TABLE OF CONTENTS
Endodontics ........................ 3
Tooth Fractures . .. . ....... . . ............. . ..... 4
SLOB Rule . ... . . ..... .. .. ... .. ....... .... . . ... 5
Apexification . . ..................... . ..... ..... 7
Pulp Capping ...... .... ...................... 7-8
Cleaning And Shaping ............ . . ..... . . ... 8-10
Endondontic Biomaterials ... ...... . ...... . . .. 10-11
Apicoectomy ......... ........... . . .......... . . 12
Endodontic Instruments .. ..... . . .... . .... . ... 13-14
Root Resorption ... .. . . ..................... 14-15
Tooth Replantation & Tooth Tissues ..... . . .. .... 15-17
Root Anatomy .............................. 17-18
Alternatives To RCT . ........ .. . .. .. ... . .. .... .. 19
Abscesses & Lesions .. ...... . .. . .. . . . . . . . .. . 20-22
Pulpitis & Necrotic Pulp .... . ........ . .. ...... 22-24
Restorations After RCT . . .. .. ................... 24
Periodontics ....................... 25
Periodontium & Gingival Fibers . . . . ..... . ...... 26-30
Flaps, Grafts, & Surgery ... . ......... . ........ 31-38
Gingivitis & Periodontal Disease ............... 39-47
Gingival Recession & Cervical Abrasion ....... . . ... 48
Hydrodynamic Theory .. ..... . ........ .. .. .... ... 49
Bacterial Plaque & CalcultJs ............... . .. 49-53
Predisposing Conditions For Periodontal Disease ..... 54
Scaling & Root Planing (SRP) & Instrumentation .. 56-60
Cementum .. . .... ... ...... . . .... ...... ..... .. 61
Occlusal Trauma & Bruxism . ............... . . 62-63
Abscesses & Cysts .......... . ............. .. 64-65
Oral Hygiene Instruction . . .. .. ... . . ... .. ..... 65-66
Chlorhexidine & LAA .... .. . .. ..... .... ....... 67-68
Oral Surgery ....................... 69
Nerves & Innervation ... .. ............. . ..... 70-72
Arteries ........... ... ......... . . ............ 73
Glands & Sinuses . . . ....................... . 74-76
Masticator Space & TMJ .. . . . ......... .. ..... 77-79
Fractures & Surgery .... ..... . .... . . . ... ..... 79-82
Anesthesia & Nitrous Oxide . . ..... .... ...... . . 83-90
Dental Emergencies & Management .. . ......... 91-93
Exodontia & Antibiotic Prophylaxis .... . ... . . ... 94-95
Ludwig's Angina & Spaces . . . .... .......... . . 96-97
Flaps & Sutures . .. ... .. ........ . ...... . .... 97-98
Impactions ..... . ...... ... .. ........ . . ....... . 99
Complications & Wound Healing .... . . . ...... 100-102
Grafts, Alveolplasty, Transplantation .......... 102-105
Implants ............................ . .. . 105-106
Lesion Biopsy . . ............ ... .. .. ....... 106-107
Medical History Considerations &
Pre-Surgical Testing ......... . . .. .... . .. 108-111
Ecchymosis, Osteoradionecrosis, & CPR ....... 111-113
PTH, Cushing's Syndrome & Diabetes . . ....... 114-117
Vital Signs & Medical History . .. . . .. ..... . ...... 118
Pharmacology .................. .. 119
Catecholamines .............. .. ........... .. . 120
Andrenergics (Sympathetics) .... . . . . . . . . . ... 121-125
Anti-Adrenergics (Beta & Alpha Blockers) .... . . 126-128
Cholinergic Fibers & Acetylcholine Receptors ... 129-130
Anti-Cholinergic Drugs .. .. ..... . ...... . . . . 131-132
Nicotinic Blockers . .... ..... .. ....... . . . .... .. 132
Drug Administration Routes & Metabolism ..... 133-136
Dea Drug Schedule & Prescription Writing .. . .. 136-137
Anesthetics & Dosages .................... 138-142
Chloral Hydrate And Nitrous Oxide ... . ........ 143-144
General Anesthesia . ............ . ....... . . 144-146
Anti-Anxiety Drugs . ......... . ...... . . ..... 146-148
Cardiovascular Drugs & Diuretics . . . . .. . . .... 149-153
Corticosteroids ... . . . . . ... . . . .. .. .. . ...... 154-155
Anti-Depressants & SSRls ....... . . ......... 155-157
Anti-Psychotics .. ....... . ... ... . ... . . .. .. ... . 157
Antihistamines ..... . ........................ 158
GI Drugs .. .. . .................... .. ...... . .. 159
Anti-Epileptics, Sulfonamides, &
Penicillin Allergies .............. . ... . .. 160-161
Penicillin, Beta-Lactamases, & Clindamycin ... 162-165
Antibiotic Prophylaxis .. . ... . ..... ... . ... . .. 166-167
Tetracyclines ... . ... ....... .. ................ 167
Macrolides & Cephalosporins ............ . .. 168-169
Parkinson's TB, & Anti-Malaria Agents ........ 170-171
Anti-Fungals, Anti-Protozoals, & Anti-Virals .... 172-174
NSAIDs (COX 1 And COX 2), Heparin & Warfarin . 175-179
Acetaminophen, Codeine, & Hydrocodone . . .... 179-181
Opioids (Narcotics) . . ..................... 181-183
Drug Efficacy & Potency .................... 184-185
Oral Contraceptives & Xerostomia .......... . .. . . 186
Anti-Neoplastic (Anti-Cancer) Drugs . ... . .. . . . .. . . 187
Anti-Diabetic Drugs ... . ... ............ ..... . .. 188
Continued on page 2
 TABLE OF CONTENTS (Cont.)
Oral Pathology .. . . ............. .. . 189 Indirect Retainers (Rests, Minor Connectors,
Proximal Plates) "" " " " ,"' .. .. , , ' , ' 321-325
Metabolic & Genetic Diseases in Dentistry", " 190-194
Chromium-Cobalt Alloys " , " " "" """" 325-326
Inflammatory Lesions"", .. ," "' , .. .. , " 194-195
Fixed Partial Dentures (FPDs) "" "" '"", , 327-329
C.T. Lesions & Oral Path Terminology " , " " " 195-200
Porcela in & PFM Properties " " " "" ". " " 329-335
Neoplasms , , .. , .. , , , , , , , , , , ' , ' , ' , .. ' , , , , 201 -206
Cements, , , , , , , , , , , , , , , , , , .. , . , .. , .... , , , , , ' 336
Odontogenic Abnormalities, ' , , , , , ' , ' , ' , , , , , 207-210
Fixed Bridges "" " " , , , , , , , , , , .. , , , , , , , , 337-339
White Lesions, , , , , , , , , , , , , , , , , , , , . , , , , , , , 210-213
Dental Lab Fabrication Techniques, , , , , , , , , , , 340-342
Blood Diseases , , .. , , , , , , , , , , , , , , , , .. , , , , , 214-217
Occlusion """"""" " ", ', ' ," " ' , ' , 342-352
Neurologic & Muscle Disorders " " "" "" ,,218-219
Impression Materials , , , , , ' .. , , , , .. , , , .. , , , 352-357
Non-Odontogenic Cysts """""" " " " " 220-221
Non-Odontogenic Tumors , , , . , , , , , , , , , , , , , , , 221-224 Gypsum "", '," "" " """" " " ." " 358-359
Provisional (Temporary) Restorations , , " ', "" ' " 360
Odontogenic Cysts, , , , , ' , , . , , , , , , , , , , , , , , , 224-226
Odontogenic Tumors " " "." "" " " "'" 226-230 Operative Dentistry .. . . . .. . ... . . . .. 361
Pigmented Lesions , , , , , , , , , , , , , , , , , , , , , , . , 230-232
Cements, Bases, & Cavity Liners , , ' , , , , , , , , , , 362-367
Pseudocysts (No Epithelial Lining) " . "" " """ 233 Caries .. , , , , , .. , , , , , , , .. , , , , , , .. .. , .. , , , 368-371
Red -Blue Lesions , , , , , , , , , , , , , , , , , , , . , , , , , 234-235
Gold, Onlays, & Inlays .. , " " "' , .. , "" ' " 371-377
Salivary Gland Tumors, , , , , , , , , , , , , , , , , , , , , 235-239
Investing & Casting, Preparation Reduction , , , , 377-380
Ulcerative Conditions, , , , , , , , , , , , , , . , , , , , , , 240-242 Com POSI'te " """ " " " " ' , " " , "' , '" 380-386
Vesiculo-Bullous Diseases, , , , , , , , , , . , , , , , , , 242-247
Amalgam, Pins, & Preparation ""." " "' " 386-396
Verrucal Papillary Lesions, , , , . , , , , , , , . , , , , , , , , , 248
Rubber Dam , , , , , , , , , , , , , , , , , , , . , , , , , , , , , 396-398
Pediatric Dentistry . . .. .... . . . . .... . 249 Dental Biomaterials , , , , , , , , , , , , , , , , . , , , , , , 398-400
Operative Hand Instruments & Burs " " , . , , , , 400-403
Pediatric Drugs " ', .. , ', " " ", .. , .. ' .. " " " 250
Operative Dentistry Study Pearls, , , , , , , , , , , , , 404-414
Primary Teeth Pulp Treatments " , ', " "" ' " 251-252
Pediatric Diseases & Conditions, , , , , , , , , , , , , 253-260 OSHA . . . .. . ....... .. .. . ......... . 415
Odontogenic Abnormalities " "" " """'" 260-262
Behavioral Management & Therapy """",, 416-420
Tooth Development, Anatomy, & Eruption " " " 262-268
Universal Precautions & Waste Management ' " 420-422
Fluoride & Sealants " "" , """ " " """ 269-277
Hepatitis, Exposure Management, & Sharps, , , , 422-425
Tooth Trauma & Treatment , , , , , ' , , , , , , . ' , , , , 277-280
MSDS & EPA , , ' , , , , , , , , , , , , , , , , , , ' , , , , , , , 425-426
Behavior Management, , , , , , , , , , . , , , , , , , , , , 280-282
Public Health (Sensitivity, Specificity,
Orthodontics .. .. ....... . .. . .... . .. 283 Prevalence, Incidence) ,,"" """" "" 426-427
Dental Index, Vital Statistics,
Occlusion & Malocclusion , , , , , , , , , , , , , , , , , , ,284-289
Randomized/Blind Studies, , , , , , , , . , , , , , , 427-430
Cephalometric Analysis & Landmarks , , , , , , , , ,290-291
Infection Control " " "" " ""' ." " " ' " 430-436
Mixed Dentition, Serial Extractions,
Space Maintenance, , , , , , , , , , , , , , . , , , , , ,292-295 Radiology . . . . . . .......... . .... . . . 437
Orthodontic Appliances, , , , , , , , , , , . , , . , , , , ' ,296-300
Radiolucency & Osteoradionecrosis " "" " "" , , 438
Bone Growth "" " " " " ', .. , ' , .. , .. " ".301-302 Digital Radiography , , , , , , , , , , , , , , , , . , , , , , , 439-440
Prosthodontics . .... .. .. ... ..... . .. 303 Filtration & Radiation Exposure , , , , , , , . , , , , , , 440-442
Types of Radiographs, , , , , , , , , , , , , , , . , , , , , , 442-447
Acrylic Resins & Complete Dentures , , , , , , , , , , 304-316
Darkroom Chemicals & Errors, , , , , , , , , , , , , , , 447-448
Removable Partial Dentures (RPD) &
Radiograph Techniques & SLOB Rule "'"" , , 448-450
Kennedy Classification " " """'. " ' " .317-318
Focal Spot, Half-Value, Kvp, Ma,
Major Connectors , , , , , , , , , , , , , , , , , ' , , , , , , , 318-319
Density, Contrast, X-Ray Tube Parts """ , 451 -453
Distal Extension & Altered Cast,
Radiograph Prescriptions and Structures , , , , , , 454-456
And Stress-Breakers, .. , , , .. , , .... .. , , .. 319-320

2
 EHRFTER 1

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 Diagnostic Aids to identify a Vertical Root Fracture:
.....
z
c 1. Fiberoptic light for transillumination.
o
c
o
2. Wedging the tooth in question and take an x-ray.
z
:::! 3. Persistent periodontal defects in an otherwise healthy tooth.
C")
4. Have patient bite forcefully on a bite stick (tooth slooth).
""
Root fractures are only visualized on a radiograph if the x-ray beam passes THROUGH THE FRACTURE
LINE. Since the fracture line can extend diagonally, an additional radiograph is taken with a steep (45°)
vertical angulation in addition to the conventional 90° degree.

Inlays can cause fractures. If a patient complains of pain during mastication since inlay placement,
suspect a fractured cusp (using a bite stick or tooth slooth helps determine which cusp is fractured).

VERTICAL TOOTH FRACTURE - symptoms and clinical tests show pulpal pathosis in a posterior
tooth, but no decay or restoration in any proximity to the pulp on the radiograph is pathognomonic of a
vertical tooth fracture.

• Radiographic exam rarely reveals the fracture because the crack is usually parallel to the x-ray
film . Radiographs (without first wedging the tooth) RARELY show vertical tooth fractures.

• Vertical fractures through root structures have an almost HOPELESS prognosis, unless the
fractured segment can be removed, and gingivoplasty &alveoplasty are performed. However,
unrealistic or overambitious case selection leads to failure.

• A tooth with a vertical root fracture has a POOR prognosis. Studies show most vertical root
fractures are caused by using too much condensation force during obturation with gutta-percha.

Anterior tooth root fractures, usually occur in a more HORIZONTAL PLANE and may be visible on the
radiograph. Anterior tooth fractures are usually due to accidental trauma (i.e. blow to the jaw/teeth). If
the fracture line is not too far down the root, it may be saved with RCT and a crown.

Therapy for horizontal root fractures is always difficult. Root canal treatment (RCT) is NOT indicated
if the fracture site remains in close proximity and if pulp retains its vitality. However, if clinical
symptoms develop, or the segments appear to be separating on the x-ray, some treatment is necessary.

CRACKED-TOOTH SYNDROME - one of the most frustrating dental conditions involving the possible
need for endodontic treatment, because its symptoms are usually characterized by a SHARP, but BRIEF PAIN
occurring unexpectedly only when the patient is chewing. Having a patient bite forcefully on a bite stick
(tooth slooth) and noticing the cusps that occlude when the pain occurs helps locate the cracked tooth .

SUBMARGINAL CURVED FLAP (SEMILUNAR FLAP) - a half-moon shaped flap raised with a
curved horizontal incision in the mucosa or attached gingiva with the concavity towards the apex. While
it is simple and does not impinge on surrounding tissue, its disadvantages outweigh its advantages, thus
it is NOT used for anterior tooth root-end surgery.
1. limited access and visibility.
2. tearing of incision corners when trying to improve accessibility by stretching the flap.
3. if a lesion is larger than expected, the incision lies over the bony defect, and healing
occurs by scarring.
4. incision extent is limited by attachments (i.e. frenum, muscles).

SUBMARGINAL TRIANGULAR & RECTANGULAR FLAP (OCHSENBEIN-LEUBKE) - requires at

least 4mm of attached gingiva and a healthy periodontium. This flap is raised by a SCALLOPED INCISION
in attached gingiva with lor 2 vertical incisions. Less risk of incising over bony defects, with no post-
surgical gingival recession. May be indicated for root-end surgery on an anterior tooth.
• Disadvantages: hemorrhage from the cut margins & scarring.
• Advantages: better access & visibility than a semilunar flap, but NOT better than a
full mucoperiosteal flap.

4
FULL MUCOPERIOSTEAL FLAP (FULL-THICKNESS) - allows MAXIMUM access & visibility. This ,...,
wide flap is raised from the gingival sulcus (elevating gingival crest & interdental gingival), and its :z:
c
c
outline precludes any incisions over bony defects, and allows various periodontal procedures (i.e. c
c::>
:z:
curettage, SRP, bone re-shaping). Can be indicated for root-end surgery on an anterior tooth. ...,
:::!
Disadvantages: it's a large flap that may be difficult to reposition, suture, make alterations, and post- en
surgical gingival recession is possible.

ELECTRIC PULP TESTER (EPT =VITALOMETER) - usually elicits a response at a HIGHER current
than normal if the tooth being tested has CHRONIC PULPITIS. EPT checks tooth sensibility/vitality by
stimulating nerve endings with a low current and high potential difference in voltage. While EPT
manufacturers give normal reference values of current the BEST way to check "normal/baseline" values
is to use it on adjacent (non-pathological) teeth, then compare the normal values with the values
obtained on the tooth in question. EPT Responses:
1. Acute pulpitis-indicated by a lower than normal current, as acute inflammation mediators
lower the pain threshold .
2. Chronic pulpitis-indicated by a response at a HIGHER current than normal.
3. Hyperemia-indicated by a LOWER than normal current, but a higher current than with an
acute pulpitis.
4. Pulp necrosis/Abscess-indicated by no response at any current level.

EPT is NOT reliable in these circumstances:

1. Pus-filled canal or a nervous patient (gives a false +).
2. Recent dental trauma, an insulating restoration, or wearing gloves (gives a false (-) response).
Do not wear gloves when using the EPT.
3. Secondary dentin deposits, moisture contamination, immature tooth (open apex), patient
taking analgesics, improper application, or weak EPT batteries.

Buccal Object Rule (SLOB Rule = Same lingual, Opposite Buccal) - a shift-cone
technique/rule that allows the dentist to determine on the radiograph which canal is the buccal and
which is lingual. Buccal object rule also allows one to determine working length of superimposed canals,
root/canal curvatures, and the facial-lingual orientation of instruments or other anatomical objects.

• The lingual surface is always CLOSEST to the cone, while the buccal surface is always FARTHER
away from the cone. To apply SLOB rule, you MUST have a reference object.

• If taken from the mesial, the lingual surface (ML canal) will appear more mesial (closer to the cone)
than buccal surface (MB canal) which appears farther distally.

• If taken from the distal, the lingual surface appears more distal (closer to the cone) than the buccal
surface which appears father mesially.

• According to buccal object rule, when the x-ray tube is repositioned either at a more mesial or more
distal angulation and a film is exposed, the root/canal farther from the film (the buccal) moves in
the SAME direction that the cone is directed. Thus, when the cone is aimed to the distal (angled
from the mesial direction), the buccal root/canal moves to the distal and appears distal to the
lingual/palatal root/canal.

• The object toward the lingual side (closer to the film) appears to shift on the film to the same
direction as the repositioned x-ray cone. If the x-ray cone is angulated mesially, the lingual/palatal
root shifts toward the same (mesial) side in the resultant radiograph, and is easily visualized.

• When treating multi-canaled bicuspids & molars, it is often difficult to determine radiographically
which canal is more toward the buccal. When a straight-on exposure is taken of a bicanaled tooth,
the canals become superimposed on the film, and visualization of each canal is impossible. If the
x-ray cone is moved to give an angled exposure, the roots will be separate on the film.

5
,..., Diagnostic tests indicated for recently traumatized teeth:
:z: 1. Soft tissue exam to observe lips, face, tongue, etc.
""
""""<:> 2. Hard tissue exam to visually look and then palpate the injured tooth and alveolus to reveal the
:z:
:::! extent of tooth mobility, any alveolar fractures, and areas of inflammation. Check for occlusal
C">
en disharmonies to help detect tooth displacements and jaw fractures.
3. Radiographic examination to reveal tooth displacement, root fractures, previous RCT,
periapical radiolucencies.
4. Other diagnostic tests. EPT (pulp vitality testing) is CONTRAINDICATED since the traumatized
pulp undergoes temporary paresthesia thus giving a false reading. A percussion test is NOT
usually performed since it is painful.
5. Observe adjacent and opposing teeth for injury.

Traumatized teeth may be fine for a long time, but many develop radiolucencies. Thus, do not
indiscriminately do root canals before checking pulp vitality. Perform RCT only in teeth that do not respond
to pulp testing (i.e. trauma to maxillary anterior teeth . A few years later x-rays reveal radiolucencies
around incisor apices). Check pulp vitality of all anterior teeth before performing root canals.

Trauma causing deep intrusion to a permanent tooth causes PULP NECROSIS and conventional RCT
is necessa ry.

Radiation Safety: Endodontic procedures involve taking multiple radiographs.

1. To protect the dentist and staff if there is no barrier available to stand behind, the stand at
least 6 feet away in the area that lies between 90-135° to the x-ray beam (an area of minimal
scatter radiation).
2. Afast (sensitive) film like "E-speed" film is preferred over slower films, since faster films
require less radiation exposure while providing a quality image.
3. Dental units should operate at 70kVp or higher. The higher kVp = lower patient skin doses
or radiation.
4. Collimation (i.e. restricting x-ray beam size so it does not exceed 2.5inch at the patient's skin)
decreases exposure.
5. Patients must be protected with a lead apron and thyroid collar for each exposure.
6. Dental personnel who may get exposed to occupational x-radiation MUST wear film badges
to record exposure, and must never exceed the max permissible dose (MPD) of 50mSv per
year per person.

Pulpotomy-removal of a portion of the pulp that is indicated for:

1. cariously exposed deciduous (primary) teeth with healthy radicular pulps.
2. traumatic or carious exposure of permanent teeth with undeveloped roots.
3. an alternative to extraction when endodontic treatment is not available.
4. emergency treatment in permanent teeth with acute pulpitis.

Pulpotomy procedures performed on fully developed permanent teeth are NOT successful. Thus, it is
only a temporary procedure for fully developed permanent teeth.

While doing a vital pulpotomy on a young, immature permanent tooth, if hemorrhage after pulpal
amputation cannot be controlled with cotton pellets even after several minutes, the next step is to
perform the amputation at a more apical level.
• Uncontrolled bleeding is a sign of inflamed pulp tissue. Radicular pulp must be uninflamed for a ----
successful pUlpotomy. It is not uncommon to find uninflamed pulp at a more apical level, especially
in cariously exposed teeth .

• If bleeding does not stop even after more apical amputation , then hemostatic agents are used as a
compromise treatment. These are closely monitored, and if pulp vitality is lost, then apexification
(pulpectomy) procedures are performed .

• Pulpotomy is the removal of the pulp chamber contents only.

6
APEXIFICATION - goal is to INDUCE FURTHER ROOT DEVElOPMENT in a pulpless tooth (dead tooth) ,....,
by stimulating the formation of a hard substance at the root apex to allow obturation of the root canal :z:
c
o
space. Apexification may be required after pUlpectomy (as at age 7, the root apex must be open). The apex c
o
:z:
closes 2-3 years after eruption . ..,
:::!
1. Isolate the field with a rubber dam, make an access cavity, and remove all pulp using (I)

reamers and files.

2. Premixed syringe of calcium hydroxide-methylcellulose paste (i.e. Pulpdent syringe) is
injected into the canal and filled to the cervical level. The paste must reach the apical portion
of the canal to stimulate tissues to form a calcific barrier. A double cement seal is made to
close off the access cavity.
3. Patient is recalled after 3 months to see if apexification occurred. If not, a fresh supply of
paste is placed. Once apexification occurs, only then is conventional RCT performed .

CALCIUM HYDROXIDE (CaOH) - its action promotes formation of a hard substance at the root apex
by creating an ALKALINE environment that promotes hard tissue deposition.

If a permanent tooth fractures, but has a fully formed root and the pulp is exposed (large exposure),
complete RCT is the treatment of choice. Apexification is NOT needed because the root is fully formed.
If the pulp exposure is small and the length of time is short (30min-lhr), then direct pulp capping with
CaOH followed by a restoration is the treatment of choice.

PULP CAPPING - placing a sedative and antiseptic dressing on an exposed healthy pulp to allow it
to recover and maintain normal function and vitality. Dycal (CaOH2 = calcium hydroxide) is the most
commonly used dressing.

• Pulp capping is overused in dentistry today, with very few indications for its use. Young pulps are more
vascularized, thus more amenable to repair. Accidental exposure of the pulp and the pulp of a
young child are two situations where pulp capping offers better success. Carious exposure of the
pulp or the pulp of a middle-aged person are not indications for pulp capping.

• Pulp cappings are more successful if the exposure was accidental (trauma or with a dental bur
=mechanican rather than carious. Also, the pulp exposure should only be pinpoint in size to expect
success. Repair occurs when a dentin bridge forms at the pulp exposure site. Even a small carious
exposure should have RCT for the best long-term prognosis.

• Pulp capping-not recommended in primary teeth with carious pulp exposures due to its high
failure rate and because pUlpotomy (having similar time requirements) is very successful. Pulp
capping can be done if a mechanical pulp exposure occurs.

• Atooth can stay asymptomatic for several weeks after pulp capping is performed, but this may only
be temporary. If pulp capping fails and the tooth becomes symptomatic, it may be nearly impossible
to treat with routine endodontics due to the severe calcifications in the root canal. Perforations may
occur when attempting to follow the obliterated canal to gain apical patency (perforations into
furcations of multi-rooted teeth have the poorest prognosis).

• Traumatic blows to teeth also cause pulp space calcification sometimes to a point where locating the
canal is very difficult. With primary teeth, trauma may cause calcifications in the pulp chamber,
which can cause a yellowish discoloration of the tooth.

• The success of pulp capping is recognized by the formation of a complete barrier of dentin at the site
of pulpal exposure.

7
 Two Pulp Capping Procedures:
I'T'I
:z: 1. Indirect Pulp Capping-a calcium hydroxide base is placed on a thin layer of questionable
""
o
dentin remaining over the pulp. It is performed when a carious exposure is anticipated. After a
""
o
:z:
:::! 3-4 month waiting period, the tooth is re-opened and remaining decay is removed. During the
n
en waiting period, hopefully secondary dentin formation occurred, allowing complete removal of the
decay without pulp exposure.
• Ex: a radiograph of a 1st molar shows gross decay that may involve a dental pulp horn. The
ideal treatment is to do an indirect pulp cap and place a sedative filling (lRM). If the tooth
remains asymptomatic, in 3-4 months you can re-enter the tooth and remove all decay with
subsequent placement of a permanent filling. *If this patient had tooth pain (aggravated by
heat and tender to percussion), and excavation of the caries revealed pulp horn exposure
without evidence of vital tissue, the emergency treatment pending eventual RCT is to place a
small cotton pellet dampened with eugenol over the exposure and seal the cavity with a
temporary material (lRM).

1. Direct Pulp Capping-placed a calcium hydroxide base directly on a pulpal exposure. Favorable
factors for direct pulp capping:
• Visual evidence of un-inflamed (pink) pulp tissue.
• Absence of cop ious hemorrhage through the exposure.
• No previous symptoms of pulpitis.
• Small non-carious exposure (mechanical pulp exposure)
• Clean cavity uncontaminated with saliva .
• Direct pulp capping is very successful in immature teeth.
• Direct pulp capping involves prompt application of a setting calcium hydroxide cement to a
small « 1mm in diameter), well isolated traumatic pulp exposure. Direct pulp capping is
expected in most instances, to stimulate formation of a reparative "dentin bridge" over
the exposure site and preserve underlying pulpal tissue in a healthy condition.
• Direct pulp capping should NOT be attempted on teeth with a history of pain, sensitivity to
percussion, or periapical radiolucencies. Instead, RCT may be indicated.
• Failure of a direct pulp capping procedure is indicated by symptoms of pulpitis at any time,
or the lack of vital response after several weeks or months.
• Adverse responses that can occur after a direct pulp capping procedure :
• Physical or microbial insult to the pulp may cause persistent inflammatory chan ges that
can culminate in partial or complete pulpal necrosis.
• Regulation of the mineralization process involved in dentin bridge formation may become
deranged, causing extensive calcification and obliteration of the pulp canal spa ce by
mineralized tissue.
• Very rarely, the differentiation of odontoclasts may be induced with the development of
internal resorptive lesions.

Criteria that must be met BEFORE a canal is obturated with gutta-percha:

• Canal must be prepared in a manner that ensures optimum canal debridement and access to the
apical area so the filling material can be condensed to obliterate the entire preparation.
• Tooth must be asymptomatic, and canal must be dry at the time of fill.
• If a bacteriologic culture test is being used, a negative culture must be obtained .

Atooth prepared for RCT that responds to thermal tests, indicates inadequate debridement (cleaning),
since a pulpless tooth should NOT respond to any stimuli . Thus, all nerve must be removed before the
canal is obturated .

Access Preparation Objectives: straight-line access, conservation of tooth structure, pulp chamber
un-roofing, and remove pulp horns.
• Root canal access is the INITIAL STEP in canal preparation. Straight-line access to the apica l
foramen must be established to ensure free movement of the instrument during debridement and
canal preparation. All subsequent treatment hinges on the correctness of the access preparation.
• All access cavities are made through the LINGUAL on anterior teeth &OCCLUSAL on
posterior teeth.
• Afacial access is recommended for maxillary primary incisors.

8
Access Preparation:
• Mistakes l: During mandibular molar access preparation, two regions tend to be "overcut" resulting
NOTES ,...,
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in undesirable over preparation of the canal access (mesial aspect under marginal ridge &lingual CI
c
CI
surface under lingual cusps). Mandibular molars tip mesially and lingually, thus if a bur is directed :z:
::::!
straight inferior, it may cause unnecessary loss of tooth structure in the mesial and lingual areas. n
~

• Mistakes l: mandibular incisors &maxillary 1st premolars are the EASIEST teeth to perforate
during access preparation due the limited access mesiodistally. Thus, care must be taken when
initiating treatment on these teeth .

DEBRIDEMENT - the removal of foreign material & contaminated or devitalized tissue from or
adjacent to a traumatic infected lesion until surrounding healthy tissue is exposed. Chemomechanical
debridement of the root canal system is the MOST crucial aspect of root canal treatment.

• Achieving GLASSY, SMOOTH CANAL WALLS is the BEST and most reliable indicator of adequacy of
root canal debridement.

• Obtaining clean canal shavings on a file or clean irrigating solution are INACCURATE measures
to determine the end point of debridement.

• MOST important consideration BEFORE filling a root canal is PROPER CLEANING (debridement) and
SHAPING (instrumentation) of the canal. Once the canal is obturated, any organisms that enter
periapical tissues from the canal are eliminated by the body's natural defenses. The MOST common
cause of root canal failure is incompletely and inadequately disinfecting the root canal system.

• SECOND most common cause of root canal failure is LEAKAGE from a poorly filled canal. This is
common even after apical curettage (i.e. RCT performed on a tooth with apical curettage of a lesion
that was found to be a cyst. 3 years later the lesion was even bigger than before). Thus, the failure was
due to LEAKAGE from a poorly filled canal. When a canal is prepared properly, any of the acceptable
filling methods will produce a successful result as long as the canal is COMPLETELY filled.

• Complete canal debridement is the MOST EFFECTIVE way to reduce canal microorganisms.
Debridement is done using various ways depending on the case, and may involve canal
instrumentation, placement of medicaments/irrigants, and/or surgery.

Objectives of Root Canal Obturation (Filling with Gutta-Percha):

1. Develop a fluid-tight seal at the apical foramen .
2. Complete filling of the root canal space.
3. Create a favorable biologic environment for the process of tissue healing.

The importance of canal obturation (filling) is SECOND only to canal debridement. -40% failures are
caused by incomplete obturation of the canal (most failures are due to incomplete debridement). If the
canal is not filled, tissue fluid and microorganisms from periapical tissues can enter the voids, causing
endodontic failure. However, if an accessory (lateral) canal is not totally filled during obturation, the
appropriate treatment is to observe the tooth and evaluate every 3 months.

After RCT is completed on a tooth with a periapcial radiolucency, it takes 6-12 months before a
marked reduction in the size of the radiolucency is evident on a radiograph. Desired periapcial tissue
changes are regeneration of alveolar bone, deposition of apical cementum, and POL re-establishment.

Indications for using solvent-softened custom gutta-percha cones: lack of an apical stop, abnormally
large apical portion of the canal, or an irregular apical portion of the canal. Tugback within 1mm of
working length is NOT an indication.
• Studies show solvent softening DOES NOT ultimately result in a better apical seal. Thus, this
time consuming procedure is not used if tugback (slight resistance to dislodgement) is achieved.
The gutta-percha cone should also have a definite apical seat (should not be able to be pushed
further apically).
• If the canal preparation is properly flared, fitting the master cone is not a time-consuming procedure.
A gutta-percha cone the same size as the last file used during preparation (MAF) is selected and
placed as far as possible into the canal, but NOT past the working length.

9
,..., • Once tugback and apical positioning are obtained, a radiograph is taken to verify cone positioning.
:z:
CI
If an accurate determination and careful enlargement are performed, the x-ray will show the master
CI
CI
c:::>
cone reaching the most apical position of the preparation or extending just 1mm short of the
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en
apical foramen. When the cone is sl ightly short, the pressure of condensation & the sealer's
lubrication action are sufficient to produce complete seating of the cone. If the cone is > lmm from
the radiographic apex, remove the cone and fit a smaller one, or instrument more in the apical third.

• MAIN reason for recapitulation (using your MAF after each increase in file size) during
canal instrumentation is to clean the canal's apical segment of any dentin filings not removed
by irrigation.

When regaining CANAL PATENCY:

• A "crown-down" sequence (larger to smaller) of instruments is used from coronal to apical.
• Rotary instruments work faster and improve the access early in the treatment compared to
heated instruments.
• Very light apical pressure is applied when using Nickel Titanium (NiTi) rotary files .
• Over-extended gutta-percha cones had to be removed by extending the file periapically.
• Glass Bead Sterilizer-sterilizes endodontic files in 15 sec at 220° C(428°F).

If a gutta-percha cone passes past the apex, a file must then be used beyond the apex to avoid breaking
the cone. Abroken cone in the periapical area can cause orthograde re-treatment failure.
• Techniques to remove gutta-percha: rotary instruments, ultrasonic, heat, heat & instrument, and
file & chemical.

CHLOROFORM - reagent of choice to DISSOLVE gutta-percha. Highly concentrated chloroform is very

effective, but use with caution because its vapor is potentially hazardous so it is dripped directly in the
canal to avoid excessive flooding.
• Other chemicals that dissolve gutta-percha: xylol, halothane, benzene, carbon disulfide, essential
oils, methyl chloroform, and white rectified turpentine.

IRRIGANTS - destroy bacteria during endodontic therapy. Irrigant's bactericidal action is much
greater than the action supplied by intracanal medicaments, thus are used GOPIOUSLY throughout the
instrumentation phase of root canal procedures.
1. Sodium Hypochlorite (NaDCIl-the most commonly used IRRIGANT in endodontics to aid in
canal preparation used in concentrations of 1%,2.6%, or 5.25%. There is no agreed single-
concentration value of NaOGI that is most effective while being the safest, thus these
percentages are all acceptable.
• 5.25% solution provides excellent germicidal solvent action, but is dilute enough to cause
only mild irritation when contacting periapical tissue. Thus, gutta-percha points can
be disinfected by placing them in 5.25% NaDCI solution for 1 minute.
• NaDCI is a good tissue solvent, has some antimicrobial effects, and acts as a lubricant for
root canal instrumentation. NaDCI is toxic to vital tissue so ALWAYS use a rubber dam.

2. Hydrogen Peroxide (3% solution)-much less solvent action than NaDCI, but a widely used
irrigant in endodontics as many clinicians use H202 & NaOGI alternately during treatment.
H2D2 has two modes of action:
• Bubbling action occurs when it contacts tissue, and certain chemicals physically foams
debris from the canal (effervescent effect).
• Liberation of oxygen strictly destroys anaerobic microorganisms.

3. Urea Peroxide (Gly-Dxide)-useful irrigant available in an anhydrous glycerol base (Gly-Dxide)

to prevent decomposition. Better tolerated by periapical tissue than NaOGI, yet has greater
solvent action and is more germicidal than H202, thus is an EXCELLENT IRRIGANT for treating
canals with normal periapical tissue and wide apices.
• Best use for Gly-Oxide is in NARROW and/or CURVED canals, utilizing glycerol's
slippery effect.

10
CHELATING AGENTS - aid and simplify preparation of highly sclerotic canals after the apex is reached
.....
with a fine instrument. Chelating agents act on calcified tissues only with little effect on periapical :z:
CI
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tissue. Chelating agents act by substituting Na+ ions that combine with dentin to form soluble salts CI
CI
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for Ca+ ions that are bound in a less soluble combination.Thus, canal edges become softer, to facilitate :::!
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canal enlargement.
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1. Ethylene Diamine Tetra-Acetic Acid (EDTA)-a chelating agent that removes the mineralized
portion (decalcify) of the smear layer. EDTA's decalcifying process is self-limiting, and can
decalcify up to a 50mm thin layer of root canal wall.
• EDTA is normally used in 17% concentration.
• RC-Prep & EDTAC are types of EDTA preparations.
• EDTA has a limited value as an irrigation solution, since the decalcifying process induced by
EDTA is self-limiting and stops as soon as the chelator is used up.
• EOTA remains active in the canal for 5 days if not inactivated. Thus, upon appointment
completion, the canal MUST be irrigated/inactivated with sodium hypochlorite (NaOCI)
containing solution .
2. EDTAC-is EDTA + Cetavlon (a quaternary ammon ium compound) with a greater antimicrobial
action than EDTA, but has more inflammatory potential to tissues. NaOCI inactivates EDTAC.
3. RC-Prep-a foamy solution that combines functions of EDTA + urea peroxide to provide
chelation &irrigation. RC-prep has a natural effervescence that is increased by irrigation
with NaOCI to help remove canal debris.

ZINC OXIDE-EUGENOL - a cement with a long history of successful use as a based root canal
sealer. The MAIN function of a root canal sealer is to FILL DISCREPANCIES between the core-filling
material and the dentin walls. This function makes it even more important than the core filling material.
ZOE (root canal sealer) functions:

• Acts as a lubricant to facilitate gutta-percha cone placement.

• Forms a bond between the gutta-percha and dentin walls.

• Exerts antibacterial activity (some exert more than others) which is highest in the period of time
immediately after its placement.

• ZOE Disadvantages: staining, slow setting time, non-adhesion, and solubility.

Most root canal sealers are some type of ZOE cement capable of producing a seal while being well-
tolerated by periapical tissues. All sealers have some radiopacity (caused by metallic salts in the
sealer), thus are visible on a radiograph . This radiopacity helps disclose any accessory canals, resorptive
areas, root fractures , and the shape of the apical foramen .
• Note: after filling a canal with gutta-percha, if there is a horizontal line of material (gutta-percha
or sealer) extending both mesially & distally from the canal to the POL space, this indicates a
ROOT FRACTURE.

Mineral Trioxide Aggregate (MTA) - MOST superior retro-filling (reverse filling = retrograde
amalgam filling) material and material of choice today. MTA seals the APICAL portion of the root canal,
and is ALWAYS after an apicoectomy alone will not yield a good result. Areverse filling (MTA) MUST
always be placed when an apical seal may be faulty (i.e. with a calcified root canal, it is impossible to
obdurate most of the canal and get an apical seal. If just the root apex where cut off (apicoectomy), the
incompletely filled canal might act as a source of reinfection. To prevent this, after the root tip is resected,
the apical foramen is found , enlarged, and filled with zinc-free amalgam to create a seal.

• Advantages: radiopaque, hydrophilic, biocompatible, non-toxic, induces hard tissue formation .

• Disadvantages: difficult to manipulate &long-setting time.

11
,..., APICOECTOMY (ROOT RESECTION = ROOT AMPUTATION) - a procedure where the buccal
:z:
CJ
CJ
tissue is flapped back, the buccal bone around the root apex and the root apex itself are removed, and
CJ
the area is curetted out. Apicoectomy is a resection of the most apical portion of the root. It is best
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::! accomplished by obliquely RESECTING the most apical portion of the involved root.
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en

• Indications: if a reverse filling (MTA) must be placed, it is necessary to gain access to an area of
pathosis, the poorly filled apical portion of the root is to be removed to the level of canal obturation.
Retreating teeth with posts are the MOST common reason for an apicoectomy and retrograde filling.

• If a tooth with previous endodontic treatment becomes reinfected, it is best to retreat it conventionally
by removing the filling material, debride the canals, and refill. However, if the tooth has been restored
with a post, core, and crown, then apical curettage, then an apicoectomy and retrofill should be
performed.

Periradicular Surgery Indications:

1. non-negotiable canal, blockage or severe root curvature in which non-surgical treatment
is impossible.
2. complications arising from procedural accidents (i.e. instrument separation, ledging,
or perforations) that cannot be handled without surgical exposure of the site.
3. failed treatment due to irretrievable posts or root fillings.
4. horizontal apical fractures where the apical end of the pulp becomes necrotic.
5. biopsy to diagnose non-odontogenic causes of symptoms (i.e. patient with a history of
previous malignancy, lip parsthesia, or anesthesia).

PERIAPICAL CURETTAGE - the same procedure as an Apicoectomy that flaps back the buccal tissue
and buccal bone removal, but DOES NOT remove the root apex. Removal and examination of the
diseased tissue and determining the extent of the lesion are the objectives of apical curettage.

SUPEROXOL - the MOST COMMON bleaching agent for endodontically treated teeth that is a 30%
aqueous solution by weight of H202 in distilled water. It is a potent oxidizing agent whose bleaching effect
is due to direct oxidation of stain-producing substances. Tooth bleaching causes color change in enamel
and dentin.

• Chairside Technique: apply heat to Superoxol-saturated cotton pellets in the tooth chamber, and
repeat until the tooth is lighter. This heat liberates the oxygen in the bleaching agent.

• The most probable post-operative complication of tooth bleaching that has not been properly
obturated is acute apical periodontitis.

• Acute Apical Periodontitis (AAP)-characterized by pain commonly triggered by chewing or percussion.

AAP alone does not indicate irreversible pulpitis. AAP indicates irritated apical tissues possibly
associated with a vital pulp with a potential reversible pulpitis. In the absence of acute pain, a
negative EPT or frank apical radiolucency, a carious tooth with sensitivity to percussion may respond
to caries control (temporary filling). If it does not respond to a sedative filling, ReT is indicated.

• Walking Bleach Technique: place a thick paste consisting of sodium perborate and 2-3 drops
of Superoxol in the tooth chamber with a temporary restoration. Several repetitions of this
technique works well.

12
ENDODONTIC INSTRUMENTS ......
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Broken Instruments: When a broken instrument (file) protrudes past the apex, surgery should be C)
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performed to remove it because it is a constant irritant (i.e. during cleaning & shaping of a canal, your C">
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K-file (#25) separates in the canal. Your first attempt to retrieve it results in a broken instrument through
the apex). To manage this case, raise a flap and remove the instrument surgically, then fill the canal with
gutta-percha.
• It is easier to retrieve an instrument if it is wedged coronal or at the curvature of the canal, but very
difficult if the instrument has passed the canal curvature.
• When an instrument breaks off anywhere in the canal and a periapical radiolucency is present and
minimal canal enlargement has been performed before the accident, surgery is indicated since the
periapical tissues have had little opportunity for healing to be stimulated. You would prepare and
obdurate to the point of blockage, and then perform an apicoectomy Sand retrofilling.
• When an instrument breaks off in the canal's apical third and is lodged tightly with no evident
periapcial radiolucency, the remaining root canal space can be filled with gutta-percha, the patient
is informed, and placed on a 3-6 month recall.
• Prognosis of a tooth with a broken instrument is best if the tooth had a vital pulp and no
periapical lesion.

NICKEl TITANIUM INSTRUMENTS (NITI) - hand-operated or engine-driven instruments to CLEAN

& SHAPE. Nili methods:
• Push & pull stroke, reaming motion, or engine-driven rotary motion (uses only a reaming motion).
• Hand instrumentation is done by either filing (push & pull) or reaming (repeated rotations).
• The instrument's action, NOT type of instrument used, determines the canal preparation's
general shape:
• Filing-a push-pull action with emphasis on the withdrawal stroke. Its efficiency is greater
with files than with reamers to remove dentin due to the greater number of flutes in contact
with canal walls during the rasping motion of removing the file. Filing action produces a
canal that is irregular in shape, thus a canal prepared with this push-pull filing action
MUST be filled with gutta-percha in a condensation procedure.
• Reaming-repeated clockwise instrument rotation especially during insertion. A reaming
action produces a canal that is relatively ROUND in shape. A reaming method is usually most
efficient if using a silver cone to fill a canal.
• Circumferential filing-a push-pull filing action that SCRAPES canal walls to create a
smooth, tapered preparation. The file is moved first towards the canal's buccal side,
reinserted, then removed slightly mesially. This is done all the way around the canal until
all dentin walls are planed. Circumferential filing technique enhances preparation when
a flaring method is used.

Important: Acanal is instrumented and shaped so it has a continuously TAPERING FUNNEL SHAPE. The
canal's widest diameter should be at the orifice (opening), while its narrowest diameter is at the
dentinocemental junction (DCJ or .5-1.0mm from the radiographic apex). Ideally, .5-1.0mm from the
canal apex is where all teeth should be filed to and filled.

BARBED BROACHES - intracanal stainless steel instruments designed to remove pulp tissue, cotton
pellet absorbent points, and other soft materials. It is NOT used for canal enlargement. The barbs are
notched out of the instrument shaft and represent a weakened point. If the broach is not used with utmost
care or is forced apically, the barbs will bend and engage the canal walls, making removal difficult.

HEDSTROM FILES - an effective "H-Type" stainless steel CUTTING instrument made using a sharp,
rotating cutter to gauge triangular segments out of a round blank shaft to produce a very sharp edge.
Used carefully with ONLY a filing action, this file successfully planes dentin walls much faster than K-
type files or reamers. S-file-a modified Hedstrom file.

13
,...., K-Type Instruments:
:z:
CJ 1. K-Files-the most useful instruments for removing hard tissue to enlarge canals. Files are
CJ
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made by twisting a blank (a square stainless steel rod producing a series of cutting flutes).
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en
The K-type file's action in the canal is a clockwise-counterclockwise motion while directing
pressure apically (can be a filing or reaming action). K-type files are the STRONGEST and
cut the LEAST aggressively. K-flex file-a modified K-type file.
2. Reamers-manufactured similar to files, but with fewer flutes. Reamers are used in canal
preparations to SHAVE DENTIN using ONLY a reaming action to enlarge canals. Reamers
remove intracanal debris with a CLOCKWISE reaming action, and place materials into
the apical portion of the canal using a COUNTERCLOCKWISE rotation.

5 Critical Factors to Manage Traumatic Avulsion Injuries:

1. Time: the time interval from injury until tooth replacement is a MAJOR factor in maintenance of
POL viability & subsequent root resorption. Teeth replanted within 30min exhibit very little
resorption, while most teeth replanted after 2hrs have extensive external root resorption
(MAIN cause of failure of replanted teeth is external root resorption).
2. Storage Media: if the tooth cannot be replanted immediately, proper storage can favorably
influence POL cell viability. MILK is the BEST storage media due to its near neutral pH (6.5-6.8)
and osmolality which is conducive for cell survival. Physiologic saline and saliva are other tooth
storage media.
3. Tooth Socket: should not be damaged by curettage or forceful replantation.
4. Root Surface: should not be scraped, dried, or manipulated with caustic chemicals.
5. Splint Stabilization: a splint that allows physiologic movement is placed for a maximum of
2 weeks to allow the initial reattachment of the POL fibers.

*When a tooth has been avulsed (out) of the mouth for> 2hrs, the treatment of the tooth socket, root
surfaces, and time required for splint stabilization changes.

Proper management of an avulsed PERMANANT tooth replanted by the dentist within 2hrs of
the accident:
• 10-14 days after replantation, clean and shape (prepare) the root canal, and place calcium
hydroxide paste into the canals. Replace this paste every 3 months for on year. After 1 year, if the
root resorption has reversed or stopped, a permanent gutta-percha filling can be placed.

Proper management of an avulsed PERMANANT tooth out for> than 2hrs of the accident:
• Ankylosis & external root resorption will probably occur within 2 years. Ankylosis caused by the
replacement gives a better prognosis than external root resorption which leads to failure.
• ReT is performed in its entirety PRIOR to replantation.
• Soak the tooth in 2.4% fluoride solution acidulated at 5.5pH for at least 20m in . Fluoride slows the
resorptive process.
• Gently curette the blood clot out of the alveolar socket and irrigate with saline.
• Rinse the tooth with saline, replant it into the socket, and splint for 4-6 weeks.

Avulsed Tooth Management:

• After 60 min of dry storage of an avulsed tooth, few periodontal ligament cells survive.
• Storage of an avulsed tooth in tap water is as bad as dry storage.
• Saliva is hypotonic, thus allows storage for up to 2hrs, but MILK has a maximum storage time
of 6hrs.
• Teeth with complete root development should be treated endodontically ASAP even if replanted
within 30 min.
• Teeth with incomplete root development that are replanted within 30 min may not require
endodontic treatment.

ROOT RESORPTION - the MOST frequent sequela to avulsed tooth replantation.

EXTERNAL ROOT RESORPTION - caused by periradicular inflammation, dental trauma (resulting

in damage to attachment apparatus), excessive orthodontic forces, impacted teeth, bleaching of non-vital
teeth. External resorption is ALWAYS accompanied by bone resorption and is the chief cause of failure
of replantation of permanent teeth (it is the main cause of failure of replanted teeth). 3 Types of
External Root Resorption:
14
 1. Surface resorption-caused by acute injury to the POL &root surface. If injury is not repeated, N ..,
healing occurs forming new cementum and POL. Root surface resorption is limited to cementum, :z
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may heal itself, and is not visible on a radiograph. c
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2. External Inflammatory resorption-external resorption in which an infected pulp may further :z
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complicate the resorptive process. Characterized by bowl-shaped resorption areas involving C">
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cementum and dentin that rapidly progresses and continues if treatment is ignored.
• Necrotic pulp and bacteria are necessary components of inflammatory resorption. Thus, this
process is arrested with immediate RCT (open the tooth, clean &shape the canal, and place
calcium hydroxide paste in the canal every 3 months for 1 year). If resorption stops after 1
year of treatment, then place a permanent root canal filling (gutta-percha). Acalcium
hydroxide-based root canal sealer is strongly recommended.
• cervical root resorption does not occur exclusively at the cervical area of the root. Pulp does
NOT playa role in cervical root resorption.
3. Replacement resorption (ankylotic resorption)-external root surface resorption that becomes
substituted by bone, causing ankylosis (common in unsuccessful avulsed tooth replant cases) .
Replacement resorption accompanies dento-alveolar ankylosis due to extensive trauma to the
tooth's attachment apparatus. It is characterized by progressive replacement of the root by bone.
Histologically, it shows direct contact between dentin and bone, with no intervening POL or
cementa I layer.
• Pathognomonic signs of external resorption: lack of mobility, metallic sound to percussion,
and infra-occlusion of the involved tooth in the developing dentition.

INTERNAL (INFLAMMATORY) ROOT RESORPTION - caused by dental trauma, partial removal

of pulp (pulpotomy), caries, pulp capping with calcium hydroxide, or a cracked tooth. Internal
resorption causes loss of pulp vitality & subsequent infection of coronal pulp causing inflammation.
Inflammation due to an infected coronal pulp is generally the cause of internal resorption. Teeth with
internal resorption have a history of trauma, crown preparation, or pUlpotomy.

• Internal resorption is often precipitated by traumatic injury to the tooth. Undifferentiated

reserve C.T. pulp cells are activated to form dentinoclasts that resorb the tooth structure in
contact with the pulp.

• Internal resorption is usually asymptomatic, and discovered on routine radiographic evaluation. The
root canal's anatomic configuration is altered and increases in size, appearing as an irregular
radiolucency anywhere along the canal space. Radiographic presentation of internal resorption is
a fairly uniform enlargement of the root canal space. The root canal "disappears" into the lesion.

• Sometimes on a radiograph, an external resorptive lesion can superimpose the canal space to mimic
internal resorption . In such cases, another radiograph is taken at a different angle since the
radiolucent lesion inside the canal space will not shift.

• Atooth with internal resorption may respond to pulp vitality tests, but when detected, a pulpectomy
should be performed. Once the pulp tissue responsible is removed, all resorption stops. To "wait and
see" may cause sufficient destruction to perforate the root.

• While internal resorption can occur ONLY when some pulp tissue is still vital, a NEGATIVE sensibility
test does NOT rule out this etiology.

• Pink Tooth-a pathognomonic sign of internal resorption (not replacement resorption), and
sometimes a sign of cervical root resorption, characterized by a pinkish appearance of the tooth due
to granulation growth undermining the coronal dentin .

INTENTIONAL REPLANTATION (REPLANT SURGERY) - a tooth that requires endodontic therapy

is purposely REMOVED from its socket, some type of canal or apical preparation and/or filling is performed,
and the tooth is RETURNED to its original socket. Replant Surgery Indications:
1. When routine endodontic therapy is impractical or impossible.
2. When a canal is obstructed via a broken instrument or calcification, and periapical surgery is
impractical (a lower molar with the mandibular canal is close proximity).
3. When perforating internal or external is present, yet surgery is impractical.
4. When previous treatment has failed, but non-surgical treatment or surgery is impractical.
15
 Intentional replantation is considered ONLY when there is no other alternative treatment to maintain
a "strategic" tooth. Long-term follow-up is required to monitor for complications, periodontal defects,
and ankylosis with replacement resorption.

Procedures essential for successful intentional replantation of an avulsed tooth include: skillful
extraction, minimum out-of-socket time, minimum root damage while the tooth is held during apical root
end preparation, and repair of any perforation or resorptive defect before replantation.
• Curettage of the socket to remove periapical pathosis is unnecessary because the socket wall should
be MINIMALLY manipulated during replantation.

Replantation of a PRIMARY TOOTH is NOT recommended due to potential danger to the permanent
successor tooth from sequels of trauma (i.e. infection, ankylosis, or damage due to manipulation
during the procedure). Thus, if a mother of a 4 year old child calls your office reporting that her child
has suffered a trauma to one of his front teeth that has avulsed out of the socket, advise the mother
to leave the tooth and come to the office immediately.

PULP - primary function of pulp is DENTIN FORMATION. Other pulp functions:

1. induction-forms dentin which then induces enamel formation .
2. nutrition-dentinal tubules are linked to the pulp to maintain pulp hydration and formation
of peritubular dentin.

MANTLE DENTIN - the first formed dentin that is laid before the odontoblast layer is organized. Thus,
the pattern of deposition and size of collagen fibers differs from circumpulpal dentin .

CIRCUMPULPAL DENTIN - represents most of the dentin formed.

SECONDARY DENTIN - forms after tooth eruption & throughout life, resulting in a gradual, but
asymmetric reduction in pulp size.

TERTIARY DENTIN (REPARATIVE DENTIN) - an irregular and disorganized dentin layer laid down
in response to any injurious or irritant stimuli.

As dental pulp ages, the number of reticulin fibers decreases (pulp becomes less cellular and more
fibrous), and the size of the pulp decreases due to the continued deposition of dentin. However, as pulp
ages, collagen fibers & calcifications within the pulp (denticles or pulp stones) both increase.
• Pulp stones-calcifications associated with chronic pulpal disease from advanced carious lesions or
large restorations.

Pulp contains myelinated (sensory) & unmyelinated (motor) nerve fibers that are afferent &
sympathetic. Unmyelinated fibers regulate the lumen size of the blood vessels. However, proprioceptors
(respond to stimuli regarding movement) are NOT found in dental pulp.
• Free nerve endings-the only nerve ending found in pulp. Free nerve ending is a specific
pain receptor. Regardless of the source of stimulation (heat, cold, pressure), the ONLY response
will be PAIN.
• Cells Found in Dental Pulp: fibroblasts (the main cell), odontoblasts, histiocytes (macrophages),
& lymphocytes.
• Cells Found in Diseased Pulp: PMN's, plasma cells, basophils, eosinophils, lymphocytes, & mast
cells (contain histamine & heparin).

At the ONSET of pulpal inflammation, these cells are involved in the cellular response: plasma cells,
macro phages, & lymphocytes, but NOT Polymorphonuclear (PMN) Leucocytes.
• The onset of pulpal inflammation is an insiduous process characterized by a chronic cellular
response of plasma cells, macrophages, and lymphocytes. There is no direct pulp exposure to caries,
thus the cellular response is not acute.
• After pulp exposure, acute inflammatory cells (mainly PMNs) are chemotactically attracted to the
area. Histologically, the tissue is likely to show signs of acute inflammation near the exposure site, and
a band of chronic inflammatory cells bit the acute inflammation and the underlying normal pulp.

16
• The response of vital pulp to microbial invasion is very resistant based on observation that even
after 2 weeks of traumatic pulp exposure, only 2mm of coronal pulp may "give in" to
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• Carious exposures in permanent teeth pulp usually require RCT. Immature (open apex) permanent :z:
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teeth with carious exposures can be treated with pulp capping or a pulpotomy. C">

• Pulp capping-not recommended in primary teeth with carious pulp exposures due to its '"
high failure rate and because pUlpotomy (having similar time requirements) is very
successful. Pulp capping can be done if a mechanical pulp exposure occurs.

APICAL portion of pulp contains more collagen than the coronal portion. This facilitates a pulpectomy
using barbed broaches or endodontic files.
• Type 1 & 3 collagen is mainly found in pulp in a 55%:45% ratio. Type 5 collagen is found in only
small amounts.
• Type 1 collagen predominates in DENTIN.
• Odontoblasts synthesize Type 1 collagen.
• Fibroblasts in pulp synthesize Type 1 & 2 collagen.

Central Zone (Pulp Proper)-area that contains large nerves & blood vessels, and is lined peripherally
by a specialized odontogenic area that has 3 layers:
1. Cell-rich zone-INNERMOST pulp layer that contains fibroblasts.
2. Cell-free zone (zone of Weill-pulp layer rich in capillaries, nerve networks, and contains
the Nerve Plexus of Rashkow.
3. Odontoblastic layer-OUTERMOST pulp layer that contains odontoblasts, and lies next to
predentin & mature dentin.
• The absence of the predentin layer predisposes dentin to internal resorption by pulp cells.
Immediately adjacent to the odontoblastic layer in the pulp, 10-47mm of the dentin matrix
remains unmineralized. If this unmineralized dentin layer is lost due to trauma or an
infectious process, it predisposes the dentin to internal resorption by odontoclasts.

MANDIBULAR TEETH ROOT ANATOMY - the lingual wall of mandibular teeth is most easily
perforated when preparing an access opening due to the lingual inclination of these teeth.

• Mandibular 1st Premolar: 25% MAY have 2 canals with 2 apical foramina. Thus, treatment can be
tricky. At least 23% can have 2 or 3 canals starting anywhere down the root. If a straight-on
preoperative radiograph of a mandibular 1st premolar shows the pulp canal disappearing in
mid root, this is an important indication that 2 canals are present. Pulpitis can cause referred pain
to the MENTAL REGION OF THE MANDIBLE.

• Mandibular 2nd Premolar: 97% have 1 canal at the apex. It has less variation than the mandibular
1st premolar. It usually has 1 root and 1 well-centered canal, with an oval access opening. The
mental foramen lies in close proximity to the root apex, so avoid overinstrumentation and overfill,
and do not misdiagnose the foramen as a premolar abscess on a radiograph. Thus, before
performing root canal therapy, ensure that all diagnostic test confirm your finding. Pulpitis can
cause referred pain to the MENTAL REGION OF THE MANDIBLE.

• Mandibular Molars: usually have a TRAPEZOIDAL outline of the pulp chamber formed by two canals
in the mesial root, and one oval canal in the distal root. -40% of cases, the distal root may have a 2nd
canal (4th canal overall). The pulp chamber is located in the mesial 213 of the crown. Look for a 4th canal
if the first canal found in the distal root lies more toward the buccal, rather than in the center.
• Mandibular 1st molar requires endodontic treatment more than any other tooth in the oral cavity.
Pulpitis can cause referred pain to the EAR.

• Mandibular Canine: the root canal is THIN mesiodistally, but WIDE labiolingually. They usually have
1 root, but in rare cases may have 2 separate roots. The access opening is a large OVAL with the
greatest width placed incisogingivally. This tooth usually has a slightly labial axial inclination of the
crown. Thus, the access opening must be directed towards the lingual surface. Pulpitis can cause
referred pain to the MENTAL REGION OF THE MANDIBLE.

17
..., • Mandibular Central Incisor: has ONLY 1 ROOT that is narrow M-D, but relatively wide labiolingually.
:z: The root may have a distal and/or lingual curvature, and 2 CANALS may be present (if so, the labial
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canal is straighter). Access opening for a mandibular central or lateral is a LONG OVAL, with the
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MAXILLARY TEETH ROOT ANATOMY:

• Maxillary Incisors &Canines: ALL have 1 root, 1 canal, &a distal axial inclination. Thus, when
penetrating along the long axis of the tooth, the bur must be slightly angled toward the distal surface
to avoid perforation of the mesial portion of the root.
• Maxillary Central Incisor: ALWAYS has 1 root &1 canal. The root is bulky with a slight distal
axial inclination, but rarely has a dilacerations. The pulp chamber access opening is OVAL-
TRIANGULAR (it is somewhat triangular, as opposed to oval). The triangle base will be the facial ,
and triangle apex is lingual. If it is not triangular, then it must be oval. Pulpitis can cause
referred pain to the FOREHEAD.
• Maxillary Lateral Incisor: is MOST likely to have a curved root. It ALWAYS has 1 root with 1
canal. The root is more slender than in the maxillary central incisor and often (55%) of the time
has a distal and/or lingual curvature or dilacerations. The access opening is OVAL. Pulpitis can
cause referred pain to the FOREHEAD.
• Maxillary Canine-ALWAYS has 1 root & 1 canal, and is the LONGEST tooth in the maxillary arch.
The access opening is OVAl. Pulpitis can cause referred pain to the NASOLABIAL AREA.

• Maxillary 1st Pemolar: ALMOST ALWAYS has 2 canals. -60% have 2 roots (1 B, 1 Palatal) each with
1 canal. The buccal & palatal roots can be completely separate, or twin projections rising from the
root's middle 1/3 to the apex (this is more common). These 2 roots are usually equal in length from
apex to cusp. However, the palatal root and canal may be wider.
• -40% of maxillary 1st premolars, only 1 root is present (usually with two separate canals). In
cross section at the cervical line, the canal is shaped like a FIGURE EIGHT (ElLIPSE). The access
is a THIN OVAl. Be careful not to perforate on the mesial (due to the mesial concavity).

• Maxillary 2nd Premolar: have a higher incidence of accessory canals (60%) than maxillary 1st
premolars. A pulpitis of this tooth MOST often refers PAIN to the TEMPORAL REGION and sometimes
NASOLABIAL REGION. If careful diagnosis does not reveal the affected tooth, other teeth and related
anatomic structures become suspect. Referred pain-occurs when a pulpitis in one tooth causes pain
in another area.
• Usually (85%) have 1 root, while (15%) 2 separate roots exist (each with 1 canal). The access
opening is also a THIN OVAL (exactly like maxillary 1st premolars).
• When only 1 canal is present in a maxillary 1st or 2nd premolar, it is usually in the CENTER of the
access preparation. If only 1 canal is found, but is not in the center of the tooth, it is probable
than another canal is present. Overfilling either premolar may force gutta-percha material directly
into the MAXILLARY SINUS.

• Maxillary Molars: have a TRIANGLE pulp chamber outline. The pulp chamber floor is formed by the
buccal canals, and the apex is formed by the palatal canal. The line connecting the mesial & palatal
canals is the longest. If a 4th canal exists, it is usually lingual to the orifice of the MB canal, and in
the MB root. The 4th canal is more common than previously believed.

• Maxillary 1st Molar: its 3 canal orifices are arranged in a TRIANGLE shape. -59% have 4th canal
(Ml) with its orifice located just lingual to the MB canal orifice. This 4th ML canal is in the MB root,
and may join the MB canal or exit through a separate foramen. If a lesion exists on the MB root prior
to ReT and does not heal in the usual time frame (6-12 months) after treatment, it is most likely due
to a missed ML canal.
• MB canal: the MB canal orifice is usually the MOST DIFFICULT to locate because it is under the
MB cusp and must be accessed from a distolingual position. It is the small canal that often splits
into two canals, and may be calcified and difficult to instrument.
• Palatal canal: is the straightest, widest, and most tapering canal. The most common curvature
of the palatal root is to the facial. The U-SHAPED radiopacity commonly seen overlying the
palatal root apex is most likely the ZYGOMATIC PROCESS of the maxilla.
• DB canal: also a small, tapering canal, but its orifice has no direct relation to the DB cusp. The
DB orifice is usually located by its relation to the MB orifice. The DB canal is found 2-3mm distal
18 and slightly palatal to the MB canal orifice.
Important: nerve endings of CN VII, IX, & X are widely distributed in the SUBNUCLEUS CAUDALIS of
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trigeminal nerve (CN V). A profuse, intermingling of these nerve fibers creates potential of referred :z:
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• Transplantation-the transfer of a tooth from one alveolar socket to another in the same person or into
another person. Transplanted teeth with partial root development have a better prognosis than fully
developed roots. Intentional replantation is NOT a substitute for endodontic surgery if it can be done.

• Orthodontic extrusion-force controlled vertical tooth movement occlusally in the socket. Orthodontic
extrusion indications: PRIOR to implant placement, untreatable subgingival pathoses (i.e. cervical
caries, cervical fracture, periodontal defects, resorptive lesions, and perforations in the cervical
area) .

• To stabilize an intentionally replanted tooth, a very effective method is to ask the patient to close in
centric occlusion for the rest of the day.

• A major disadvantage of endodontic implants is the lack of an apical seal.

• Crown lengthening-a procedure to apically position the gingival margin and/or to reduce cervical
bone. Used to treat subgingival caries, perforations, and resorptions.

• Root submersion-involves resection of tooth roots 3mm below the alveolar crest, then cover with a
mucoperiosteal flap. Submerged roots will prevent alveolar resorption and maintain better
proprioception .
• Indications: rampant caries, adverse periodontal conditions, repeated failure of prosthetic cases,
and especially useful in medically compromised or handicapped patients requiring better denture
control. Sometimes, root submersion is performed to avoid formation of an esthetic defect that may
result after extraction.

THERMAL SENSITIVITY - the EARLIEST and MOST COMMON symptom of pulpal edema/inflamed
pulp (acute pulpitis) is thermal sensitivity to hot and/or cold stimuli. Usually involves increased and
persistent pain to cold.

• Best method to elicit the most accurate thermal response is to INDIVIDUALLY ISOLATE the suspected
teeth with a rubber dam, then bathe each tooth in hot or cold water. All other methods may stimulate
the tooth in only one section of one surface, thus are less accurate. Thermal tests may yield a false-
negative in immature, recently traumatized teeth, or due to premedication with an analgesic.

• As caries enter dentin, it spreads laterally at the DEJ due to the increased organic content and
involvement of many dentinal tubules. Tomes fibers-react, cause fatty degeneration and later
decalcification (sclerosis).

• As caries progresses, dentin destruction is followed by bacterial invasion of the tubules and complete
dentin destruction. Once odontoblasts are involved, pulpal changes occur (i .e. initially vascular
dilation and local edema) .

• The only reliable clinical evidence that secondary dentin has formed is DECREASED TOOTH
SENSITIVITY (seen a few weeks after placing a filling). When dentinal tubules become completely
calcified, dentin is insensitive.

19
 Teeth conditions that usually DO NOT require endodontic treatment if managed properly because pulp
remains vital:
1. Cementoma (periapical cemental dysplasia)-usually occurs in the anterior region of
the mandible, starting as a radiolucent lesion that eventually calcifies. Cementoma DOES
NOT affect pulp vitality.
2. Traumatic bone cyst-not a true cyst since there is no epithelial lining. Found mainly in
young people and is asymptomatic. Appears as a radiolucency that scallops around teeth
roots. Teeth are usually vital. No treatment.
3. Globulomaxillary cyst-a developmental cyst found at the junction of the globules and
maxillary processes of the maxilla, between the lateral incisor and canine roots. This cyst
arises from cells in a fissural line of bone. Teeth are vital.

Conditions that usually require Endodontic Treatment:

1. Apical Scar-a periapical granuloma, cyst, or abscess that heal with scar tissue. It's a well-
circumscribed radiolucency resembling a granuloma. Tooth is non-vital, so endodontic
treatment is necessary.
2. Radicular Cyst-usually occurs in a pre-existing granuloma, is rarely painful, and appears as
an apex radiolucency of a non-vital tooth. Endodontic treatment is necessary.
3. Chronic Dental Abscess-often the cause of a sinus tract in the gingival tissue of children. It is
often the result of a periapical granuloma, appearing as a radiolucent area at the apex of a
non-vital tooth. Afistula is often found leading from an abscess cavity. Tooth pain stops
upon drainage. Endodontic treatment is necessary.
4. Chronic Periapical Granuloma-asymptomatic, associated with a non-vital tooth, and the
MOST common sequelae of pulpitis. Endodontic treatment is necessary.

PERIAPICAL ABSCESS - a condition that results from a pulpal infection that extends through the
apical foramen into the periapical tissues. MOST COMMON OF ALL DENTAL ABSCESSES. It is a localized
collection of pus in the alveolar bone at the root apex after pulpal death with the infection extending into
the periapical tissue.
• FIRST SYMPTOM is slight tooth tenderness that later develops into a severe throbbing pain (acute
abscess) with swelling of the overlying mucosa.
• Tooth will NOT respond to EPT or cold tests, but may respond to heat.
• Emergency treatment: establish drainage (ideally through the canal) and prescribe antibiotics &
analgesics to relieve the acute symptoms, followed by conventional RCT at a later date.
• For endodontic infections that do not respond to penicillin, clindamycin is recommended as it
produces high bone levels, and is effective against anaerobic bacteria, but must be used with caution
due to the potential for pseudomembranous colitis.
• Acute Osteomyelitis-occurs in the jaws, most commonly caused by a DENTAL INFECTION. It is not
a common disease, but is a serious sequela of a periapical infection that often results in a diffuse
spread of infection throughout the MEDULLARY SPACES, with subsequent necrosis of a variable
amount of bone.
• Acute or subacute osteomyelitis may involve the maxilla or mandible. The disease usually
remains fairly well-localized to the area of initial infection in the maxilla. In the mandible, bone
involvement is more diffuse and widespread.
• Clinically, the afflicted person has severe pain, temperature/fever, and regional
lymphadenopathy. The teeth in the involved area are loose and sore making eating difficult,
if not impossible.
• Radiographically: AO progresses rapidly and demonstrates little radiographic evidence of its
presence until it has developed for at least 1-2 weeks. At that time, diffuse lytic changes in bone
appear. A "moth-eaten" radiolucency is evident.
• Treatment: establish & maintain drainage, and prescribe antibiotics to prevent further spread
and complications.

PERIODONTAL ABSCESS - an acute abscess that develops through the periodontal pocket that
involves alveolar bone loss, pocket formation, and periodontal pathologic conditions. Tooth is usually
palpation & percussion positive, and responds to EPT (unlike the periapical abscess). Bacteria
associated with the periodontal abscess are gram (-) rods (i.e. Capnocytophaga species, Vibrio-corroding
organisms, Fusobacterium species).

20
GINGIVAL ABSCESS - a RARE abscess that occurs when bacteria invade through a break in the
gingival surface. Caused by mastication, oral hygiene procedures, or dental treatment.

CHRONIC APICAL ABSCESS (SUPPURATIVE APICAL PERIODONTITIS) - a long-standing,

low-grade infection of the periapical bone with the root canal being the source of the infection. It is
generally asymptomatic, and sometimes so painless that it may go undetected for years until revealed
by an x-ray. Treatment is conventional root canal therapy.

• Chron ic apical abscess may follow an acute alveolar abscess or unsatisfactory RCT. Radiographs
reveal a diffuse radiolucency & POL thickening. The tooth may be slightly loose, or tender to percussion.

• Chronic apical abscess is differentiated from cysts & granulomas because cysts & granulomas are
well-defined radiolucencies .

PHOENIX ABSCESS (suppurative apical periodontitis = recrudescent abscess) - an apical lesion

(acute abscess) that develops as an acute exacerbation of a chronic apical abscess. It develops as the
granulomatous zone becomes contaminated or infected by root canal elements. Diagnosis is based on acute
symptoms (pain to percussion) and radiographic examination (reveals a large periapical radiolucency).
• A massive invasion of pulpal contaminants will result in the formation of an acute abscess
(Phoenix abscess).

Important: 30%-50% of bone calcium must be altered before radiographic evidence of periapical
breakdown occurs. This alteration occurs at the junction between the cortical and cancellous bone.

ACUTE APICAUALVEOLAR ABSCESS (AA) - a localized collection of pus inside alveolar bone at
the root apex after pulpal death, with the infection extending into the periapical tissue. FIRST SYMPTOM
of AA may be slight tooth tenderness, that later develops into a SEVERE THROBBING PAIN to percussion
with swelling of the overlying mucosa.

• The tooth becomes more painful, elongated, and loose. At times, the pain may decrease or completely
disappear. The patient may appear weak, irritable, and have a fever.

• AA diagnosis is based on history, exam, and radiographs . An AA tooth will not respond to EPT or cold
tests, but MAY respond to HEAT.

• Treatment: establish drainage & debride the canal system of necrotic tissue to relieve the acute
symptoms. At a later date, perform conventional RCT. (Note: if the abscess ruptures through the
periosteum into soft tissue, the patient's symptoms will subside).

GRANULOMA - a growth of granulomatous tissue continuous with the POL due to pulpal death with
diffusion of toxic products into the periapical area. Is usually asymptomatic. Radiographically, a well-defined
area of rarefaction (radiolucency) with some irregularities is evident. Clinically, the tooth is NOT sensitive.

CYST - inflammatory response of the periapex that develops from pre-existing granulomatous tissue
(granuloma), characterized by a central, fluid-filled, epithelium-lined cavity, surrounded by a
granulomatous tissue &peripheral fibrous encapsulation. Often associated with a chronically infected
and potentially mobile tooth, but is usually asymptomatic.
• Radiographically: evident as a well -defined area of rarefaction (radiolucency) that is limited by a
continuous radiopaque, sclerotic border of bone.

Important: a granuloma or cyst is ONLY differentially diagnosed by a HISTOLOGIC EXAMINATION.

21
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COMBINED PERIODONTAL-ENDODONTIC LESION - endodontic treatment takes precedence over
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periodontal management. Combined endodontic-periodontal therapy is widely used because the
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combined endo-perio lesions, endodontic procedures are performed first, and when necessary, are
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followed by periodontal treatment.

• Ex: If bone loss extends from the cemento-enamel junction (CEJ) to the tooth apex on a radiograph,
probing depth are above normal all around the tooth, but at one point the probe drops precipitously
to an even greater depth, and vitality test is negative. This patient may require endodontic
treatment followed by periodontic treatment.

• In these cases, the value of precise pocket probing and correct appraisal of pulp vitality is crucial.
In some doubtful cases, it is best to wait until after RCT is complete to see if spontaneous resolution
(pocket closure and osseous fill-in) will occur before surgical periodontal procedures are begun.

• Periodontal therapy is initiated first ONLY in the case of a primary periodontal lesion, with
subsequent secondary endodontic involvement.

• A common clinical finding of a periodontal problem is PAIN to LATERAL PERCUSSION on a tooth

with a wide sulcular pocket.

• Periodontic-Endodontic Abscess-a combined lesion that usually shows radiographic involvement

of the periodontium & apex of the involved tooth.

Probing Lesions:
1. Conical-Shaped Probing Lesion-a periodontal probing defect that cannot be managed by
endodontic treatment alone that is typical of a periodontal problem. Periodontal Lesions
characteristically show bone loss that starts at the crestal bone level and progresses apically.
Thus, probing defect is conical-shaped. Periodontal lesions may not be amenable to ReT alone
even if it is associated with a pulpless tooth. However, endodontic treatment must be completed
PRIOR to treating the periodontal problem.
2. Blow-Out (acute) Probing Lesion-a clue for diagnosis is a non-vital (necrotic) pulp that can
completely heal after RCT. Atooth with this lesion shows normal sulcus depth all around the
tooth until the area of swelling is probed. At this point, the probe drops to a level near the root
apex. Probing depths in all other areas are within normal limits.
3. Narrow Sinus Tract Lesion-probing reveals normal depths all around the tooth except at one
very narrow area . Thus, the probe can pass down the root surface to some distance (sometimes
to the apex) . The tooth is pulpless (non-vital). Once RCT is complete, the lesion completely heals
within one week. Another clue for diagnosis is a non-vital (necrotic) pulp.

REVERSIBLE PULPITIS (PULPAL HYPEREMIA = PULPAL INFLAMMATION) - most commonly

caused by bacteria. Pain is not spontaneous, but requires an external irritant to evoke a painful response
(i.e. cold, sweets). Pains are SHARP & BRIEF, stopping when the irritant is removed. Radiographs
appear normal (may show deep caries or cavity preparation).

• Tooth is usually percussion negative, and with thermal tests, the pulp responds more readily to cold
than to hot (the response leaves shortly after the irritant is removed).

• A short, painful response to cold suggest pulpal hyperemia . Pulpal hyperemia is an excessive
accumulation of blood in the pulp due to vascular congestion. It is the engorgement of pulpal vessels
with blood . Once the causative agent (i.e. bacteria or a restoration in hyperocclusion) is removed or
adjusted, the pulp usually returns to normal.

• Pulpal hyperemia is congestion of blood within the pulp chamber caused by physical, chemical,
or bacterial insult. After restoration placement, teeth often become hyperemic and sensitive to cold
for a few days. The pain is not spontaneous, and does not last after the stimulus is removed. Th is
short pain duration and low intensity is what distinguishes pulpal hyperemia from the pain of acute
pulpitis ("irreversible pulpitis").

22
• Pulpal hyperemia caused by bacterial insult is a limited inflammation of the pulp. The tooth can
recover if the caries is eliminated by timely operative treatment.
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• Hyperemic teeth respond on a lower level of current on the EPT (electric pulp tester) than a '"
normal tooth.

• The most effective way to reduce pulp injury during tooth preparation is to minimize dehydration
of dentin.

IRREVERSIBLE PULPITIS ("ACUTE PULPITIS") - condition characterized by SPONTANEOUS PAIN

with periods of cessation (intermittent in nature). Clinical symptoms severity varies as the inflammatory
response increases. Pain varies from a mild & readily tolerated discomfort, to a severe, throbbing, and
excruciating pain that is spontaneous, intermittent, and LINGERS AFTER THE IRRITANT IS REMOVED.

• Pain is usually not readily localized by the patient, but is diffuse in nature.

• Irreversible pulpitis is an acute inflammation of the pulp characterized by intermittent spasms of pain
that becomes continuous. In the early stages, it may appear as a very severe hyperemia . As the
condition continues, the pain is gnawing or dull-throbbing, and is generally increased by heat and
relieved by cold.

• Lying down or bending over intensifies the pain because the overall increase in cephalic blood
pressure is relayed to the confined pulp tissue.

• Tooth may be tender to percussion (tooth is usually percussion positive), heat may intensify the
pain response, while cold may relieve it (in advanced stages). Usually HOT &COLD cause severe and
lasting pain. Thus, thermal test is the best aid to diagnose an irreversible pulpitis.

• When the pulp becomes severely inflamed as indicated by a thermal stimulus producing pain that
lasts long after the stimulus is removed (longer than 10 seconds), this suggests "irreversible pulpitis"
and the pulp is unlikely to recover after removing the caries. Pulpal pain (spontaneous or elicited by
an irritant) that lingers more than 10-15 seconds.

• Radiographs do NOT disclose periapical pathology.

• Sometimes it is hard to distinguish between reversible and irreversible pulpitis, in which case caries
control (placing a temporary filling) is a conservative approach toward making the final diagnosis.
If a tooth responds well to the temporary filling, the there is no need for RCT at this time.

• Treatment: RCT (complete pulp removal).

NECROTIC PULP (PULP DEATH) - may have no painful symptoms and does not respond to EPT
at any current level, but the tooth sometimes responds to heat, but will not respond to cold. Atooth
affected with a necrotic pulp may have no painful symptoms and may appear discolored. EPT is valuable
because there will be no response at any current level.
• Treatment: RCT or extraction.

Significant Bacteroides species involved in pulpal-peri radicular infection are Porphyromonas &
Prevotella which received a separate genus (undergone taxonomic revision) due to their distinct
characteristics. Predominant bacterial species isolated from INFECTED ROOT CANALS include:
• Eubacterium, Peptostreptoccus, Fusobacterium, Porphyromonas, and Prevotella species.
• Streptococcus species may not be as important in the progession of a carious lesion (leading to pulp
exposure) as much as it is in the initiation of the lesion . Strict anaereobes playa major role in
periapical pathoses.

23
,."
Virulence Factors involved in periradicular pathosis:
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• Enzymes-neutralize antibodies and complement components.
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en and hemolysis.
• Fatty acids-affect chemotaxis and phagocytosis.

Vital pulp resists bacterial invasion. Even if vital pulp is exposed to microorganisms for 2 weeks, the
bacterial penetration may extend no> 2mm into the pulp. In contrast, non-vital pulp is a fertile ground
for bacterial growth and leads to necrosis.

Endodontic Therapy Contraindications:

1. non-restorable tooth OR non-strategic tooth (i.e. tooth not in occlusion).
2. tooth with insufficient periodontal support.
3. tooth with a vertical root fracture.
4. tooth with massive internal or external resorption .
5. tooth with a canal unsu itable for instrumentation or surgery (i.e. broken instruments,
dentinal sclerosis, sharp dilacerations).

Any teeth not contraind icated are EXCELLENT candidates for successful endodontic therapy.

HEMOPHILIA - a medical condition that is NOT a contraindication to conventional endodontic

therapy, but is strongly recommended that the dentist obtain clearance from the patient's physician
before treatment.

Example of a Special Case: a previously traumatized tooth may show complete obliteration of the pulp
chamber & canal, but the POL may appear normal. The patient will be asymptomatic and the tooth will
not respond to pulp vitality testing. Treatment of choice: observe as long as the tooth remains
asymptomatic & no periapical changes are evident.

Restoring Endodontically Treated Teeth:

Amajor disadvantage of posts (dowels) is it does not reinforce the tooth structure, but WEAKENS IT.
• All posts designs are predisposed to leakage.
• At least 4mm of gutta-percha MUST remain to preserve the apical seal.
• Threaded screw posts may actually increase the chance of fracture. Thus, parallel-sided posts
and tapered posts are preferred.
• Pins increase stresses and microfractures in dentin, thus should not be used.
• Cusps adjacent to lost marginal ridges should be restored with an ONLAY.

Restoration Options for Endodontically Treated Posterior Teeth: Endodontically treated posterior teeth
are more prone to fracture than non-treated posterior teeth due MAINLY to destruction of coronal tooth
structure and reduced structural integrity.
• Restoration of occlusal opening only: in rare instances, the access opening and caries destruction
do not encroach on the cusps and marginal ridges. These teeth may be restored with an occlusal
amalgam. However, a cuspal coverage restoration provides fracture protection
• Onlays: in most cases, it is required that root canal treated teeth be protected from fracture by a cusp-
coverage restoration. The minimum (most conservative) preparation is an onlay that covers cusps
and marginal ridges.
• Crown: a full-coverage crown is preferred when the remaining coronal tooth structure does not afford
sufficient tooth structure for an onlay.
• Crown with Post & Core: to reinforce the treated tooth and provide suitable coronal tooth structure
for an optimum crown preparation, a post & core is indicated. Be very careful when placing posts as
perforations and vertica l root fractures can occur.
• If performing a pulp-chamber-retained amalgam, you must place amalgam 3mm into each canal
for retention.

24
CHAPTER 2

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25
 THE PERIODONTIUM &FIBERS
PERIODONTIUM - tissues that surround and support the teeth consisting of the gingiva, POL,
cementum, alveolar & supporting bone. The main functions are to support, protect, and nourish the
teeth.
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• Attachment apparatus-consists of the alveolar bone proper, POL fibers, and cementum that
o attaches the root to alveolar bone.
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• Gingival apparatus-describes the gingival fibers and epithelial attachment.

• Gingival ligament-consists of dentogingival, alveologingival, and circular fibers .

• Indifferent Fiber Plexus-small collagen fibers located in the POL that run in all directions, and are
associated with the larger principal collagen fibers.

ALVEOLAR PROCESS - the part of the maxilla and mandible that HOUSES TEETH and consists of two
main parts.
1. Alveolar bone proper-the only essential part 0 the bone socket (alveolar process) that is always
present. It is a thin inner layer of compact lamellar bone that immediately surrounds the root
where POL fibers attach. It is a perforated cribiform plate through which vessels and nerves pass
between the POL and bone marrow. It consists of two layers of bone (compact lamellar bone &
layer of bundle bone (the layer that POL fibers insert into). Alveolar bone proper helps form the
attachment apparatus.

2. Supporting alveolar bone-is not always present, but surrounds the alveolar bone proper to
provide SUPPORT to the socket (alveolar process) and consists of:
• Cortical plate (compact lamellar bone)-forms the outer & inner plates of alveolar processes,
and is thicker in the mandible than in the maxilla.
• Spongy bone (cancellated bone)-fills in the area between the cortical plates of bone. Spongy
bone is NOT present in the anterior region of the mouth (here the cortical plate is fused to
the cribiform plate). This is also true over the radicular buccal bone of maxillary posterior teeth.

Gingiva Components:
1. FREE GINGIVA (unattached or marginal gingival-the collar of tissue not attached to the tooth
or alveolar bone composed of:
1. gingival margin-the most coronal part of the free gingiva.
2. free gingival groove-separates free gingiva from attached gingiva; only present in
33% of adults.
3. gingival sulcus-the shallow groove between the marginal gingiva & tooth surface, bound
by sulcular epithelium laterally, and by JE apically.
4. interdental (interproximal) gingiva-occupies the interdental spaces coronal to the
alveolar crest.

GINGIVAL FIBERS (SUPRACRESTAL C.T. FIBERS) - Type I collagen fibers that support and
attach the gingiva to tooth and alveolar bone. Gingival fibers are found ONLY within the FREE GINGIVA
(not in attached gingiva or mucogingival junction). Gingival fibers are continuous with the POL (which
is also C.T that surrounds the root and connects the root to alveolar bone by its principal fibers). Gingival
fibers are designated by their orientation:

1. Alveologingival fibers-insert in the crest of the alveolar process and spread out through
the lamina propria into the free gingiva. Also helps form the gingival ligament.

2. Circular fibers (Circumferential fibers)-resists ROTATIONAL FORCES applied to a tooth, and

help form the gingival ligament. These fibers encircle the tooth around the most cervical part
of the root, and insert into cementum and lamina propria of the free gingiva and alveolar crest.

26
 3. Dentogingival fibers-extend from cementum apical to the epithelial attachment (JE) and
travel laterally and coronally into the lamina propria of the gingiva. Also help form the
NOTES
gingival ligament.

4. Dentoperiosteal fibers-extend from cervical cementum over the alveolar crest, to the
periosteum of the cortical plates of bone.
..,
."

5. Transseptal fibers: connect two adjacent teeth (tooth-to-tooth) and are sometimes ::!
o
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classified within the PDL principal fibers, although they are actually tooth-to-tooth fibers, o
:z
not tooth-to-bone fibers. These fibers extend from tooth-to-tooth, coronal to the alveolar crest, ...
:::!

and are embedded in cementum of adjacent teeth. They are not found on the facial aspect, and '"
have no attachment to the alveolar crestal bone. They maintain integrity of the dental arches.

ATTACHED GINGIVA - the gingiva attached to underlying periosteum of alveolar bone and to cementum
by C.T. fibers and epithelial attachment. Present between the free gingiva and more movable alveolar
mucosa. Attached gingiva contains KERATINIZED EPITHELIUM &LAMINA PROPRIA of dense, well-
organized fiber bundles with few elastic fibers. It is firmly joined to underlying tooth structure,
periosteum, &bone, and structured to withstand frictional stresses of mastication and brushing.

• NARROWEST BAND of attached gingiva is found on FACIAL SURFACES of the mandibular canine &
first premolar, and lingual surfaces adjacent to mandibular incisors &canines. Narrow attached
gingival zones may also occur at the MB root of maxillary first molars (associated with prominent
roots and sometimes with bony dehiscences), and at mandibular third molars.

• Width of FACIAL attached gingiva ranges from 1-9mm. It is WIDEST on the facial surface
of the maxillary lateral incisor, &narrowest on facial surfaces of mandibular canine &
first premolar.

• "functionally adequate" zone of gingiva-a zone that is keratinized, firmly bound to tooth and
underlying bone, -2mm or more wide, and is resistant to probing and gaping when the lip is distended.

BOUNDARIES that define the ATTACHED GINGIVA extend from the mucogingival junction (MGJ) to the
free gingival groove (base of the sulcus).

• Mucogingival Junction-separates attached gingiva from alveolar mucosa. However, the free gingival
groove separates the free gingiva from attached gingiva.

• Free gingiva-extends from the free gingival groove (sulcus base) to the gingival margin.

ATTACHED GINGIVA is normally CORAL PINK in color and firmly bound down to underlying tooth structure,
periosteum, and bone. Its color varies depending on the degree of keratinization, thickness of
epithelium, presence of melanin, and number of blood vessels.

STIPPLING - the irregular surface texture of the attached gingiva that resembles an orange peel's
surface. Stippling occurs at the intersection of epithelial ridges that cause the depression, and the
interspersing of C.T. papillae between these intersections that form the small orange peel bumps.

• In the absence of stippling, edema of underlying C.T., inflammatory degradation of gingival collagen
fibers, and normal variation in gingival topography may result in areas of the attached gingiva .

ALL ORAL MUCOSA is STRATIFIED SQUAMOUS EPITHELIUM regardless if it is keratinized or nonkeratinized.

• Non-Keratinized Oral Mucosa: buccal & alveolar mucosa , tongue's inferior (ventral) surface, soft
palate, floor of mouth, specialized mucosa, and lining mucosa , gingival col, and crevicular epithelium,
• Alveolar Mucosa-functions as a LINING TISSUE, located APICAL to the attached gingiva on the
facial & lingual surfaces. Consists of a thin, NON-KERATINIZED epithelium, loosely textured,
contains elastic fibers in the mucosa and submucosa, and is loosely bound to periosteum of
alveolar bone. Alveolar mucosa is well-adapted to permit movement, but cannot withstand
frictional stresses.

• Keratinized Oral Mucosa: hard palate &attached gingiva .

27
 Functional Oral Mucosa:
1. Masticatory mucosa-com posed of free & attached gingiva, and mucosa of the hard palate.
The epithelium of these tissues is KERATINIZED, and the lamina propria is a dense, thick,
firm C.T. of collagenous fibers. Important: the surface epithelium of the gingiva is highly
impermeable, which makes it resistant to bacterial invasion.

,...,
."
2. lining Mucosa (Reflective Mucosa)-mucosa that lines most of the oral cavity EXCEPT the
""
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gingiva, anterior palate, and dorsum of the tongue. lining mucosa is a thin, movable
CI
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• Mucogingival junction-the junction of the lining mucosa with the masticatory mucosa.

3. Specialized Mucosa-consists of non-keratinized epithelium that covers the tongue

dorsum and taste buds

PERIOOONTAlliGAMENT (POL) - a complex, specialized, soft, fibrous C.T. containing numerous

cells, blood vessels, nerves, & extracellular substances consisting of fibers (gingival & prinicipal), &
ground substance. POL is a HIGHLY VASCULAR & CElLULAR C.T. that surrounds the roots of teeth and
bridges root cementum with alveolar bone. Most POL fibers are collagen , while ground substance
consists of various proteins and polysaccharides. When the tooth loses its function , the POL becomes
very thin and loses its regular arrangement of fibers .

• POL is hour-glass shaped with the narrowest part at the middle of the root.

• POL occupies the space between cementum and the periodontal surface of alveolar bone.

• Cementum and alveolar bone are the tissues immediately adjacent to the POL.

• MOST ABUNDANT CEllS in the POL are FIBROBLASTS. Fibroblasts are ovoid or elongated cells
oriented along the POL principal fibers and exhibit pseudopodial-like processes.

• Epithelial Rests of Malassez-remnants of Hertwig's epithelial root sheath, found as groups of

epithelial cells in the POL Some epithelial rests degenerate, while others become calcified
(cementicles).

POL Functions:
1. Physical Functions: attaches tooth to bone via its principal fibers and absorbs occlusal forces
by acting as a cushion to reduce the impact of forces generated during mastication on alveolar
bone. Orthodontic treatment is possible because the POL continuously responds and changes
based on the functional requirements imposed on it by externally applied forces. 4 human
dentition features that directly affect POL health & its hard tissue anchorage to resist
occlusal forces:
1. anterior teeth have slight or no contact in MIC (intercuspal position).
2. occlusal table is < 60% of the overall F-L width of the tooth.
3. occlusal table is generally at right angles to the tooth's long axis.
4. mandibular molar crowns are inclined 15-20% toward the lingual. Thus, mandibular molars
root apices are positioned more facially, while the crowns are positioned more lingually.

2. Formative Functions: formation of C.T. components by the activities of C.T. cells (cementoblasts,
fibroblasts, and osteoblasts).

3. Resorptive Functions: by activities of C.T. cells (fibroclasts, osteoclasts, and cementoclasts).

4. Nutritive Functions: through blood vessels to cementum, bone, and gingiva.

5. Sensory Functions: carried by the trigeminal nerve (CNV), proprioceptive and tactile sensitivity
is imparted through the POL (sensation of contact between teeth).PDL contains 2 types of
nerve endings:
1. free, unmyelinated endings: convey PAIN.
2. encapsulated, myelinated nerve endings: convey PRESSURE.

28
PDL's average thickness in an adult is -.25mm in normal function. POL thickness depends on :
1. Age (POL becomes thinner, thus decreases in thickness with age) due to increased deposition
of cementum and bone which occurs mainly in the mandibular canine region.
2. Stage of eruption
3. Function of the tooth (POL is thicker in functioning teeth, than in non-functioning teeth, and is
th icker in areas of tension, and thinner in areas of compression)
4. Trauma history (POL may not exist due to ankylosis (fusion of the tooth to bone). ,..,
."

::!:!
c
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Specialized cells of the PDl: function to resorb and replace cementum (cementoclasts or cementoblasts), c
:z:
POL (fibroclasts or fibroblasts), and alveolar bone (osteoclasts or osteoblasts). ::::!
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en

PDL is composed primarily of Type I COLLAGEN FIBERS. PDL does not contain MATURE elastin fibers,
but contains two IMMATURE elastin forms (Oxytalan & Eluanin).

• Oxytalan fibers-run parallel to the root surface in a vertical direction, and bend to attach to
cementum in the cervical third of the root. Oxytalan fibers regulate vascular flow.

PDL is a specialized form of C.T. derived from the DENTAL SAC that surrounds the root and attaches
the root to its bony socket. PDL is composed mainly of C.T. fibers (Type I collagen fibers) that are
arranged into two groups:
1. Gingival Fibers-C.T. collagen fibers found in the free gingiva, but are continuous with the POL
C.T. fibers, thus are often considered part of the POL. Gingival fibers SUPPORT the marginal
gingiva and interdental papillae.
• Gingival fibers: circular, dentogingival, dentoperiosteal, alveologingival, & transseptal fibers
(sometimes considered POL principal fibers).

2. Principal Fibers-collagen fibers of the POL that include: alveolar crest fibers, horizontal,
oblique, apical, & interradicular fibers . Principal fibers CONNECT ROOT CEMENTUM TO ALVEOLAR
BONE. They are distinguished by their location and direction.
• Sharpey's Fibers-the terminal portions of the POL principal collagen fibers that are embedded
into the cementum and alveolar bone.

POL PRINCIPAL FIBERS (TOOTH-TO-BONE FIBERS) - bundles of Type I collagen fibers grouped
based on the direction they extend from the root cementum to alveolar bone. The terminal portions of the
PDL collagen fibers that are embedded/anchored into cementum and alveolar bone are SHARPEY'S
FIBERS. The diameter of Sharpey's fibers is much greater on the BONE SIDE than cementum side.
1. Horizontal fibers-run perpendicular from alveolar bone to cementum, and RESISTS LATERAL FORCES.

2. Alveolar crest fibers-extend from the cervical cementum of the tooth to the alveolar crest, and
function to counterbalance the occlusal forces on the more apical fibers and resist
lateral movements.

3. Oblique fibers-are the most numerous fibers in the periodontal ligament. They attach apical to
the horizontal fibers and run diagonally toward the crown of the tooth inserting to the alveolar
bone there. Because they are the most numerous, these fibers are believed to be primarily
responsible in absorbing the chewing forces on the tooth. They are hence the main support of the
tooth . Oblique fibers RESIST FORCES ALONG THE TOOTH'S LONG AXIS (masticatory forces).
Mostly commonly found in the root's middle third.

4. Apical fibers-radiate apically from cementum to bone. Apical fibers offer INITIAL RESISTANCE
to tooth movement in an OCCLUSAL DIRECTION.

5. Interradicular fibers-are found ONLY ON MUlTI-ROOTED TEETH, extending from cementum in

the root furcation area to bone within the furcation.

29
 GINGIVAL CREVICULAR FLUID (GCF) - in health, GCF is a transudate that emerges from the
gingival sulcus. GCF may contain a variety of enzymes and cells, particularly desquamating epithelium
& neutrophils being shed through the sulcus. An increase in GCF flow is the first detectable sign of
inflammation. Once inflammation has occurred, GCF is called inflammatory exudate which contains a
higher level of serum proteins and leukocytes.
""C
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:::c • Nutrient materials for the gingival epithelium cells are supplied mainly from capillaries in
o subjacent C.T.
c >,
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...
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CI> Dentojunctional Epithelium-the gingival epithelium that faces the tooth, composed of non-keratinized
stratified squamous epithelium and is divided into:

1. Sulcular epithelium-epithelium that lines the sulcus and connects directly with the JE.

2. Junctional Epithelium-a specialized epithelium surrounding each tooth, It begins at the sulcus
base, It is a collar-like band of stratified squamous epithelium firmly attached to the tooth by
HEMIDESMOSOMES. At its beginning, it is -10-20 cell layers thick, while at its apical end it is
only a few cell layers thick. JE has two layers (basal & suprabasallayers). In IDEAL GINGIVAL
HEALTH, the JE is located entirely on enamel above the CEl
• Epithelial Attachment (Junctional Epithelium)-the special part/structure of the junctional
epithelium and inner layer of cells of the JE that actually provides the attachment (it
attaches gingiva to the tooth surface or to compatible restorative materials). Epithelial
attachment consists of a lamina lucida, lamina densa, & hemidesmosomes,

Histologically, the best way to distinguish free gingiva from the epithelial attachment is the epithelium
of the epithelial attachment DOES NOT CONTAIN RETE PEGS while the free gingival does, Rete Pegs-
epithelial projections that extend into the free gingival C.T.

• C.T. papillae-projections that extend into the overlying epithelium ,

CERVICAL LINE (CEJ) CONTOURS - are closely related to the attachment of the gingiva at the
tooth's neck. The GREATEST contour of the cervical lines & gingival attachments occur on the MESIAL
SURFACE OF ANTERIOR TEETH (mesial surface of the maxillary central incisor has the greatest cervical
line curvature).

• All teeth generally have a greater proximal cervical line (CEJ) curvature on the MESIAL than the
distal. Also, the proximal cervical line (CEJ) curvatures are greater on incisors and get smaller when
moving toward the last molar where there may not be a curvature,

• CEJ (cemento-enamel junction) of ALL teeth curves in 2 directions: toward the apex (on facial &
lingual surfaces), and away from the apex (on mesial & distal surfaces).

• In the absence of periodontal disease, the configuration of the crest of the interdental alveolar
septa is determined by the CEl's position on adjacent teeth.

• The width of the interdental alveolar bone is determined by the tooth form present. Relatively flat
proximal tooth surfaces call for narrow septa, while in the presence of an extremely convex tooth
surface, wide interdental septa with flat crests are found,

30
FLAPS, GRAFTS, &SURGERY
AUTOGENOUS FREE GINGIVAL GRAFT - an autogenous graft of gingiva placed on a viable C.T.
bed where initially buccal or labial mucosa were present. Usually, the donor site from where the graft
is taken is an edentulous region or palatal area. The graft epithelium undergoes degeneration after it
is placed, then sloughs. The epithelium is reconstructed in -1 week by the adjacent epithelium and ."
I'T'I
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proliferation of surviving donor basal cells. In 2 weeks, tissue reforms, but maturation is not complete C
C
until 10-1 Gweeks. The healing time required is proportional to the graft's thickness. The greatest amount c
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of shrinkage occurs within the first 6 weeks. ::::!
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• Free gingival graft-involves removing a section of attached gingiva from another area of the mouth
(usually the hard palate or an edentulous region) and suturing it to the recipient site. FGG success
depends on the graft being immobilized at the recipient site. AFGG is used to increase the zone of
attached gingiva and possibility of gaining root coverage. The difficulty in getting complete root
coverage lies in the fact that an avascular graft is placed over a root surface also devoid of blood supply.

• FGG retains NONE of its own blood supply and is totally dependent on the bed of recipient blood
vessels. The FGG receives its nutrients from the viable C.T. bed.

• MAIN reason a FGG fails is disruption of the vascular supply before engraftment. Infection is the
second most common reason of FGG failure.

Free Gingival Graft Indications:

• Prevent further recession and successfully widen (increase the width) of attached gingiva.

• cover non-pathologic dehiscences &fenestrations.

• performed with a frenectomy to prevent reformation of high frenal attachments.

• cover a root surface with a narrow denudation. FGG mayor may not yield a successful result when
used to obtain root coverage (the result is not highly predictable in root coverage cases).

• used therapeutically to widen attached gingiva after recession occurs, and to prophylactically
prevent recession where the band of attached gingiva is narrow, and of a thin, delicate consistency.

• correct localized narrow recessions or clefts, but NOT DEEP WIDE RECESSIONS. In such cases, the
laterally repositioned flap (a pedicle graft) has a greater predictability. FGG is rarely used on facial
or lingual surfaces of mandibular 3rd molars (especially facial).

• FGG Healing: involves revascularization of the graft. The graft's top layers are revascularized last.
Thus, the epithelium dies off (degenerates), producing the necrotic slough. During healing, the
epithelium of FGG degenerates (necrotic slough), and re-epithelization occurs by proliferation of
epithelial cells from adjacent tissue and surviving basal cells of the graft tissue.

FREE MUCOSAL AUTOGRAFT - a graft that differs from a FGG in that the transplant is C.T. without
an epithelial covering.

• Epithelial differentiation is induced by the underlying C.T. so that free grafts of dense C.T. taken from
keratinized areas result in the formation of keratinized tissue even when transplanted to non-
keratinized zones. This procedure is more difficult than FGG, and is often used on CANINES where
little keratinized gingiva exists to create a band of gingiva-like tissue.

• During healing, the epithelium of FGG degenerates (necrotic slough), and re-epithelization occurs by
proliferation of epithelial cells from adjacent tissue and surviving basal cells of the graft tissue.

31
 Root Amputation & Hemisection MUST be done in conjunction with endodontic therapy of a particular
tooth. Endodontic therapy is performed first, followed by the periodontal therapy:

• Root Amputations-the separation of an individual root from the crown. Most root amputations
involve MAXILLARY lst &2nd MOLARS (commonly involved periodontal sites). Burs and diamond
stones are used to sever the crown and root before extracting by root tip forceps. Once the root
,...,
.."
amputation is complete, the remaining apical area of the crown and furcation region are recontoured
:::c
c::> similar to the shape of a pontic so maximal access is provided for oral hygiene.
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• Hemisection-the vertical sectioning of the tooth through BOTH the crown and root. Usually, a
hemisection is used in a mandibular molar region were the crown is divided through the bifurcation
region. 50% of the tooth is extracted if one specific root has excessive loss in osseous support,
and the remaining half of the molar tooth is now treated as a premolar.

DISTAL WEDGE (PROXIMAL WEDGE) flAP - the simplest distal flap procedure/approach used
for retromolar reduction. This procedure is often performed after wisdom teeth are extracted because the
bone fill is usually poor, leaving a periodontal defect. This region is occupied by glandular and adipose
tissue covered by unattached, non-keratinized mucosa. Only if sufficient space exists distal to the last molar,
a band of attached gingiva may be present (in this case, as distal wedge operation can be performed).

• Distal Wedge flaps are performed in these areas: maxillary tuberosity region, mandibular
retromolar triangle area, and distal to the last tooth in the arch, or mesial to a tooth that
approximates an edentulous area.

• Many designs have been presented for the distal wedge flap procedure. However, the basic concept
involves making at least 2 incisions distal or mesial to the tooth, and carrying these incisions parallel
to the outer gingival wall to form a wedge (the wedge base is the periosteum overlying the bone,
and apex is the coronal gingival surface). Detaching the wedge from the periosteal base and
elminating involved tissues in the distal pocket region reduces tissue bulk, and allows access to the
underlying bone.

OSSEOUS RECONTOURING SURGERY - main goal is to ELIMINATE PERIODONTAL POCKETS. The

existing bony topography is changed to eliminate periodontal pockets. This surgery does not cure
periodontal disease, but provides the patient the opportunity and access to maintain their own
periodontium and dentition with routine oral hygiene procedures.

• Before using osseous resection or recontouring to treat an infrabony defect, the dentist should
consider these treatment alternatives: maintenance with periodic root planning, bone grafts,
reattachment-fill procedures, hemisection or root amputation.

• In some surgical procedures, it is necessary to leave interradicular bone exposed. This usually results
in bone loss of no clinical consequence.

• Osseous resection surgery should NOT be done until etiologic factors that caused the osseous defects
are arrested . Clinically detectable inflammation must be eliminated by SRP and by the patient's
ability to maintain optimal plaque control.

• The MOST critical factor to determine if a tooth should be extracted or have surgery (prognosis) is
AMOUNT OF ATTACHMENT LOSS (the amount of apical migration of the epithelium attachment).
Amount of attachment loss is the most important factor in the determination of a prognosis of a
tooth with periodontal disease (more accurate than probing depth, tooth mobility, and presence of
furcation involvement).

32
PRIMARY OBJECTIVE of Surgical Flap Procedures in treating periodontal disease is to provide access NOTES
to root surfaces for debridement.

• Surgical Flap Goals to treat periodontal disease: to reduce or eliminate periodontal pockets,
regrowth of alveolar bone, maintain biological width, and establish adequate soft tissue contours.

• Flap techniques vary with the goal sought, but the common goal of all flap procedures is to PROVIDE -c
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ACCESS for instrumentation. It allows the clinician to visualize the roots so calculus can be removed c:::>
CJ
more com pletely. c:::>
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• Without direct visualization provided by a flap, it is rare that a clinician can effectively root plane
beyond 5mm of probing depth or into root furcations of lesser depth. Flaps also make removal of
granulomatous tissue from the region of the periodontal defect difficult. It is important to remove
this since it contains epithelium and potential presence of bacterial infiltration.

• If a patient fails to demonstrate adequate oral hygiene during initial therapy (SRP), surgery is
contraindicated because after surgery, the incidence of disease recurrence is greater if oral hygiene
remains poor. The best course of action is to continue to stress oral hygiene, and maintain areas
with SRP (scaling & root planing).

PERIODONTAL flAP - a segment of marginal periodontal tissue that is surgically separated coronally
from its underlying support and blood supply, and attached apically by a pedicle of supporting vascular
C.T. Flap procedures are the MOST COMMON of all periodontal surgical techniques. Flaps should be
uniformly thin and pliable, the flap base must be uniformly thin (-2mm thick), and all flap corners
should be ROUNDED.

4 Rules of Flap Design:

1. flap base is WIDER than the free margin to allow sufficient blood circulation to the flap's
free margin.

2. lines of incision must not be placed over any defect in bone to prevent delayed healing.

3. incisions that traverse a bony eminence (canine) is avoided. The mucosa covering bony
eminences is thin and healing is slow, and may result in an ugly scar formation . Incisions
made in tissues that harbor uncontrolled infection may cause rapid infection spread (do
not do this). Most periodontal surgical procedures are performed only after anti-infective
therapy is complete.

4. all flap corners should be rounded, since sharp points delay healing (healing will occur
without complication if basic surgical principals are followed).

Deep periodontal pockets are often treated by flap surgery. These cases often result in reduced pocket
depth by formation of a long junctional epithelium (soft tissue reattachment), even if there is no change
in the position of the gingival margins. The best indicator of success of a periodontal flap procedure
is postoperative maintenance and plaque control by the patient.

Most Commonly Used Flaps:

1. Full-Thickness Mucoperiosteal Flaps-include the surface mucosa (epithelium, basement
membrane, C.T. lamina propria), and contiguous periosteum of the underlying alveolar bone.
This flap involves reflecting ALL of the soft tissue and periosteum to expose the underlying bone.
Afull-thickness flap is used where attached gingiva is thin « 2mm wide). Apically &Coronally
positioned flaps are full thickness flaps.
• Modified Widman Flap (MWF)-a full-thickness flap that is a modification of the replaced flap .
MWF is used in open flap debridement and regenerative periodontal procedures, and is a
mainstay of periodontal surgery on single-rooted teeth and on flap surfaces of molars affected
by moderate pockets and infra bony defects .
• MWF objectives: gain access to underlying bone & root surfaces, reduced pocket depth by
establishing a new attachment at a more coronal level, preserve an adequate zone of
attached gingiva, and to provide an environment for healing by primary closure.

33
 NOTES • MWF indications: pocket bases located coronal to the mucogingival junction, where there
is little or no thickening of marginal bone, when shallow to moderate pocket depths can
be reduced, and when esthetics is important (anterior region).

• Repositioned Flaps: include replaced flaps, MWF, and excisional new attachment procedures.
They all heal by repair (i.e. by a long junctional epithelium and C.T. adhesion or attachment),
-c and are considered pocket reduction procedures. Pocket reduction is achieved mainly by gains
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2. Partial-Thickness Periodontal Flap-includes ONLY the mucosa epithelium and a layer of the
underlying C.T. The mucosa is separated from the periosteum by sharp dissection. Alveolar bone
is not exposed. These flaps are used to prepare recipient sites for free gingival grafts, or when a
dehiscence or fenestration is present on a prom inent root. A partial thickness flap is used when
attached gingiva is thick (> 2mm).

One determinant of how the flap will be raised (either a full or partial thickness flap) is the thickness
(amount) of attached gingiva prior to surgery. Full thickness &partial thickness periodontal flaps can be
displaced, but palatal flaps cannot be displaced (due to the absence of unattached gingival on the palate).

POSITIONED flAPS - procedures in which the flap's coronal margins are advanced (lifted, but the
flap is not freed-up) apically, coronally, or laterally from an area adjacent to the recipient site to a new
location relative to the site they occupied before the procedure. Like repositioned flaps, most positioned
flaps heal by repair. In positioned flap procedures, the flap's vascular supply is maintained (unlike in the
free gingival graft).

Types of Positioned Flaps:

1. Pedical Flap (Laterally Positioned Flap)-a positioned full-thickness flap performed to correct
defects in morphology, position, or amount of attached gingiva. It is usually a full-thickness
flap that is attached at its base with its free end adjacent to the defect (recipient site). The
defect is covered by stretching the flap laterally until the free end comes over it.
• Indications: areas where narrow gingival recession is adjacent to wide band of attached
gingiva that can be used as the donor site. Used to correct or prevent recession by providing
root coverage, creating a wider band of gingiva, and in the absence of recession to widen
the zone of gingiva.

• Positioned &Repositioned flaps are really pedicle flaps that are all physically attached
at their apical base by a pedicle of lining mucosa and an intact blood supply.

• Important factors to evaluate before performing a laterally positioned flap: presence of

bone on the facial surface of the donor tooth, gingiva thickness and width of attached gingiva
at the donor site.

• Double Papilla Flap-a variation of the laterally positioned flap that uses the same principals,
except the gingiva between the teeth (papilla) on either side are placed over the exposed root.

2. Apically Positioned Flap-a full-thickness, mucoperiosteal flap with a relatively high degree of
predictability that is the "work horse" of periodontal surgery/therapy. This flap's objective is to
surgically eliminate deep pockets by positioning the flap apically while retaining the attached
gingiva. Most commonly used in conjunction with osseous surgery as surgical access is obtained
for osseous surgery, treatment of infra bony (intra bony) pockets, and root planing.
• Indications: moderate or deep pockets, furcation-involved teeth, and crown lengthening.

• Contraindications: patients at risk for root caries, as excessive root surfaces are often exposed
AFTER performing an apically positioned flap, and where tooth exposure would be unesthetic.

34
~-

• In the course of flap surgery, after gaining access to underlying osseous tissue and
performing the required therapy, the apically positioned flap is sutured to a place at a
more apical level, exposing the alveolar margin. When this is done, additional attached
gingiva granulates from the PDL and covers the barely exposed bone. This additional tissue
joins the apically positioned attached gingiva to form a broader zone of gingiva. Note: on
the palatal surface of maxillary molars, you need to trim the flap margin to proper length
during the procedure.

3. Coronally Positioned Flap-a full-thickness mucoperiosteal flap almoSt exclusively used to

restore gingival height and the zone of attached gingiva over isolated areas of gingival recession.

There is no necrotic slough of positioned flaps because positioned flaps carry their vascular supply
with them. In a FGG, healing involves revascularization of the graft. The graft's top layers are
revascularized last. Thus, the epithelium dies off (degenerates), producing the necrotic slough.

Internal bevel incision-basic incision in most periodontal flap procedures where the flap is reflected to
expose the underlying bone & root. It has 3 objectives:
1. Remove the pocket lining.

2. Conserve the relatively uninvolved outer gingiva surface, which if apically positioned,
becomes attached gingiva.

3. Produce a sharp, thin flap margin to adapt to the bone-tooth junction.

GINGIVOPLASTY - surgical procedure to reshape the gingiva & papilla of a tooth to correct
deformities and provide the gingiva with normal & functional form. The overall objective is NOT to
elim inate periodontal pockets, but to provide a more physiological tissue contour. While portions of the
gingiva are excised during a gingivoplasty, it is the reshaping (not the excision) of gingiva that defines
a gingivoplasty. Gingivoplasty is commonly used to correct tissue contours that result from ANUG.

GINGIVECTOMY - surgical procedure that eliminates pocket depth by resecting the tissue coronal
to the pocket base. The final aspect of the gingivectomy is to bevel (contour) the wound's coronal margin
to provide the most physiological shape and marginal thickness so adequate oral hygiene techniques
can be performed.

• Indications: treating pseudopockets, hereditary gingival enlargement, suprabony pockets, and

hyperplasia caused by Dilantin therapy.

• Contraindications: infrabony pockets (defects) and lack of attached tissue. Limitations include
compromised esthetics with longer teeth, lack of access to bony defects, and having a broad, open
wound post-surgically.

• Factors to consider when electing to perform a gingivectomy rather than a periodontal flap: pocket
depth (if the base of the pocket is located at the mucogingival junction or apical to the alveolar crest,
do not perform a gingivectomy); need for access to bone; and amount of existing attached gingiva.

OSTECTOMY - removal of osseous defects or infrabony pockets (pockets below the crest of bone)
by elimination of bony pocket walls. This bone removed is supportive in nature, but is sacrificed
because eliminating the pocket is worth the price of the loss in attachment apparatus. After removing
the osseous pocket walls, some re-contouring is done to provide optimal osseous architecture for the
overlying gingival tissues to conform to and be maintained.

• Major contraindication of removing crestal bone: if the removal will weaken an adjacent tooth's
bony support.

35
 N Osseous Oefects: the pattern of bone loss from periodontitis can be horizontal or vertical:
1. HORIZONTAL BONE LOSS-the pattern of interproximal bone loss parallels the CEJ of adjacent
teeth. Horizontal patterns are usually generalized by involving multiple teeth in a segment.
• SUPRABONY POCKETS-the pattern of bone loss (destruction) is HORIZONTAL, and is not
intraosseous. Transseptal fibers are usually normally arranged, but form at a more apical level,
and the pocket base (epithelial attachment) is CORONAL to the crest of alveolar bone.
Supra bony pockets may be further classified as a:
• Gingival pocket ("relative or "pseudopocket")-a condition where there is expansion of
the marginal tissue coronally (not apical movement) of the epithelial attachment.
Pocketing occurs WITHOUT attachment loss.

• Periodontal pocket ("true pocket")-a deepened gingival sulcus where the epithelium
undergoes ulceration. Characterized by APICAL MIGRATION of the epithelial attachment
(inner layer of cells of the JE) beyond its physiological level which is normally at or near
the CEJ.

2. VERTICAL BONE LOSS-pattern of interproximal bone loss does not parallel the CEJ, and
are found around ISOLATED teeth.
• Periodontal Osseous Defects (lNFRABONY POCKETS)-are generally classified by the number
of bony walls remaining that surround the tooth. With infrabony pockets, the pocket base
(epithelial attachment) is APICAL to the crest of alveolar bone so there is actually a defect
or hole within the bone (intraosseous). For a defect to have a bony wall, it must be
intraosseous (i.e. partially or completely within alveolar bone; i.e. ramps, hemiseptums,
interdental craters, intra bony defects, & moat defects) . Infrabony pockets are associated
with VERTICAL (ANGULAR) BONE LOSS that creates holes/defects within the bone, and are
classified as follows:
1. One-wall defects: Hemiseptum- if only the proximal wall is present. Ramp-if only a facial or
lingual wall is present.

2. Two-wall defects: (i.e. interdental crater).

3. Three-wall defects: an intrabony pocket; offer the best opportunity for bone graft containment
and periodontal regeneration procedures.

4. Four-wall defects: a circumferential or moat defects. Four-walled moat defects also offer the
best opportunity for bone graft containment and periodontal regeneration procedures.

5. Zero-wall defects: alveolar dehiscences & fenestrations. Do not treat with osseous surgery.

6. Combination defect: combination lesion that is more complex with more walls apically
than coronally.

Important: INFRABONY DEFECTS/POCKETS ARE CONTRAINDICATIONS FOR MUCOGINIGVAL SURGERY.

With infra bony pockets, interproximally the transseptal fibers run in an angular direction not horizontally.
Transseptal fibers extend in a sloping configuration from the cementum below the pocket base along the
bone and down over the crest of bone to the cementum of the adjacent tooth.

OSSEOUS CRATERS - concavities in the crest of the interdental bone confined within the facial &
lingual walls. Craters comprise 113 (35.2%) of all defects, and 2/3 (62%) of all mandibular defects.
Osseous craters are MORE COMMON in posterior segments than anterior segments, and are best treated
with OSSEOUS SURGERY (recontouring).

When evaluating an osseous defect, the ONLY WAY TO DETERMINE the number of walls left surrounding
the tooth is by EXPLORATORY SURGERY.

• Radiographs 00 NOT SHOW the number of walls left surrounding the tooth, the exact configuration
of the defect, or the location of epithelial attachment. This is because a dense buccal and/or
lingual plate of bone tends to mask the defect and blocks it out on the radiographs. Thus, the number
of osseous walls remaining can only be determined by exploratory surgery.

36
• TWO MOST CRITICAL FACTORS to determine the prognosis of a periodontally involved tooth are
MOBILITY &ATTACHMENT LOSS (the most critical). Periodontal osseous defects are classified by
the number of osseous walls present/remaining at the time of their surgical exposure, and may have
1,2,3, or 4 walls.
• To measure attachment loss use a periodontal probe from an established reference point (CEJ
or restoration margin) for initial measurement. Probings are repeated after appropriate time
intervals and any changes are noted (i.e. if a probing depth is 4mm and recession is 3mm, ,..,
"'tI

total attachment loss = 7mm). =:!

o
o
o
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:::!
OSTEOPLASTY - reshaping or recontouring the alveolar bone that does not provide attachment for C">

periodontal fibers (non-supporting bone) without removing supporting alveolar bone. It is similar to '"
a gingivoplasty in that it is not directed toward eliminating the pocket walls, but recontours &
reshapes the underlying osseous structures. In this technique, the non-supporting bone is removed (this
means the osseous reduction does not reduce the bone that the POL is attached).

• Non-supporting bone-alveolar bone not directed related to tooth support (i .e. bony exostoses,
edentulous ridges, tori, flattened interdental contours and ledges) . Walls of some osseous defects
may be comprised of non-supporting bone.

Clinically, a bone grafting procedure is MOST likely successful with a 3-Walled Defect. The success of
periodontal bone grafting varies directlywith the number of bony walls of the defect (vascularized, osseous
surface area), and inversely with the surface area of the root against which the graft is implanted .

• Anarrow 3-walled infrabony defect yields the greatest success, then a 2-walled defect, then a 1-
walled defect (infra bony defect/hemiseptal defect = the least successfu l).

Sometimes the graft may take even when the bone graft is piled on the crest of the interdental septum .
Clinically, the chances of success are best in a 3-walled infrabony pocket and least successful in a
through-and-through furcation defect on a maxillary molar.

Root resorption is the most common side effect of an autogenous bone graft in managing an infra bony
pocket and often extends into dentin and the pulp chamber. Other postoperative problems that sometimes
occur after osseous or marrow transplants: infection, graft exfoliation, various and sometimes
prolonged healing rates, and rapid defect recurrence.

DEHISCENCE - a loss of buccal or lingual bone overlaying the tooth root, leaving the root area only
covered by soft tissue.

ALLOGRAFT - a graft taken from one human (donor) and placed in another human (recipient). Afreeze-
dried decalcified bone graft taken from a human donor and placed in a periodontal defect in another
patient is an allograft.

Osseous Grafting Techniques: osseous coagulum, autogenous intraoral bone, il iac crest bone, Freeze-
dried bone allograft (FDBA) with autologous bone, porous, coral-derived hydroxyapatite, and Undecalcified
freeze-dried bone allograft (UOFA).

• Hemopoietic marrow is the bone donor graft with the greatest osteogenic potential.

37
 GUIDED TISSUE REGENERATION (GTR) - placement of non-resorbable barriers or resorbable
membranes & barriers over a bony defect. GTR BLOCKS the re-population of the root surface by long
junctional epithelium & gingival C.T. to allow POL and bone cells to re-populate the periodontal defect
(this technique assumes that only the POL cells have the potential to regenerate the tooth's attachment
apparatus) .
.."

"'
=:!
• GTR's physical blockade uses non-resorbable barriers (expanded polytetrafluoroethylene ePTFE) or
<:>
CJ resorbable membran~s and barriers (Type I bovine collagen, calcium sulfate, or polyactic acid).
<:>
:z:
:::!
C'>
VI • If a non-resorbable barrier is used , then 6-10 weeks after placement, a second surgical procedure
is performed to retrieve the non-resorbable barrier.

• Tissue Regenerative Procedures are applicable and predictable under these circumstances:
1. patient exhibits exemplary plaque control both before and after regenerative therapy.
2. patient does not smoke.
3. there is occlusal stability of the teeth at the regenerative site.
4. osseous defects are vertical. The more walls of bone remaining, the greater likelihood
of regenerative success.

Surgical Dressing Materials:

1. Should be conveniently prepared and placed.
2. Should be soft and flexible for proper adaptation, while providing stability and flexibility when set.
3. Should be non-irritating to the oral tissues.
4. Should have a smooth surface to help resist plaque accumulation.

Eugenol was previously the most popular and most effective agent in the periodontal dressing, but was
found to cause its own tissue injury and necrosis. Today, commercially available periodontal dressings
currently DO NOT CONTAIN EUGENOl. "Noneugenol-containing periodontal dressings include:

• Chemical cured: PerioCare-a paste-gel & Coe-pak-a paste-paste.

• Visible-light cured: Baricaid that comes in a syringe.

Advantages of Placing a Periodontal Dressing After Surgical Procedures: protects the surgical wound,
minimizes patient discomfort, helps maintain tissue placement, and helps prevent post-operative
bleeding. Periodontal dressings DO NOT enhance the healing rate of the tissues.

• Periodontal dressings do not have a well-defined effect on wound healing processes or on

surgical outcomes (i.e. gains of periodontal attachment or reduced probing depths).

• All dressings must be used according to the manufacturer's instructions and are removed within
7-10 days. However, before removing, ensure that the sutures are not embedded in the dressing and
ensure the dressing is not locked interproximally.

COLLAGEN found in the gingival has a turnover rate significantly greater than collagen found in tendons
and the palate.

• The most common form of the various collagen types in the mucosa is TYPE 1 collagen. Type I
collagen in the gingiva is not the same biochemicaly as found in other parts of the body and skin.

• Collagen turnover rate in norrmal gingiva is not as rapid as in the periodontal ligament (POL), but
is much greater than in other tissues (i.e. skin, tendons, and palate).

• Collagen accounts for -60% of gingival protein.

• Vitamin Cis required for hydroxylation of praline and lysine which are essential for collagen formation.

38
GINGIVITIS &ANUG
JUNCTIONAL EPITHELIUM - in health, the JE is a collar-like band of stratified squamous epithelium
10-20 cells thick near the sulcus, 2-3 cells thick at the apical end, and .25-1.35mm long. It is the
stratified non-keratinizing epithelium that surrounds the tooth like a collar, and is attached by one broad
surface to the tooth, and by the other to the gingival C.T. ,..,
."

::!

• JE has 2 basal laminas (1 faces the tooth (internal basal lamina) and 1laces C.T. ""
""
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(external basal lamina). :::!
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'"
• Proliferative cell layer-responsible for most cell divisions and is in contact with C.T. (next to external
basal lamina).

• JE desquamative (shedding) surface-located at its coronal end, which also forms the bottom of the
gingival sulcus. The JE is more permeable than the oral or sulcular epithelium, serving as the
preferential route for the passage of bacterial products from the sulcus into the C.T. and for fluid and
cells from the C.T. into the sulcus.

LONG JUNCTIONAL EPITHELIUM - refers to the JE in disease, and differs from the JE in health. In
disease, migration of the JE occurs, along with C.T. degeneration under the attachment. As the JE
proliferates along the root surface (gets longer), the coronal portion detaches. Barrier membranes (often
used to treat bony defects) help prevent the long JE from forming.

Epithelium Attachment - the attachment apparatus (i.e. internal basal lamina &
hemidesmosomes) that connects the JE to the tooth surface. The epithelium attachment is not the
same as the JE (which is the entire epithelium). For a new attachment to form after periodontal
treatment, complete removal of calculus, altered cementum, diseased JE, and pocket epithelium must
occur, and there must be undifferentiated mesenchymal cells.

Clinical Criteria to Diagnose Gingivitis: (bacterial plaque is the etiology of gingivitis. Without plaque,
there is no gingivitis. Gingivitis is the PREDOMINANT periodontal disease.

1. gingiva color: normal color ranges from coral pink to various stages of pigmentation.
• Erythema-an intense red color of the gingiva.
• Cyanosis-the most common color change (bluish-purple hue) found with periodontal disease.

2. gingiva contour: has a normal range, but is influenced by missing teeth, teeth position, etc.
Papillae should fill interproximal spaces, and gingival margins should be scalloped in form.

3. gingiva tone: the normal consistency of the gingival tissue should be resilient and fibrotic from
the free gingival groove, apical to the mucogingival junction. Gingiva texture should include
stippling (orange-peel appearance) of the attached gingiva.

4. gingiva size: healthy gingiva tissues should be well-contoured to the underlying osseous
architecture with the free gingival margin thin enough to allow a "knife-edge" thickness at
the dentogingival margin.

5. plaque &calculus: the best way to evaluate the amount and distribution of plaque is using
disclosing solution.

There are NO radiographic features of gingivitis (radiographic appearance of bone appears normal).
However, there are radiographic features of periodontitis.

39
 3 Stages of Disease in Developing Gingivitis:
1. Transient (incipient) Stage-occurs within 2-4 days after cessation of oral hygiene. The earliest
changes are visible microscopically consisting of a margination of leukocytes (PMNs) in vessels
close to the junctional epithelium. Sloughed epithelium cells and bacteria are found in the
gingival sulcus.

""1:1
m 2. Developing Stage-the area of collagen destruction becomes larger and is occupied by fluid that
::!:!
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contains serum proteins: fibrin, immunoglobulins (especially IgG), complement, inflammatory
0
:z cells, principally lymphocytes (B or T cells), and macrophages. In the developing stage,
::::!
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lymphocytes are the predominant cell.

3. Chronic Stage-the cytologic characteristics of the inflammatory infiltrate in the gingival lamina
propria are changed. Plasma cells predominate the chronic stage. IgG is produced by most of
the plasma cells, with a few cells present containing IgA (mostly in saliva). IgM containing cel ls
are rarely seen.

IgG - the immunoglobulin most abundant in the gingival exudates common in gingivitis.

Significant levels of immunoglobulins are found in both epithelial and C.T. compartments. Although
severe periodontal disease has been reported in people suffering abnormalities in neutrophil function
(neutropenia), increased or more severe periodontal disease has not been reported in young people with
other compromised immune functions (i.e. Tor B cell deficient states).

ACUTE NECROTIZING ULCERATIVE GINGIVITIS (ANUG) - also called "Vincent's infection" or

"trench mouth". ANUG is a condition that presents pathognomic signs and symptoms. Fusiforms,
spirochetes, & Prevotella intermedia are involved in ANUG's etiology. Treponema denticola is the
intermediate-sized spirochete associated with ANUG. Histologically, deeper areas of the lesion contain a
zone of spirochetal infection.

ANUG's 2 most important clinical Signs:

1. interproximal necrosis & pseudomembrane formation on marginal tissues-only affects
the gingiva. There is no attachment loss with ANUG.

2. History of soreness/pain and bleeding gums caused by eating and brushing.

ANUG (acute necrotizing ulcerative gingivitis = Vincent's Angina) - an anaerobic

infection of the gingival margins causing ulceration and, if untreated, destruction of the gingiva and
underlying bone. The interproximal areas are affected first. Spirochetes invade the epithelium and C.T.
Prevotella intermedia, Fusobacterium species and Selenomonas species are also seen in the necrotic
zones superficial to the zone of spirochete infiltration.
• Prevote/la Intermedia & Spirochetes (intermediate-sized spirochetes) are the principal bacteria
associated with ANUG.

ANUG Signs & Symptoms: fetor oris (offensive odor), low-grade fever, lymphadenopathy, and malaise.
NEUTROPHIL is the dominant WBC involved in the inflammatory infiltrate of ANUG.

• ANUG occurs most often in adults ages 18-30. Factors that predispose someone to ANUG: a history
of gingivitis, tobacco smoking, gross neglect (poor oral hygiene), fatigue, stress, poor nutrition, and
immuno-compromised patients.

• ANUG Treatment: debridement, hydrogen peroxide (or warm saline) rinses, and antibiotic therapy
(penicillin V) if there is systemic involvement (i.e. fever, malaise, lymphadenopathy). Patients with
HIV-associated ANUG require gentle debridement and antimicrobial rinses.

Acute Gingivitis-gram (+) bacteria predominate (Actinomyces filament & Streptococci species) .

• As gingivitis develops (early lesion is 4-7 days), the area of destruction becomes larger with
persistence of inflammation. Leukocytes invade C.T. and are dominated by lymphocytes (3/4 of all
cells), macrophages, plasma cells (secrete IgG), and mast cells (release histamine).
40
3 Major Phenomena of Inflammation:
1. Increased vascular permeability-inflammatory tissue exudates forms due to increased
NOTES
permeability of blood vessels at the inflammatory site (edema).

2. Leukocytic cellular infiltration-involves mainly neutrophils, caused by chemotactic agents C5a

& leukotriene 84 (LTB4) that function to phagocytize bacteria and elaborate proteolytic enzymes.
.,
,..,
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3. Repair-occurs either by regeneration or replacement. c
c
c
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ACUTE INFLAMMATION - the INITIAL protective response of tissue to irritation or injury (especially C">
en
bacterial infections) involving vascular and cellular responses. Polymorphonuclear Neutrophils (PMNs)
=neutrophhilic leukocytes are initially the most abundant inflammatory cells in acute inflammation,
which predominate in the Cellular phase.

• PMNs (neutrophilic leukocytes) are the first line of defense and first cells to migrate into the
gingival sulcus when inflammation caused by plaque formation in the initial lesion of gingivitis
occurs. PMNs are the first line of defense and migrate toward the injured site (gingiva) as a result
of the chemotactic properties of plaque.

• Cells involved in acute inflammation

2 Phases of Acute Inflammation:

1. Vascular Phase-involves basophils, tissue mast cells, & platelets which release HISTAMINE.
• Vasoconstriction (temporary)-narrowing of blood vessels caused by contraction of smooth
muscle in vessel walls that are visible as blanching of the skin.

• Vasodilation-widening of blood vessels to increase blood flow to the infected area .

• Increased vascular permeability-allows diffusible components to enter the infected site.

Inflammatory tissue exudates forms due to increased permeability of blood vessels at
the inflammatory site (edema) .

• Note: Eosinophils are NOT in the vascular phase, but are the predominant inflammatory
cells in allergic reactions and parasitic infections.

2. Cellular Phase: Polymorphhonuclear neutrophils (leukocytes) predominate and are the first
defense cells to migrate to the injured tissue via chemotaxis (C5a & leukotriene 84 (LT84) are
the chemotactic factors for neutrophils). PMNs engulf matter by phagocytosis. The engulfed
matter becomes a phagosome and combines with lysosomal granules to form a phagolysosome
that digests the engulfed particle.
• Leukocytic cellular infiltration-involves mainly neutrophils caused by chemotactic agents
C5a & leukotriene 84 (LT84) that function to phagocytize bacteria and elaborate
proteolytic enzymes.

• Macrophages appear late in the cellular phase and represent a TRANSITION between acute
and chronic inflammation.

4 LOCAL Signs of Acute Inflammation usually accompanied by loss of function:

1. Redness (rubor)-caused by dilation of capillaries.

2. Heat (calor)-capillary dilation allows increased blood flow through vessels, with the associated
high metabolic activity of neutrophils and macrophages.

3. Swelling (tumor)-caused by increased capillary permeability.

4. Pain (dolor)-caused by lysis of blood cells which triggers bradykinin and prostaglandin
production. Pain is a cardinal symptom of inflammation that may result from histamine
and bradykinin release, and from direct nerve damage or pressure by the tissue exudates.

5. SYSTEMIC effects of acute inflammation: fever, tachycardia, and leukocytosis (especially neutrophils).
41
 MAST CELLS - participate in the early phase of inflammation (i.e. an early lesion of gingivitis), and
are found in C.T., contain numerous basophilic granules, and release substances (heparin & histamine)
in response to injury or inflammation of body tissues. Mast cell content in human gingiva is high, and
increases as gingival inflammation increases.

• Histamine-MAJOR HISTAMINE STORAGE SITES are mast cells, platelets, and basophils. Histamine
,...,
.."
is released when tissues are damaged, and is important in the VASCULAR PHASE of acute
:=!
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CJ inflammation (causing vasodilation and increased vascular permeability).
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VI • Anaphylactic response-characterized by the degranulation of mast cells when antigen-antibody
complexes affix to cell surfaces.

CHRONIC GINGIVITIS - the number of gram (-) anaerobic organisms increases. Fusobacterium ,
Prevotelia intermedia, and Capnocytophaga species comprise %of the flora. Spirochetes become evident,
and Actinomyces species (filaments) remain.

• As gingivitis reaches the chronic stage (established lesion whose time varies from weeks, months,
or years), there is an increase in PLASMA CELLS (still secreting IgG) and B-LYMPHOCYTES that
invade deep into C.T. This stage can persist for years with or without moving to the advanced lesion
(periodontitis).

• Chronic Inflammation-the protective tissue response to irritation or injury that persists LONGER
than several days, with an accumulation of lymphocytes, plasma cells, but mostly macrophages
(macrophages dominate). There is more proliferative than exudative, and necrosis occurs and recurs
(as opposed to repa ir by regeneration). Fibrosis occurs causing progressive tissue damage and loss
of function. Polymorphonuclear Leukocytes (PMLs) are the main cell components that cause
chronic inflammation.

• When chronic gingivitis progresses to periodontitis (advanced lesion), lymphocytes, plasma celis,
and macrophages continue to invade the C.T. along vascular pathways and destroy the gingival fibers.
Changes within the supporting bone occur as the inflammatory process continues. *Neutrophils are
the MOST NUMEROUS cell in the inflammatory exudates of an acute periodontal abscess.

PELLICLE - a glycoprotein deposit (dental plaque) derived from salivary constituents that rapidly
covers and is selectively adsorbed onto a freshly cleaned tooth surface. Pellicle formation is the 1st
step in plaque formation. Pellicle Components: albumin, lysozyme, amylase, immunoglobulin A, praline-
rich proteins, and mucins.

• Primary Pellicle Colonizers: gram (+) bacteria like Streptococcus sanguis, Streptococcus mutans,
& Actinomyces viscosus.

• Secondary Pellicle Colonizers: gram (-) species like Fusobacterium nucleatum, Prevotella
intermedia, and Capnocytophaga species.

• Tertiary Pellicle Colonizers: Porphyromonas gingivalis, Campylobacter rectus, Eikenella corrodens,

Actinobacillus actinomycetemcomitans, and oral spirochetes (Treponema species).

The overall pattern observed in dental plaque development is a very characteristic SHIFT from an
early predominance of gram (+) facultative aerobes, to a later predominance of gram (-) anaerobes.
The MAJOR factor in determining the different bacteria is OXYGEN. The redox potential of the gingival
sulcus greatly influences the bacterial composition.

The MOST abundant bacteria in a HEALTHY SULCUS are STREPTOCOCCUS & ACTINOMYCES species.
Gram (+) cocci (Streptococci) & filamentous bacteria (Actinomyces) are most abundant in a healthy sulcus.
• Streptococcus Viridans-consist of a variety of alpha-hemolytic streptococci (i.e. S. salivarius,
mutans, sanguis, and mitis) that are all COMMON ORAL FLORA.

42
• Normal Flora of the Oral Cavity:
• Gram (+): Streptococcus, Peptostreptococcus, Actinomyces, Lactobacillus.
NOTES
• Gram (-): Veillonella, Fusobacterium, Corynebacterium, Campylobacter, Eikenella.

At birth, the oral cavity is usually sterile, but microorganisims appear -lO-12hrs after birth. After one
year, these bacteria are present:
,.,.,
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• Streptococci (S. salivarius is most abundant) . S. mutans and sanguis do not appear until teeth ::!:!
Q

are present. ""

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• Staphylococci, Neisseria, Actinomyces, and Fusobacterium.

• By age 4-5, the oral flora resembles an adult's oral flora.

PREGNANCY GINGIVITIS - a nonspecific gingivitis and definitive diagnosis is made on the physical
state of pregnancy. There is an exaggerated and modified response of the gingiva to local factors
(plaque), considerable loss in tissue tone, a color change to bright red, with marginal rolling and
papillary enlargement that obliterates embrasure spaces. The prominent clinical finding is gingival
hemorrhage (bleeding) upon gentle pressure.

• If a women is in her 1st or 2nd trimester, scaling, polishing, and OHI can be performed. If she is
well into her 3rd trimester, prudent treatment may be to just give OHI and reappoint her after
childbirth for scaling and polishing.

• Gingival changes evident DURING PREGNANCY probably (but not definetly) result from the
effect of PROGESTERONE, and an increase in the number of MAST CELLS found throughout
the gingival tissues.

• Pregnancy gingivitis is associated with increased levels of PREVOTELLA INTERMEDIA in the inflamed
sites. These bacteria crave steroid hormones (Le. Progesterone) for their own metabolism.

• Gingival pathology IS NOT found during pregnancy if no etiologic factors accumulate (plaque) or are
not present prior to the pregnancy.

LOCALIZED ACUTE GINGIVITIS - the most common form of gingival periodontal disease in
school-aged children.

DESQUAMATIVE GINGIVITIS (DG) - a chronic gingival disease characterized by erythematous,

erosive, vesiculobullous, and/or desquamative involvement of the free and attached gingiva . Most
patients are postmenopausal FEMALES ages 40-70yrs. DG is a poorly understood, painful condition
where the outer gingiva layer desquamates (peels away), exposing an acutely red surface.

• Many diseases and conditions are associated with this gingival disease, but most are dermatologic.

• Plaque's role is vague in desquamative gingivitis.

• Usually occurs due to an allergic reaction or is associated with skin diseases (i.e. lichen planus,
BMMP, bullous pemphigoid, and pemphigus vulgaris). This condition generally resolves when the
allergic reaction or skin disease is treated and cleared up.

• Treatment: depends on the underlying condition . Pemphigus, pemphigoid, and psoriasis may require
system ic steroid thera py. Topical corticosteroids (Triamcinolone, Kenalog in Orabase) are effective
in treating the oral lesions.

• Histologically, where non-ulcerated areas are found, stratified squamous epithelium is significantly
atrophic. Rete pegs are short or absent. Inflammatory cells (mainly plasma cells), may be found on
the basal layer.

43
 N HEREDITARY GINGIVOFIBROMATOSIS - a rare GENETIC DISEASE that is a progressive
proliferation of the gingiva (especially collagenous elements). Clinically, there is generalized diffuse
gingival enlargement, often extensive enough to cover the teeth . The tissue is dense and firm , with
considerable distortion of normal contour. Gingival color is normal, but erythematous changes are a result
of secondary bacterial involvement.

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• There is a striking lack of inflammatory cells, proliferating capillaries, and vascular engorgement
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en INflAMMATORY GINGIVAL ENLARGEMENT - a form of gingivitis that is easily differentiated from
simple gingivitis. Clinical findings include an increase in gingival size, distortion of normal form, and
change in tissue tone. There is significant increase in sulcular depth and pocket formation occurs
(pseudopocket or relative pocket). It is a pseuodpocket because it is caused by expansion of the
marginal tissue coronally, rather than apical movement of the epithelial attachment beyond its
physiological level. Histologically, there is a greater degree of sulcular proliferation through rete pegs
than in simple gingivitis.

• Medications (specifically Dilantin, Cyclosporine A, &Nifedipine) cause the highest incidence of

fibrous gingival hyperplasia.

• Drugs that induce OVERGROWTH (hyperplasia) of gingival tissues: Phenytoin (Oilantin),

Cyclosporine A(Sandimmune), &Nifedipine (Procardia). Gingival overgrowth is related to the level
of plaque accumulation. The highest incidence of drug-induced hyperplasia occurs with
PHENYTOIN (OILANTlN).

• Dilantin Hyperplasia-a progressive proliferation response to the gingiva associated with the use of
sodium Dilantin (Phenytoin) . Studies show administration of Dilantin does not cause a significant
increase in fibroblastic activity. The occurrence of the gingivitis IS NOT automatic with the drug
therapy if the level of oral hygiene is maintained and no pre-existing gingival disease exists. Studies
show between 50-60% of patients taking Dilantin will develop hyperplasia. Asignificant difference
in comparing this hyperplasia to hereditary gingivofibromatosis, is the finding that there is an
increased accumulation of inflammatory cells in Dilantin-induced hyperplasia .
• 20% of patients on calcium channel blockers (i.e. Nifedipine), and 20-30% of patients on
cyclosporine A (an immunosuppressant), are susceptible to drug-induced gingival 0
vergrowth/hyperplasia.

• Pseudopocketing ("gingival pocket" or "relative pocket")-a condition where pocketing occurs

WITHOUT ATTACHMENT LOSS due to expansion of the marginal tissue CORONALLY (not apical
movement of the epithelial attachment beyond its physiological level).

AGINGIVECTOMY can be done to correct the gingival contours for Hereditary Gingivofibromatosis &
Inflammatory Gingival Enlargement that is drug-induced.

PERIODONTITIS - inflammation that affects and destroys the attachment apparatus (bone
destruction). Periodontitis history is marked by APICAL MIGRATION of the junctional epithelium from the
CEJ, loss of C.T. attachment &POL, and bone destruction. Periodontitis usually progresses slowly and
painlessly, but is arrested with proper therapy.

• Periodontitis ALWAYS begins with gingivitis due to local irritation, primarily plaque, and the
inflammation then spreads from the gingiva and soft tissues into the underlying structures. Gingivitis
and periodontitis cannot be induced without bacteria (plaque).

• Chronic gingivitis/Gingivitis does not always lead to periodontitis, and may exist for long periods
without advancing to periodontitis. However, gingivitis & periodontitis MUST ALWAYS be induced by
bacteria (plaque).

• The presence of periodontal pockets CANNOT be determined from radiographs.

To diagnose periodontitis, radiographic evidence of bone loss MUST be evident. Bitewing x-rays are
44
the MOST accurate to assess alveolar bone resorption. If extensive bone loss has occurred, vertical
bitewings should be taken because they reveal more of periodontium.

• MORE THAN 30% of the bone mass at the alveolar crest must be lost for a change in bone height
to be recognized on radiographs.

• Areduction of only 0.5-1.0mm thickness of cortical plate is sufficient to permit radiographic ..,
-0

visualization of destruction of the inner cancellous trabeculae. The crest of alveolar bone is :!:!
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affected in periodontal disease. In health, the crest lies 1-2mm below the CEJ of the adjacent teeth . o
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• In peridontitis, these radiographic changes are visible: loss of lamina dura, horizontal or vertical
bone resorption, and thickening (widening) of the periodontal ligament space.

• Bleeding, pocket depths> 5mm, and changes in tissue color and tone cannot lead to a diagnosis
of periodontitis WITHOUT radiographic evidence of bone loss.

• Radiographs as a diagnostic tool in periodontal disease CANNOT determine a definitive diagnosis of

furcation involvement, and CANNOT accurately depict the morphology or depth of interdental craters
that sometimes appear as vertical defects.

Radiographic Changes in Periodontal Disease:

1. Early periodontitis-areas of localized erosion of the alveolar bone crest (blunting of the
crest in anterior regions, and rounding of the junction between the crest and lamina dura
in posterior regions).

2. Moderate periodontitis-destruction of alveolar bone extends beyond early changes in

the alveolar crest, and may include buccal or lingual plate resorption, generalized
horizontal erosion, or localized vertical defects and possible clinical evidence of tooth mobility.

3. Advanced periodontitis-bone loss is so extensive that the remaining teeth show excessive
mobility and drifting, and are in danger of being lost. There is usually extensive horizontal
bone loss or extensive bony defects.

4 stages of the Periodontal Lesion: initial, early, established, & advanced.

Additional clinical criteria that MUST be evaluated during a periodontal exam (besides color, tone,
contour, & gingiva size):
1. Level of free gingival margin in relation to the CEJ: the normal level of epithelial attachment
should be on enamel or at the CEJ (this places the free gingival margin 2-3mm coronal to the
sulcular base).

2. Periodontal pocket depth: all measurements> 3mm are recorded for sulcular depth, including
any reading that locates the free gingival crest < 2mm at or below the CEJ.
• Shallow pockets attached at the level of the apical third of the root connote more severe
destruction than deep pockets attached at the root's coronal third. When the gingival margin
coincides with the cementoenamel junction (CEJ), the loss of attachment = the pocket depth.
• Provides the most accurate assessment of periodontal pocket depth.

3. Loss of Attachment: determined by measuring the distance between the CEJ to the base of
the attachment.
• Attachment level-the position of the junctional epithelium at the base of a sulcus (pocket).
In health, the JE is on enamel or at the CEJ. In disease, the JE migrates apically along the root
surface. It is measured from an established reference point (CEJ or restoration margin) to the
attachment with a periodontal probe. The periodontal pocket is measured from a changeable
point (margin of free gingiva) to the attachment level.

4. Mobility: there are three grades of tooth mobility. 1,2, and 3. Grade 3 is the most severe and has
the poorest prognosis

45
 NOTES 5. Bleeding: physiologically, bleeding from the gingival sulcus should not be caused by gentle
provocation . Bleeding in the absence of local irritants may indicate a systemic disease. Bleeding
is the most reliable indicator of gingival or periodontal inflammation.

6. Exudate: the presence of exudates (specifically suppuration) is evaluated by digital pressure

on the buccal and lingual of each tooth .
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7. Mucogingival complications: the involvement of the gingival component in the disease state
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The two MOST critical parameters for the prognosis of a periodontally involved tooth are ATTACHMENT
LOSS (most critical) and TOOTH MOBILITY.

• Attachment loss is the MOST significant clinical criteria in regard to the prognosis of a periodontally
involved tooth (much more significant than periodontal pocketing). Attachment loss is the most
significant factor because with attachment loss, supportive structures are being destroyed.
Pocketing can increase or decrease depending on the amount of inflammation without attachment
loss. However, extensive attachment loss and gingival recession can be accompanied by shallow
pockets (poor tooth prognosis).

• Clinically, the most common sign of occlusal trauma is tooth mobility.

PERIODONTAL POCKET PROBING - provides the MOST ACCURATE assessment of periodontal

pocket depth.

• Periodontal pocket-a pathologic space between a tooth and pocket wall. Its depth is measured from
the gingival margin to the clinical attachment level. Pocket depth is measured using a calibrated
periodontal probe. The most important reason for using the periodontal probe is it DETERMINES
LOSS OF ATTACHMENT. Probing measurements are taken BEFORE & AFTER SRP procedures to evaluate
the tissue response and effectiveness of treatment.

• Periodontal probing provides the MOST ACCURATE ASSESSMENT of periodontal pocket depth. The
true topography of vertical osseous defects cannot be determined by radiographs alone (as bone
levels may be high, but pockets may be deep). Extensive bone loss may exist, yet be unaccompanied
by pockets if the gingiva has receded.

During PROBING, the periodontal probe is adapted in the interproximal areas so it touches the contact
area with the tip angled SLIGHTLY BELOW &BEYOND the contact area. The probe is angled -10° on each
interproximal surface so the probe tip is placed apical to the contact point of adjacent teeth and may
detect any interdental crater. However, usually the probe is directed PARALLEL to the tooth's long axis.

• Periodontal measurements are taken by inserting the probe UNDER the marginal gingival and
gently moving the tip down to the junctional epithelium (JE) which feels soft, elastic, and resilient.
In a healthy site, the probe tip stops within the JE and in a diseased site it penetrates into C.T. In
severe disease, the probe tip may penetrate to the alveolar bone.

• The probe is inserted along the long axis of the tooth into the pocket with gentle pressure (-25gm
of force) until resistance is met. This force depresses the thumb pad -1-2mm. The probe is walked
around each tooth surface. This method is less painful and more efficient, provides a complete and
accurate assessment of the depth of epithelium attachment, and detects bony defects better.

• Clinical probing depth is ALWAYS GREATER than the histologic sulcus or pocket depth. Probing
accuracy is only within +/- Imm.

• The calibrated periodontal probe should have a tapered shaft -0.5mm in diameter at the tip. It
is important to have uniform instruments throughout the practice to ensure standardization.

46
NABER'S 2N (HAMP PROBE) - used to detect and clinically diagnose 4 types of FURCATION NOTES
involvement according to the GLICKMAN FUR CATION CLASSIFICATION:

1. Grade I: incipient bone loss. Furcation probe can feel the depression of the furcation opening.

2. Grade II: partial bone loss (Cul-de-sac). Furcation probe tip enters under the roof of the furcation.

3. Grade III: total bone loss/destruction with through-and-through opening of the furcation. The
furcation entrance is not visible. The bone loss is at the furcation is tothe extent that a probe
can be passed through the furcation from buccal to the lingual (and vice versa). In trifurcated
teeth, the probe can be passed from one aspect to another (from the ML to the buccal). In these
cases, the furcation is still covered by gingival.

4. Grade IV: a Grade III furcation where the furcation entrance is visible.

Findings That Complicate Furcation Involvement and account for some painful symptoms:

• Caries of cementum & dentin, tooth resorption in the furcation, abscess formation in the furcation,
and involvement of pulp via lateral canals in the furcation.

• Adefinitive diagnosis of furcation involvement is made by careful clinical probing with a Naber's (2N)
or Hamp probe. Radiographs are helpful, but are used ONLY as an adjunct to the clinical examination.

MAIN objective of treating involved furcations is to ELIMINATE FURCATION INVOLVEMENT using various
treatment methods (however, not all treatments can eliminate the furcation, as some treatments only
increases accessibility for plaque removal). Bone grafts have relatively little effectiveness in treating
furcations . However Guided Tissue Regeneration (GTR) can treat Grade II furcations with good
success. Furcation involvement of maxillary 2nd molars have the POOREST PROGNOSIS after therapy.

MOST COMMON ERROR during periodontal probing is EXCESSIVElY ANGLING the probe when inserting
it interproximally beyond the long axis of the tooth. This gives greater probing readings than are
actually present.

• Tilting the probe can affects measurement accuracy. If the probe is angled too much it will extend
past the contact area. If it is not inserted far enough, it will be at the line angle rather than under
the contact area. Both mistakes result in inaccurate readings. Thus, the probe tip should be flAT
against the tooth near the gingival margin with probe approximately PARALLEl WITH LONG AXIS OF
THE TOOTH FOR INSERTION.

• Probe tip should ALWAYS be kept in contact with the tooth to prevent soft tissue injury. The probe
is gently "walked" along the JE in an up and down motion (circumferential probing) always remaining
under the gingival margin. It is critical that the probe be walked along the entire gingival sulcus since
the depth of the epithelial attachment varies.

• SIX probing measurements for each tooth are recorded (3 on the buccal (DB, B, MB) & 3 on the
lingual (DL, L, MU. These measurements are the distance in mm from the pocket base (junctional
epithelium) to the free gingival margin.

• In the presence of inflammation, the probe may extend apical to the most coronal extent of the JE
(pocket base) and give a slightly greater probing depth than is actually present.

Patients at risk for subacute bacterial endocarditis must be premedicated BEFORE periodontal
probing. Bacteremia can occur even with mastication or brushing, but it does not last long. The
important consideration is the presence or absence of periodontal inflammation . Inflammation leads to
longer duration bacteremia with resultant risks for patients at risk of acute bacterial endocarditis.

47
 If the periodontal probe contacts an obstacle once inserted into the gingival sulcus, attempt to MOVE
PAST THE OBSTACLE and then continue to move the probe apically. Often when probing, probe passage
may be blocked by a hard, unyielding ledge of calculus. Thus, gently lift the probe away from the tooth
and place it against the tissue wall of the pocket and attempt to proceed apically again .

If the obstacle was calculus, and has now been bypassed, the probe will move deeper into the pocket until
,..,
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the JE is reached (sulcus base). The probe tip should then be placed back against the tooth once the
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obstruction has been bypassed. Important: the probe should be inserted PARALLEl to the tooth's
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of deepest penetration .

GINGIVAL RECESSION - measurement of the migration of the free gingival margin APICAL to the
CEJ (measured as a positive value). The recession measurement added to the probing depth indicates the
amount of periodontal attachment that has been lost at that site. When the gingival margin is coronal
to the CEJ, recession measurement has a negative value.

• MOST COMMON etiologic factor/cause of gingival recession is TOOTHBRUSH ABRASION (injury).

This type of recession is common on the left canines of right-handed people (or right canines of
left-handed people).

• Gingival recession can also occur secondary to periodontal therapy. This may have additional
significance in the older patient, namely increased risk for cervical abrasion, dentinal sensitivity,
and most important, predisposition to root caries.

• The hygienist or dentist should evaluate the brushing technique and monitor hard and soft tissue
conditions at each recall visit. Faulty placement, overaggressive movement or pressure, or use
of a hard toothbrush can cause hard and soft tissue damage.

• Sometimes these areas will become sensitive if the root is exposed and the patient complains of
COLD SENSITIVITY. This hypersensitivity will sometimes subside over time with daily plaque removal
using a SOFT TOOTHBRUSH to help desensitize the root surface by allowing remineralization of
the root surface.

• The rationale of in-office densensitization procedures is not completely understood. Some procedures
may depend on denaturation of the superficial end of TOMES FIBERS or of nerve endings in dentin.
Other procedures are designed to deposit an insoluble substance on the nerve or fiber endings to
act as a barrier to stimuli, while others procedures stimulate secondary dentin formation (reparative
dentin), thus insulating the pulp from external stimuli.

TOOTHBRUSH TRAUMA (ABRASION) - usually occurs on CANINES &PREMOLARS (the most

prominent teeth in the dental arch). Oral health maintenance is enhanced by using a SOFT-BRISTlE
toothbrush with a dentifrice of optimum abrasiveness and dental floss. Ahard-bristle toothbrush can
cause gingival recession and abrasion of enamel or cementum, thus is avoided.

• The abrasive quality of dentrifices affects enamel, but abrasion is a greater concern for patients
with exposed dentin since dentin is abraded 25x faster, &cementum 35x faster than enamel. This
can lead to root surface abrasion and root sensitivity.

• Hard tissue damage from oral hygiene procedures is mainly due to abrasive dentifrices, while
gingival lesion can be produced by a toothbrush alone.

• Toothbrush trauma (abrasion) can cause recession of the marginal gingiva, soft tissue lacerations
(including attached gingival and alveolar mucosa), v-shaped notches in the cervical areas of teeth, &
gingival clefts (narrow grooves that extend from the gingiva crest to the attached gingiva). The location
of these alterations if usually INVERSElY related to the right-or-Ieft handedness of the patient.

Important: in gingival atrophy (recession), tissues appears otherwise normal, the gingiva is thin, finely

48
textured , and pale pink with normal papillae. In addition, the gingival sulci are very shallow, and plaque N
is minimal.

HYDRODYNAMIC THEORY - the most accepted theory as to the CAUSE OF ROOT SENSITIVITY which
postulates that the pain associated with root sensitivity is caused by indirect innervation caused by
DENTINAL FLUID MOVEMENT IN THE TUBULES that stimulates mechanoreceptors in the pulp.
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DENTINAL HYPERSENSITIVITY - a problem in patients immediately after periodontal surgery that ""
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causes clinical exposure of root surfaces (dentinal tubules are not adequately sealed). Cold sensitivity :z:
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is the main symptom. Plaque and food debris that remain on exposed root surfaces, often lead to C")
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increased sensitivity. To reduce dentinal sensitivity to thermal change after removing a periodontal
dressing, KEEP THE ROOTS FREE OF PLAQUE. There are other treatments to reduce dentinal
hypersensitivity, however none of the following are totally effective. Often, diligent oral hygiene alone
solves the problem of sensitivity.

1. topical fluorides: sodium fluoride (2.0%) & stannous fluoride (8%). Acidulated phosphate
fluoride is contraindicated due to its high acid pH.

2. fluoride mouth rinses: OTC sodium fluoride (0.05%) or prescription acidulated phosphate-fluoride
(0.04%) and sodium fluoride (0.2%).

3. desensitizing toothpastes: contain either strontium chloride, potassium nitrate, or sodium citrate.
Recommend patient to use with a low abrasive dentifrice.

4. iontophoresis: electroplating fluoride to root surfaces.

5. dentin bonding agents: applied to the root surface (i.e. All-Bond, Scotch bond, Gluma,
Amalgam-Bond).

6. root coverage with gingival surgery (FGG)

ATTACHED GINGIVA - measured from the projection of the sulcus base (periodontal pocket) onto the
gingiva surface to the mucogingival junction (MGJ). The amount of attached gingiva is calculated by
subtracting the sulcus/pocket depth from the width of gingiva from the free gingival margin to the
mucogingival margin.

BACTERIAL PLA~UE - is the KEY ETIOLOGIC AGENT in the cause/initiation of gingivitis and
periodontal disease. Plaque is an accumulation of a mixed bacterial community in a DEXTRAN MATRIX.
It is formed on a cleaned tooth surface within minutes, and is composed of 80% water &20% solids
(95% of this 20% is bacteria). The clinician's goal and the goal of oral hygiene is to remove this etiologic
agent. After a prophy, plaque is most likely to accumulate on interproximal tooth surfaces first.

Plaque is a SOFT deposit that accumulates on teeth. Plaque is a complex microbial community with>
1010 bacteria/mg. In addition to bacteria cells, plaque contains a small number of epithelial cells,
leukocytes, and macrophages. The cells are contained in an extracellular DEXTRAN matrix formed from
bacterial products and saliva . The extracellular matrix contains protein, polysaccharide, and lipids.
Dextrans-insoluble & sticky, and contribute to plaque's ability to adhere to teeth. Plaque also contain
inorganic compounds (largely calcium and phosphorus) which are derived from saliva. Plaque's
inorganic content is greatly increased with the development of calculus. Calculus formation involves the
calcification of dental plaque.

Plaque can be supragingival or subgingival, and different bacteria may be found in plaque (cocci, rods,
&filaments) , and their properties change with time, diet, and location .

Constituents of PLAQUE: the overall pattern seen in dental plaque development is a very characteristic
shift from an early predominance of GRAM (+) FACULTATIVE bacteria, to a later domination of GRAM
(-) ANAEROBIC bacteria, as the plaque mass accumulates and matures. As PLAQUE AGES, the number
of gram (+) aerobic bacteria (i.e. cocci) DECREASES, while the number of gram (-) anaerobic bacteria
(i.e. rods, fusiform filaments, spirochetes) INCREASES.
49
 Stages of Plaque Formation:
1. Acquired Pellicle Formation: the pellicle is derived from salivary constituents that are selectively
adsorbed onto the tooth surface. Pellicle is composed of albumin, lysozyme, amylase,
immunoglobulin A, proline-rich proteins, and mucins. The pellicle is essentially structureless
and bacteria-free, and forms on a clean tooth surface within minutes due to its salivary origin.
It also forms on crowns, dentures, porcelain teeth, etc .
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2. Bacterial Colonization: within a short time after cleaning a tooth, the pellicle-coated tooth
o surface is colonized by gram (+) bacteria (i.e. Streptococcus sanguis, Streptococcus mutans,
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M & Actinomyces viscosus) . These are the primary colonizers.
'" 1. Primary Plaque Colonizers: GRAM (+) facultative bacteria that are the constituents of
EARLY (YOUNG) plaque, appearing within a short time after cleaning a tooth. Streptococcus
sanquis, Streptococcus mutans, &Actinomyces viscosus.

2. Secondary Plaque Colonizers: are GRAM (-) bacteria (Fusobacterium nucleatum, Prevotella
intermedia, & Capnocytophaga species) found in plaque after 1-3 days of accumulation.

3. Tertiary Plaque Colonizers: consists of GRAM (-), ANAEROBIC RODS that appear 1 week after
plaque accumulation (Porphyromonas gingivalis, Campylobacter rectus, Eikenella
corrodens, Actinobacillus actinomycetemcomitans/AA, and oral spirochetes
(Treponema species).

3. Maturation Stage: saliva continues to provide agglutinating substances and other proteins to
the intercellular matrix, and bacterial intercellular adhesion results. The crystalline structure
will increase and eventually calcifies into calculus.

Supragingival Plaque: plaque that is attached or tooth associated, dominated by gram (+) aerobic
facultative cocci (Streptococcus sanguis, mutans, &Actinomyces viscosus). Saliva and diet alter its
bacterial composition.

Subgingival Plaque: plaque that is unattached or loosely adherent (more closely associated with the wall
of subgingival tissues than with attached (supragingival plaque). Dominated by anaerobic, gram (-)
rods. Saliva and diet do not alter bacterial composition. As pockets form, gram (-) anaerobic rods prevail.
Bacterial species found are:

• Porphyromonas gingivalis, Fusobacterium nucleatum, Prevotella intermedia, Bacteroides

forsythus, Campylobacter rectus, and Treponema denticola and other Treponema species.

Bacteria produce low molecular weight compounds (i.e. hydrogen sulfide &butyrate) that can induce
some of the early signs of inflammation. However, the chronic signs of periodontitis (i.e. inflammation,
collagen &bone loss) are mainly caused by bacterial products entering the tissue and activating
inflammatory and immune processes.

CALCULUS - MINERALIZED, MATURE PLAQUE covered on its surface with non-mineralized plaque,
material alba, desquamated epithelial cells, and formed blood elements. Calculus is the MOST important
plaque retentive factor. The microbiologic etiologic factor in periodontal diseases is DENTAL PLAQUE,
while dental calculus is the most significant LOCAL contributing factor. The primary reason to remove
calculus from teeth is because calculus harbors plaque microorganisms. Structurally, calculus retains
much of the histologic morphology of its plaque precursor.

• Calculus forms on natural teeth, dentures, and other dental prosthesis (crowns, bridges).

• Calculus is classified as SUPRAGINGIVAL or SUBGINGIVAL depending on its location.

• Calculus is classified as SALIVARY or SERUMAL depending on the source of the inorganic salts that
comprise it.

50
• INORGANIC materials comprise -70%-90% of calculus composition, while ORGANIC material and
WATER comprise the remainder. Calcium and phosphates with small amounts of magnesium and
carbonate (derived almost entirely from saliva). At least 2/3 of the inorganic matter in calculus is
CRYSTALLINE (mainly appatite/hydroxyapatite). Calculus also contains octacalcium phosphate,
tricalcium phosphate (whitlockitel, & brushite.

• ORGANIC components of calculus comprise (10-15%) and include microorganisms (same as in ..,
."

plaque) , desquamated epithelial cells, leukocytes, and mucin. ::!:!

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• Calculus exerts its pathogenic potential as a contributing factor that fosters plaque formation and
promotes it retention on teeth.
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• The rough surface of calculus is usually covered with a layer of plaque biofilm. Calculus "presents"
plaque via the biofilm to periodontal soft tissues.

3 Phases of Calculus Formation: AVERAGE TIME for this entire calculus formation process to
occur is 12 days.
1. Pellicle formation: begins to form within minutes.

2. Plaque maturation: microorganisms grow together to form a cohesive plaque layer.

3. Plaque mineralization: occurs both supragingivally and subgingivally. Calculus is mineralized

plaque that is formed by bathing the plaque in a highly concentrated solution of CALCIUM &
PHOSPHORUS (saliva) .

SUPRAGINGIVAL CALCULUS - the main source of its minerals is from SALIVA. Supragingival
calculus occurs ABOVE the free gingival margin and is white or pale yellow, and easily removed by a
professional cleaning. It occurs most often on the tongue side of mandibular incisors and cheek side
of maxillary molars due to the presence of the salivary ducts that secrete saliva rich in minerals needed
for its formation .

• SALIVARY PELLICLE is the most COMMON MECHANISM that allows supragingival calculus to attach
to smooth enamel surfaces.

SUBGINGIVAL CALCULUS - is darker due to blood breakdown pigments, harder, and more dense
than supragingival calculus. The source of minerals for subgingival calculus is CREVICULAR flUID.
Subgingival calculus occurs BElOW the free gingival margin and is much darker due to blood
breakdown products. It is more difficult to remove than supragingival calculus, and is usually distributed
EVENLY throughout the mouth, and is FORMEO FROM GINGIVAL CREVICULAR FLUID SECRETION.

• The attachment of subgingival calculus is complicated by irregularities like cemental tears,

cemental voids once occupied by Sharpey's fibers, resorption bays, and other CEMENTUM DEFECTS.

Other Contributing/Complicating Factors in Periodontal Disease:

• Food impaction/retention: overlapping, malposed, tilted or drifted teeth are often associated with
food impaction or retention. If food is not removed , it leads to inflammatory periodontal disease.

• Open & loose contacts: leads to food impaction and possible retention.

• Overhanging margins of restorations and improperly designed prostheses: can provoke or initiate
periodontal disease, as there is a direct correlation between surface roughness or marginal
irregularities of a tooth, and plaque retention.

• Soft or sticky consistency of diet: food debris collects between teeth and along the gingiva, and can
be a prominent cause of inflammation.

• Violation of biologic width: if restorative materials invade biologic width permanent periodontitis will
produce apical migration of the junctional epithelium.

• Occlusal traumatism
51
 PLAQUE SCORE - obtained using plaque disclosing solution to help visualize plaque for the patient
and clinician. Also used at multiple visits to show patients improvement in their level of oral hygiene.

Endotoxin (LPS =lipopolysaccharide base) - a constituent of gram (-) microorganisms that

is an important agent in the pathogenesis of inflammatory periodontal disease. Gram (-) bacteria cell
""C
walls consists of a lipopolysaccharide base (endotoxin) that has great pathogenic potential. Typically, LPS
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::!:! containing gram (-) cell wall extracts can promote bone resorption, inhibit osteogenesis, chemotaxis
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• Plaque bacteria produces ENZYMES (hyaluronidase, collagenase, chondroitin sulfatase, elastase,
and proteases) that may initiate periodontal disease.
• Collagenase-enzyme produced by Bacteroides species that catalyzes collagen
degradation (hydrolysis).

• Hyaluronidase-enzyme produced by Streptococcus mitans &salivariusthat destroys the

amorphous ground substance.

• Chondroitin Sulfatase-enzyme produced by Diptheroidsthat also destroys amorphous

ground substance.

• Antibodies {immunoglobulins)-are produced by plasma cells in response to oral bacteria or their

byproducts. The most numerous are IgG which neutralizes bacterial toxins by enhancing phagocytosis.

• The most likely source of bacteria found in diseased periodontal tissue is SUBGINGIVAL PLAQUE.
The probability that bacterial endotoxins playa major role in gingival inflammation is evident by a
reduction in inflammation upon removal of plaque and a reduction of the inflammatory state with
antibiotic treatment.

The frequency of maintenance visits for a patient who had previous periodontal treatment depends
on 2 factors:
1. appearance and clinical condition of the gingival tissues. This will determine if the patient
is maintaining adequate plaque control.

2. ability and performance in home care. This will determine the effectiveness of the patient's
ora I hygiene.

The main goal of the dentist, hygienist, and patient is to maintain good oral health to prevent disease
recurrence. This is the main objective of the MAINTENANCE PHASE of periodontal therapy. The primary
cause of disease recurrence is the dental team's failure to motivate the patient to practice effective
plaque control.

The first year after treatment is critical, since the patient has already demonstrated susceptibility to
periodontal disease (the cause of which tends to be persistent and recurrent). The appearance and
condition of the gingival tissues determines if the patient is maintaining adequate plaque control.

• BLEEDING during circumferential probing indicates that crevicular epithelium is ulcerated due to
active periodontal disease. Bleeding scores (bleeding) is the MOST RELIABLE indicator of the
presence of gingival or periodontal inflammation.

• After periodontal treatment, the first recall visit should be scheduled at 3 months. With excellent
plaque control and maintenance of periodontal health, the interval can be lengthened to 4-6 months.

The new periodontitis classification system is more descriptive and not as temporal as the previous
system . The terms adult, juvenile, early onset, and prepubertal ARE NOW REPLACED with various forms
of chronic and aggressive disease. The term refractory periodontitis has been removed as a distinct
disease entity, since the current thinking is that any type of periodontitis may be refractory.

52
Aggressive Periodontitis (formerly Juvenile Periodontitis or Early Onset}-occurs in two forms:
1. Generalized Aggressive Periodontitis (formerly Rapidly Progressive Periodontitis}-Prevotella
intermedia & Eikenella corrodens predominate. Occurs between ages 12-25, and is
characterized by rapid, severe periodontal destruction around most teeth, with episodic, rapid,
and severe attachment loss.

2. Localized Aggressive Periodontitis (formerly Localized Juvenile Periodontitis}-gram (-) ....,

,...,
::c
anaerobes Actinobacillus Actinomycetemcomitans (AA) and Capnocytophaga species c:::>
c:::>
(ochraceus) predominate. Prevotella intermedia and Eikenella corrodens may also be present c:::>
:z:
to a lesser extent. Occurs in otherwise healthy adolescents ages 12-19, characterized by rapid :::!
n
en
and severe attachment loss confined to incisors and 1st molars.
• One outstanding negative feature is the relative absence of local factors (plaque) to explain
the severe periodontal destruction that is present.

• Possible etiologic factors are a genetic predisposition or a dysfunction of neutrophils

(a chemotactic defect).

• AA & Capnocytophaga species (specifically C. Ochraceus) are also associated with

periodontitis in juvenile diabetes.

Bacteria associated with PERIOOONTAL HEALTH are gram (+), nonmotile, facultative anaerobes. In the
healthy mouth, more than 350 species of bacteria are present. Periodontal infections are linked to less
than 5% of these species. Healthy and disease-causing bacteria are grouped into two categories:
1. harmless/helpful bacteria-are gram (+) nonmotile, facultative anaerobic bacteria (coccal
and rod forms). Streptococcus species (Streptococcus gordinii) and Actinomyces species
are associated with periodontal health.

2. In periodontal disease, the bacterial balance shifts to gram (-), motile, strictly anaerobic
bacteria. Inflammatory disease and injury cannot develop without these gram (-) motile bacteria.
Bacteria most implicated in periodontal disease and bone loss include:
• Actinobacillus actinomycetemcomitans (AA}-associated with aggressive periodontal
disease (formerly early onset) and localized aggressive periodontitis (formerly localized
juvenile periodontitis).
• Porphyromonas gingivalis-associated with chronic periodontitis (formerly adult periodontitis).
• Bacteroides forsythus-strongly linked to periodontal disease.
• Treponema denticola, sokranskii-associated with deep periodontal pockets & ANUG.
• Prevotella intermedia-associated with deep periodontal pockets & ANUG.
• Eikenella corrodens, Campylobacter rectus, Fusobacterium nucleatum,
Peptostreptococcus micros, Prevotella nigresens, enteric rods.
• Pseudomonas & Eubacterium species have also been implicated as periodontal pathogens.

Recent Reclassification of Periodontal Microorganisms

Previous Name New Name

Bacteroides gingivalis Porphyromonas gingivalis

Bacteroides endodontalis Porphyromonas endodonta Iis
Bacteroides intermedius Prevotella intermedia
Bacteroides melaninogenicus Prevotella melaninogenica
Bacteroides denticola Prevotella denticola
Bacteroides loescheii Prevotella loescheii
Wolinella recta Campylobacter rectus
Wolinella curva Campylobacter curvus

53
 PERIODONTITIS BACTERIA

Adult Periodontitis Refractory Periodontitis Rapidly Progressive

Bacteria: Bacteria Periodontitis Bacteria:

..,
.."
• Porphyromonas gingivalis • Porphyromonas • Porphyromonas
::!!
o
o • Prevotella intermedia gingivalis gingivalis
o
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:::!
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en • Campylobacter rectus • Campylobacter rectus nodatum, & timidum)
• Fusobacterium nucleatum • Prevotella intermedia • Prevotella intermedia
• Spirochetes • Fusobacterium
nucleatum
• Campylobacter rectus
• Eikenella corrodens

RAPIDLY PROGRESSING PERIODONTITIS - most commonly seen in YOUNG ADULTS (20-25 yrs),
characterized by marked inflammation, rapid bone loss, and periods of spontaneous remission. Most
of these patients have depressed neutrophil chemotaxis.

JUVENILE PERIODONTITIS - (onset at puberty age 12-14)-caused by principal bacteria AA,

capnocytophaga ochraceus, Prevotella intermedius, and Eikenella corrodens. 2forms of Juvenile Periodontitis:
1. Generalized Juvenile Periodontitis-Prevotella intermedius and fikenella corrodens
predominate. Occurs between ages 12-25 characterized by rapid, severe, periodontal
destruction around most teeth. It appears to be associated with systemic disease (diabetes
mellitus type 1, Down syndrome, neutropenias, Papillon-Lefevre syndrome, and leukemias).
2. Localized Juvenile Periodontitis-gram -negative anaerobes Actinobacillus
Actinomycetemcomitans (AA) and Capnocytophaga ochraceus predominate. Prevotella
intermedius and Eikenella corrodens may be present to a lesser extent.
• UP occurs in healthy adolescents ages (12-19) characterized by severe periodontal
destruction around either maxillary/mandibular first molars or maxillary/mandibular
anterior teeth.
• An outstanding negative feature is the relative absence of local factors (plaque) to explain
the severe periodontal destruction which is present. Possible etiologic factors include a
genetic predisposition or a dysfunction of neutrophils (] chemotactic defect).
• AA and Capnocytophaga ochraceus are also associated with periodontitis in juvenile diabetes.

Conditions that PREDISPOSE a patient to the development of inflammatory periodontal disease or

exacerbation of an existing disease: pregnancy, neutropenia, agranulocytosis, and leukemias. While
bacterial and immune factors playa major role, genetic, systemic, and functional factors are also involved .

• Genetic factors may predispose or trigger periodontitis. Factors governing leukocytic levels,
migration, and chemotaxis may predispose a person to infection and influence host response.

• Individuals with a defective immune response (i .e. as seen in agranulocytosis &neutropenia) are
notably susceptible to crestal alveolar bone loss and abscesses. Occassionally, the periodontium is
the site of lesions with initial foci elsewhere, (i.e. as in tuberculosis or cancer).

• Systemic disease (Le. diabetes mellitus) may lead to an increased incidence and severity
of periodontitis.

• Agranulocytosis-an abnormal condition of the blood, characterized by a severe reduction in the

number of granulocytes, causing fever, prostration, and bleeding ulcers in the mouth, rectum , and vagina.

• Neutropenia-an abnormal decrease in the number of neutrophils in blood. Associated with acute
leukemia, infection, rheumatoid arthritis, vitamin B12 deficiency, and chronic splenomegaly.

• Leukemias-malignant neoplasms of immature white blood cells. Patients with acute leukemias have
more oral complications that people with chronic leukemias. The gingiva is grossly enlarged, bluish-
54 red in color, has a soft, spongy consistency, and the papillae are blunted.
Evidence suggests that periodontal disease may be an AUTOIMMUNE DISORDER where the body's immune
factors (cytokines) attack the person's own cells and tissues. These possible immune factors are
interleukin-l beta, interleukin-4, tumor necrosis factor-alpha, and prostaglandin E-2.

• Bacteria that form plaque and calculus release toxins that stimulate the immune system to
overproduce powerful infection-fighting factors called CYTOKINES (i.e. TNF-alpha, IL-l beta, IL-4,
and PGE2). Usually, cytokines are important for healing. In excess however, cytokines cause ,...,
-.::r
::c
inflammation, severe damage, and overproduce the enzyme COLLAGENASE that breaks down c::>
c::>
proteins and the C.T. that supports the teeth. This inflammatory response may have damaging effects c::>
:z:
on the C.T. that supports the teeth and in organs throughout the body (including the heart). ::::!
n
(I)

• Awide variation in host response to bacterial challenge between patients exists. Some people
with heavy plaque accumulation and high proportions of pathogenic organisms appear relatively
resistant to bone and attachment loss. Others develop extensive periodontal destruction just by small
amounts of plaque and low proportions of putative pathogens.

• Patients with abnormally exuberant inflammatory responses often have a hyper-inflammatory

monocyte/macrophage phenotype, thus secrete greatly increased levels of pro-inflammatory
mediators like IL-l beta, IL4, TNF-alpha, and PGE2 in response to bacterial byproducts.

Periodontal disease can be associated with these systemic diseases and conditions:

• Down's syndrome, HIVIAIDS, hormone imbalances, uncontrolled Type 1 & II Diabetes mellitus.

• People suffering from Types I & II Diabetes have 15x the risk of developing periodontal disease as
compared to the non-diabetic population. Much evidence exists on the link between DM-I and DM-
II and periodontal disease, as diabetes causes abnormalities in blood vessels.

• Several rare white blood cell disorders, genetic predisposition, medications, smoking, and osteoporosis.

Most systemic diseases and conditions that may affect periodontal diseases generally alter host
barrier and host defense mechanisms. While many conditions cause gingival inflammation and ulcers,
not all people develop periodontal disease. Certain factors place people at higher risk:

• Smoking-the single MAJOR preventable risk factor for periodontal disease that can cause bone
loss and gingival recession even in the absence of periodontal disease. Studies indicate that
smoking and nicotine increase inflammation by reducing oxygen in gingival tissue and trigger an
overproduction of immune factors (cytokines-specifically interleukins). This overproduction damages
cells and tissues. The risk of periodontal disease increases with the number of cigarettes smoked per
day. Smoking cigars and pipes carries equal risk as cigarettes.

• Evidence supports the link between Diabetes Mellitus Types I &" and periodontal disease (these
people have 15x greater risk than the non-diabetic population). Diabetes causes abnormalities in
blood vessels and high levels of specific inflammatory chemicals (i.e. interleukins) that greatly
increase the risk of periodontal disease.

• Osteoporosis-loss of bone density associated with periodontal disease in post-menopausal women.

Some treatments for osteoporosis (i.e. bisphosphonates) may reduce bone loss, including the bony
structures that support teeth.

• Autoimmune conditions-Crohn's disease, rheumatoid arthritis, lupus erythematosus, and CREST

syndrome are associated with a higher incidence of periodontal disese.

55
 SCALING & ROOT PLANING & INSTRUMENTATION
MAIN OBJECTIVE OF ROOT PLANING is to provide optimally smooth root surfaces to reduce the potential
for bacterial accumulation , which is done to achieve soft-tissue reattachment. Root planing is the
instrumentation applied to the root surface to remove deposits and smooth the root.
........,::!:!
c::>
CJ
SCALING & ROOT PLANING (SRP) - techniques of instrumentation applied to the root surface to
c::>
:z: divest it of plaque, calcified deposits, and softened or roughened cementum. When thoroughly performed,
::::!
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CI>
these techniques produce a smooth, clean, hard polished root surface. Cementum, dentin, and calculus
are removed during root planing.

• SRP is the primary treatment for periodontal inflammation. In simple cases, SRP reduces shallow
pockets and the number of bacteria in these shallow pockets, and may be the only treatment necessary.

• In severely advanced periodontal disease where surgery may not be possible, SRP is the only feasible
treatment.

• Since plaque and deposit removal is the definitive treatment for periodontal inflammation, SRP is
more often used than any other type of therapy. Commonly observed clinical changes one week after
SRP include reduced pocket depths and reduced gingival inflammation.

• BEST CLINICAL AID to determine if subgingival calculus is removed is using an EXPLORER &BITE-
WING X-RAYS which shows the presence of any interproximal calculus.

SCALING & ROOT PLANING - the purpose is to remove calculus, bacteria, and endotoxins.
• When extensive SRP must be performed, the best approach is to schedule a SERIES of appointments
to scale and root plane a segment or quadrant of teeth at a time thoroughly and completely. DO NOT
do gross debridement (subgingival and supragingival) of the entire mouth, then schedule a series
of appointments for fine scaling and polishing.

If the curette tip breaks off when scaling subgingivally, the appropriate actions to take to remove the
tip are:

• Gently examine the gingival sulcus using a curette in a spoon-like stroke attempting to pull the
fragment out, take a periapical radiograph of the area, and place the patient in an upright position.
NEVER use a push stroke to force the tip out of the sulcus as this could force the tip deeper into
the sulcus.

• The procedure should be stopped immediately and patient placed in an upright position. Before
proceeding subgingival, check the mouth floor and mucobuccal fold for the fragment, then take a
periapical radiograph before going any further to locate the fragment. Do not alarm the patient, to
prevent the patient from becoming frantic.

• The best way to prevent curette breakage is to use proper sharpening techniques to maintain the
original instrument design and discard instruments when the blade starts to thin out. A thinner
blade is weaker and breaks more easily.

• Instruments must be sharp if SRP is to be completed efficiently with minimal tissue trauma. Asharp
instrument requires fewer strokes, provides greater control, and increases tactile sensitivity.
With a dull instrument, the handle must be grasped much firmer with more pressure applied to the
tooth surface, causing fatigue due to heavy-handedness, burnished calculus, decreased tactile
sensitivity, and inefficient use of time.

• Tactile sensitivity-the ability to distinguish degrees of roughness and smoothness on the

tooth surface.

56
INSTRUMENT SHARPENING - The sharpening technique used is an important consideration when
it comes to maintaining the instrument's original shape. Manual sharpening is preferred over using
mandrel mounted stones, as manual sharpening helps prevent unnecessary blade reduction that can
occur when using a rapid cutting mounted stone.

• A wire edge is produced when the sharpening stroke direction is away from, rather than into or
towards, the cutting edge. Avoid producing a "wire edge" by always finishing with a down stroke.

• Sharpen instruments at the first sign of dullness.

• Then angle between the blade face and stone is kept at 100-110°. When sharpening instruments
with a flat stone, the angle between the instrument and stone is 100-110°.

• The technique to sharpen Gracey curettes is essentially the same as for Universal curettes. However,
the Gracy's cutting edge is offset and curves, unlike the universal's cutting edge.

• Lubricate the stone. Oil is used with natural stones (Arkansas & India stones) and water with
artificial/synthetic stones (Carborundum, Ruby, & Ceramic stones) . Lubricant allows metallic
particles removed from the instrument during sharpening to become suspended in the lubricant to
help prevent scratching and "glazing" of the stone.

• Choose sharpening stones appropriate for the instrument (flat, cone, coarse). Ensure that the
sharpening stone is sterile when sharpening any instrument while working on a patient.

• Establish proper angle between the stone and instrument. Maintain a firm grasp of the stone and
instrument, but avoid excess pressure.

• Aproperly sharpened instrument with NO rounded surface area WILL NOT REFLECT LIGHT.

SRP Notes:
• There is potential for abscess formation in a deep pocket only when a superficial scaling is performed .
• OHI may be more effective if a patient can see healing tissue in an area that has been completely
debrided and can compare it to tissue in an untreated area .
• A patient who had a gross debridement will see a marked visual improvement of the oral cavity, and
may not understand the importance and necessity of the deep SRP appointments. This may cause the
patient not to follow through with scheduled treatment, and the patient's periodontal condition will
fu rther deteriorate.
• Post-evaluation therapy should take place -4-6 weeks (the time for repair of the dentogingival
junction) after periodontal therapy has been complete.
• If bleeding or swelling is noted in localized areas of the mouth during the re-evaluation appointment,
check for and remove any residual calculus deposits that may remain.
• In root planing, the working stroke begins at the apical edge of the junctional epithelium (base of
the pocket).

Eliminating the cause of periodontal inflammation is NOT an objective of curettage. However, the
objective of scaling & root planing includes the elimination of the cause of inflammation. In addition
to removing plaque, stain, and calculus, SRP also removes "disease affected" cementum containing
embedded calculus, whole bacteria, and toxic bacterial debris (i.e. endotoxin).

Factors to Consider in Selecting Root Planing Instruments: calculus deposit location, area of the mouth
to be instrumented, and adaptation of gingiva to the tooth.

Anatomic features of teeth often limit the effectiveness and efficiency of SRP calculus removal. It is
difficult to perform a thorough SRP on the mesial surfaces of maxillary premolars, proximal surfaces
of mandibular incisors, and trifurcations of maxillary molars.

• Mesial surfaces of maxillary premolars and proximal surfaces of mandibular incisors are most
likely to have flutings. Also, root proximity is a major problem when performing SRP on mandibular
incisors. Trifurcations on maxillary first molars are the most difficult of all to root plane.

57
 NOTES • If while root planing you find only a thin ring of calculus in the bottom third of a deep pocket, you can
assume the calculus previously extended the full length of the pocket, but the top part was previously
removed. Likewise, if after SRP the patient returns in one week with hard , black deposits of calculus
around the gingival margin, this indicates a reduction in inflammation occurred after the procedure,
and old calculus is now exposed.

,....,
.."
• The BEST CRITERION to evaluate the success of SRP is NO BLEEDING ON PROBING (since BOP
::!!
o
o
indicates active inflammatory periodontal disease).
o
:z:
:::!
C"'>
en
Periodontal Hoes &Files are used almost EXLUSIVELY for HEAVY accessible SUPRAGINGIVAL CALCULUS
removal as their cutting edges are designed to function at RIGHT ANGLES (90 to the tooth surface.
0
)

Due to their blade thickness, they lack adaptability and tactile sensitivity. They may be used subgingival
for gross calculus removal ONLY if the tissue is flexible and easily displaced. Since they are for gross
calculus removal only, they should always be followed by a curette.
1. Hoes-have a wide, single straight cutting edge that cannot adapt to curved tooth surfaces
(injury to tooth and tissue can occur). The entire cutting edge length must be kept against
the tooth and only vertical pUll-type strokes are used. The cutting edge (blade) is angled 90°
to the tooth surface, and is turned at a 90-100° angle to the shank, and the cutting edge
is beveled at a 45° angle to the end of the blade (this angle is maintained when sharpening
the hoe).
• Hoes are most effective on buccal and lingual surfaces. However, mesial &distal adaptation
is poor, if not impossible. Maintaining a two-point contact with the tooth (cutting edge and side
of shank) increases hoe stability.

2. Files-primary function is to CRUSH or FRACTURE heavy calculus, but the entire deposit is not
removed . The file is always followed by root planing with a curette, and works best on buccal
and lingual surfaces, next to edentulous areas, and to reduce amalgam overhangs. While
their size and lack of adaptability make interproximal use difficult, files work well on the distal
surface of the 3rd molar where access is often limited. Vertical pull-strokes are used with files

Currettes can be used with vertical, oblique, horizontal, or circumferential pull-type strokes.
Currettes are used for subgingival SRP, supragingival calculus removal, and gingival curettage.

1. Universal Curettes (Crane-Kaplan 6, McCall 17118, Columbia 4R/4L)-designed primarily to

remove SUBGINGIVAL CALCULUS deposits on ALL tooth surfaces. Universal's have 2 cutting
edges at 90 0 to the root surface, and can be used in any region of the mouth.

2. Gracy Currettes-have 1 cutting edge at 60° to the root surface. Designed to instrument specific
tooth surfaces in specific regions of the mouth .
• Gracy 1-2: have a short shank distance. Used on interproximal surfaces of anterior teeth &
buccaillingualipalatal surfaces in posterior teeth.

• Gracy 3-4: designed with a short modification of the shank, and are used in the same
regions as Gracy 1-2.

• Gracy 5-6: available in two different shank lengths, and are used in the same region as
the Gracy 1-2.

• Gracy 7-8: referred to as universal because of their application to several and tooth surfaces.
They have limitations on the distal surfaces of posterior teeth.

• Gracy 9-10: have a long contra-angle design to instrument buccal and lingual surfaces
of molar and premolars.

• Gracy 11 -12: easily applied to MESIAL surfaces of posterior teeth from both the buccal and
palatal/lingual. The cutting edge is on the outside of the elbow.

• Gracy 13-14: provided excellent access to the DISTAL surfaces of posterior teeth . The
cutting edge is on the inside of the elbow.

• Gracy 15-16: provided excellent access to the DISTAL surfaces of posterior teeth.
58
An instrument's SHANK design influences the instrument's intended use:
• Rigid, thick shank: is stronger, less flexible, and provides less tactile sensitivity. Stronger, more rigid
shanks are used to remove heavy calculus deposits.

• Less rigid, more flexible shank: provides more tactile sensitivity. Used to remove fine calculus and
for root planing.
..,
-0

• Straight shanks are used in anterior areas, while longer (contra-angled) shanks are used in posterior =:!
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areas. o
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IDEAL ANGULATION of a currette's facial surface is between 70-80° to the tooth surface to allow the
curette blade to be properly activated against the tooth surface.

• Stroke-the action of an instrumenting the performance of the task for which it was designed.
Instruments are often given the name of the task being performed . Probing Stroke (Walking Stroke)-
upward and downward movement within a periodontal pocket.

• Exploratory Stroke (Assessment Stroke)-used to assess the smoothness or roughness of the tooth
surface and the effectiveness of instrumentation. Instrument handle is grasped lightly to increase
tactile sensitivity.
• Explorer-when using the periodontal explorer to detect calculus, a LIGHT instrument grasp
(not firm) is used to increase tactile sensitivity. The lateral side of the instrument tip is
placed in contact with the tooth surface when exploring for calculus.

• Scaling Stroke-a short, powerful "pull" stroke to remove calculus (more pressure). The scaling motion
is preferably initiated in the forearm and transmitted from the wrist to the hand with a slight flexing
of the fingers. Wrist rotation is synchronized with movement of the forearm .
• The sequence and control of strokes is important. If heavy lateral pressure is continued with
long, even strokes, it will produce a smooth, but "ditched" root surface. To avoid this, deliberate
transition from short, powerful scaling strokes, to longer, lighter root planing strokes must
be made as soon as the calculus and initial roughness are removed.

• Preferably, the motion to initiate a SCALING STROKE is generated from the FOREARM.
Although fingers may be used to initiate the scaling stroke in some situations, a powerful
scaling stroke cannot be initiated in the wrist or fingers. Hence, is not carried out
independently without using the forearm. The modified pen grasp is the most useful
grasp for periodontal instruments.

• Root Planing Stroke-long, overlapping strokes for final smoothing of the root surface, usually in a
"pull" motion (less pressure). Pulling strokes are safer than pushing strokes, as pushing strokes
can cause calculus to become embedded in soft tissue. Strokes can be directed vertically, horizontally,
or obliquely (diagonally) . The pressure applied becomes lighter as the surface becomes smoother.
When root planing, vertical strokes should be used first, then oblique, then horizontal strokes.
light pressure should be used with root planing strokes to maximize tactile sensitivity.

AIR SYRINGE - used to DETECTsupragingival &subgingival calculus. Supragingival calculus is often

seen more easily when it is dry (saliva conceals it), and deflecting the gingival tissue slightly makes
subgingival calculus easier to detect.

• It is NOT used during scaling to locate the epithelial attachment.

59
 GINGIVAL CURETTAGE - a surgical procedure performed when the cutting edge of the curette is
directed AGAINST THE SOFT TISSUE WALL of the pocket. Curettage-is only the treatment of the pocket
wall (removal of sulcular epithelium and inflamed C.T.). The objective of gingival curettage is to remove
chronically inflamed, diseased epithelial lining and microorganisms from the pocket to reduce edema
and pocket depth .

..,
.."
"., Curettage removes the diseased soft tissue lining the periodontal pockets. It is a manual process
<=I
CI that permits a deeper and more complete cleansing than ultrasound. It does not add any significant
<=I
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benefits for shallow pockets. Local anesthesia is often used. Fine scaling instruments (curettes) have
C">
en two functions:

1. scrape and clean root surfaces.

2. plane root surfaces to smooth and remove the outer layer of diseased material.
• Contraindications: Firm and fibrotic gingival tissues, areas of acute periodontal inflammation,
an extremely thin lateral gingival wall, wide or tortuous infrabony pockets, and bi-and
trifurcation involvement.

• Indications: when gingival inflammation persists after careful and thorough root planing,
treating shallow (up to 4mm) pockets where gingival tissues are highly edematous (patients
with edematous & granulomatous inflammation respond better to curettage than patients
with conditions of fibrous hyperplasia).
• As maintenance treatment for areas of recurrent inflammation and where pocket reduction
surgery has previously been performed .
• To reduce inflammation prior to pocket elimination and to remove chronically inflamed
periodontal tissues

• Often performed with root planing to promote soft-tissue attachment (re-epitheliazation)

which occurs within 7-10 days.

• MOST important factor to determine the amount of shrinkage is the DEGREE OF EDEMA in
the tissue. Healing begins with blot clot formation. Neutrophils predominate im mediately
after curettage (for the first 12hrs).

• In gingival curettage, the curette's blade face is positioned at a 70° angle to the soft tissue
pocket wall or sulcular epithelium. The curette is positioned at the pocket base, pressure is
applied with the finger on the outside of the pocket with smooth, even vertical strokes.

• To establish the correct working angle once a curette is inserted subgingivally, the shank is
moved away from the tooth to open the blade angle to the tooth surface. At proper working
angulation (70-80°), the lower shank of a Gracey curette is PARALLEL to the tooth surface,
while a Universal curette's lower shank is tilted slightly toward the tooth.

• The curette blade is held at an angle> 90° (compared to _70° for SRP). Digitally support the
free gingival/pocket wall increases the cutting stroke effectiveness. Use Horizontal strokes to
treat facial and lingual surfaces (stroke length is determined by tooth contour; usually long and
continuous strokes achieve best results). Irrigate frequently while performing the procedure.

• Post-operative healing involves shrinkage of the gingival wall, pocket depth reduction, and
formation of a long junctional epithelium.

60
PERIODONTAL CURETTE - a narrow, delicate instrument with either 1 or 2 cutting edges (working
surfaces) with rounded edge ends. Usually, curettes are in paired forms allowing access to opposite
surfaces. Curettes are usually smaller than scalers and are designed to permit atraumatic entry into the
subgingival space. The tactile sensitivity of most curettes is greater than scalers. Thus, curettes are well
suited for subgingival calculus detection and removal, and root planing. The most effective instrument
for subgingival SRP is a sharp curette.
,...,
..."

:!
• Periodontal curette is the instrument that is least traumatic and most effective for NON-SURGICAL C)
CI
ROOT PLANING. C)
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en
• Most effective and efficient way to perform root planing is using curettes with short, even working
strokes, followed by longer strokes.

• Final root planing strokes are LONGER & LIGHTER than scaling strokes, and become lighter as the
cementum becomes smoother.

• Exploratory SRP strokes differ in angulation, pressure, length, and direction.

CHISEL - best designed to remove supragingival calculus deposits in interproximal areas (especially
on anterior teeth). It has a single, straight cutting edge, and the end of the blade is flat and beveled at
a 45° angle.

COINCIDENTAL CURETTAGE (lNADVERTENTIINCIDENTAUACCIDENTAL) - performed when

the soft tissue wall of a pocket is removed by the offset cutting edge during a root planing procedure.

CEMENTUM - main function of cementum is ATTACHMENT of the POL principal fibers. Cementum also
functions to compensate for loss of tooth surface due to occlusal wear by apical deposition of vital cementum
throughout life. Cementum also protects the root surface from resorption during vertical eruption and tooth
movement, and has a reparative function that allows reattachment of C.T. after periodontal treatment.

Cementum contains 2 types of Collagen Fibers:

1. Sharpey's Fibers-the terminal portions of the PDL principal fibers that are embedded in the
cementum and run PERPENDICULAR to cementum on one end and alveolar bone on the other end .

2. Type I Collagen Fibers-contained within cementum and run PARALLEL to the cementum surface.

RADICULAR CEMENTUM - cementum found on root surfaces whose thickness INCREASES with age.
It is thicker apically than cervically, and its thickness ranges from O.05mm-O.6mm.

• Cellular Cementum-found on the APICAL THIRD of the root, and contains cementocytes in lacunae
in its cementum matrix. It occurs more frequently on the apical third of the root and in furcations. It
is usually the thickest to compensate for attritional wear of the occlusal/incisal surfaces and passive
eruption of the tooth . Cellular cementum is formed AFTER the tooth reaches the occlusal plane.

• Acellular Cementum-the FIRST cementum to be formed, does not contain any cells in its matrix,
and usually covers the root's CORONAL TWO-THIRDS (cervical third or half of the root). It is thinnest
at the CEJ and plays a major role in TOOTH ANCHORAGE.

CORONAL CEMENTUM - forms on the enamel covering the crown.

If VITAL cementum is resorbed or nicked in surgical procedures, the defect is repaired by the
deposition of new cementum. Repair cannot occur where pockets exist or where the gingiva has receded
and cementum is exposed. Exposed cementum that forms part of the clinical crown is often removed
during scaling, root planing, or brushing.Deposition of new cementum continues periodically throughout
life, whereby root fractures may be repaired .
Cementum is indistinguishable on radiographs .

61
 OCCLUSAL TRAUMA - trauma to the periodontium from functional or parafunctional forces causing
damage to the attachment apparatus of the periodontium by exceeding its adaptive and reparative
capabilities. There are 2 forms of occlusal trauma:

1. Primary Occlusal Trauma-excessive occlusal forces applied to a tooth/teeth with normal

supporting structures (no periodontal disease). It's a condition where pathologic occlusal
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forces are the primary etiology for observed changes in the periodontium. It is usually reversible
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2. Secondary Occlusal Trauma-occurs when the periodontium is already compromised by

inflammation and bone loss. Consequently, occlusal forces that may otherwise be well tolerated
in a healthy periodontium now have deleterious effects due to preexisting periodontal disease.
Teeth with a reduced adaptive capacity and compromised periodontium may then migrate when
subjected to certain occlusal forces . Factors like frequency, duration, and velocity of those occlusal
forces (not just their magnitude), may be of greater significance in the development of tooth
hypermobility (a common clinical sign of occlusal trauma).

BRUXISM - an aggressive, repetitive, or continuous grinding, gritting, or clenching of the teeth

(cupping/hollowed out areas on the occlusal table of the most terminal tooth) during the day and/or
night in other than functional activities (i.e. chewing or swallowing). Opinions differ on the primary cause
of bruxism, but occlusal prematurities, muscle tenSion, and emotional factors have been implicated.

• Signs &symptoms: POL widening and thickening of lamina dura, sore muscles and jaw pain, TMJ
dysfunction and difficulty opening the mouth, increased tooth mobility (especially in the morning),
occlusal wear facets .

• Excessive forces produced by bruxism can cause increased tooth mobility.

• Treatment: behavioral, emotional, and interceptive modalities.

TOOTH MOBILITY - the movement of a tooth in its socket due to an externally applied force. Mobility
is measured by the examiner pushing the tooth gently in a F-L direction using the blunt ends of two metal
instruments. The use of a finger is not acceptable to assess mobility. Mobility Scale:

1. 0 mobility = when a tooth is not mobile.

2. 1 mobility = when a tooth moves O.5-1mm .

3. 2 mobility = when a tooth moves 1-2mm.

4. 3 mobility = when a tooth moves> 2mm or if a tooth is mobile and depressible in an

occlusal apical direction.

ABNORMAUPATHOLOGIC MOBILITY - tooth mobility past the physiologic range because it

exceeds the limits of normal mobility values. The periodontium may not necessarily be diseased at the
time of examination.

OCCLUSAL SPLINTING - the primary reason for splinting teeth is to IMMOBILIZE excessively mobile
teeth for patient comfort. Temporary stabilization is achieved by splinting one or more mobile teeth to
each other and to more stable teeth in a position that facilitates a more AXIAL and EVEN distribution of
occlusal forces (generally performed on teeth with reduced periodontal supporfJ. The rationale for
splinting is improved patient comfort, function and plaque control, better distribution of occlusal forces,
and improved tooth stability during clinical procedures.

• There is no reason for splinting non-mobile teeth as a preventive measure. Splinting is only one
type of measure used to treat periodontal disease, and should be used with other needed measures
like root planning, OHI, pocket elimination, and occlusal adjustment.

62
• Loose teeth splinted to adjacent teeth may become stabilized. When many teeth are loose, adjacent N
sextants should be included in the splint. Teeth tend to loosen B-L, yet may remain firm M-O. Even
when teeth do not tighten, the splint serves as an orthopedic brace that permits useful function to
loose teeth.

• Avariety of methods can be used to achieve temporary stabilization. Whichever method used, special
attention is paid to make the splint amenable to oral hygiene procedures and instructing the patient ,..,
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Types of Splints: :::::!
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1. External Splints-includes ligatures, tooth-bonding plastic splints, welded band splints, '"
continuous clasps, and night guards. These devices may be unesthetic or unhygienic, lack
durability, rigidity, and/or fit. However, these splints are prepared easily and economically,
and tooth structure is not removed (very conservative).

• Night Guards-an acrylic splint whose primary purpose of a night guard in periodontal trauma is to
modify and control BRUXISM or to REDIRECT forces into a non-traumatic pattern. Night guards
should be made of hard acrylic, have no sharp edges and be comfortable. Night guards should occlude
evenly with mandibular teeth and permit the patient to move the mandible freely in all excursions.
Also called centric relation splints, occusal appliances. Goal is to allow condyles to seat in their most
anterior superior position (centric relation) and to have posterior (point contacts) in CO and no
posterior contact in any eccentric movement.
• Functions: stabilize the dentition, modify the nature of the habit (bruxism), act as a splint
after periodontal surgery, and assist in controlling recurrence of the drug-induced
gingival enlargement.

• Night guards are usually worn at night, but may also be worn during the day.

• Bruxism clinical signs: TMJ symptoms, muscle soreness, cracked teeth/fillings, wear facets
on teeth, and widened POL spaces on radiographs.
2. Intracoronal Splints-include acrylic or amalgam with an embedded wire and acrylic or
acrylic-and-gold provisional splints. Tooth structure is removed, and these splints are more
serviceable than external splints. However, the materials wear and break, depend on the bonding
medium strength, and tend to create plaque harbors that lead to caries, calculus deposition,
and inflammation .

MOST COMMON SIGN OF OCCLUSAL TRAUMA IS TOOTH MOBILITY. Other clinical signs are migration of
teeth and teeth tenderness to percussion .:

• Radiographic signs of trauma due to occlusion: widening of the POL space, thickening of the lamina
dura, angular bone loss and infrabony pocket formation, root resorption, and hypercementosis.

• Radiographic changes seen on teeth that are no longer in function : reduced trabeculation of bone
and narrowing of the POL space.

• Trauma from occlusion is reversible (the body can repair the damage if the excessive occlusal
forces are eliminated). Periodontal pockets are not caused by occlusal trauma. A local irritant
and inflammation are necessary to cause apical shift of the epithelial attachment (JE).

• Other findings associated with excessive occlusal forces: alternating areas of resorption and repair
of alveolar bone, fibrosis of alveolar bone marrow spaces, cemental resorption leading to dentinal
resorption, cementa I tears, ankylosis, occasional pulpal necrosis and calcification.

Reasons to Perform Selective Grinding in the Natural Dentition:

• Achieve a more favorable direction and distribution of forces .

• Coordinate the median occlusal position with the terminal hinge position of the mandible.

• Eliminate prematurities in excursive movements to gain group function or canine protected occlusion.

63
 • Direct occlusal forces centrally along the long axis of the tooth.

• Improve or maintain masticatory performance.

• Accomplish occlusal adjustment without reducing vertical dimension and by reta ining an acceptable
interocclusal distance .
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Contra indications to Selective Grinding in the Natural Dentition:
• When pulp chambers are large or in the presence of tooth sensitivity.
• When major occlusal discrepancies may require orthodontics or reconstruction.
• Patients who are poor candidates for full-mouth reconstruction due to psychologic factors.

Steps involved in adjusting occlusion: eliminate prematurities in centric relation (CR), in protrusive
movements, and in lateral excursive movements. Then re-establish the physiologic occlusal anatomy
and carefully polish all ground surfaces.

ABSCESSES:
• Periodontal probing will reveal deep pockets associated with the periodontal abscess. Vita lity tests,
thermal and electric tests will exclude the pulp as the unlikely cause of symptoms as the tooth with a
periodontal abscess is usually vital. Methods to distinguish a periodontal abscess from a pulpal
(periapical) abscess is done via periodontal probing, EPT, thermal testing. However, a periapical
radiograph is not a good diagnostic method to distinguish a periodontal and a pulpal abscesses.

• MOST COMMON symptom a patient will report with a periodontal abscess is ACUTE PAIN that is
constant, severe, and dull throbbing. Thermal changes do not elicit or modify the discomfort.
The onset of this discomfort is rapid and becomes progressively more intense. The patient may also
notice an increase in tooth mobility, and say it is difficult to close their teeth together without striking
the involved tooth first, causing increased pain.

• The periodontal abscess can be an acute exacerbation of chronic periodontal disease and may
occur when the infection passes into the tissue through the pocket epithelium . Such abscesses are
often the result of blockage of the narrow openings of tortuous or deep infrabony pockets.

• Radiographic findings associated with the periodontal abscess are NOT specific. There may be no
change radiographically in the early acute lesion . However, often there is a localized discrete
radiolucency lateral to the root or in a furcation which can cause rapid alveolar bone destruction .

• Treatment of the acute periodontal abscess is determined initially by whether there is localization
of the abscess (if there is, drainage is the treatment). If the abscess is not localized, the patient is
placed on antibiotics (Penicillin V) and instructed to rinse with warm saline. Clindamycin can be used
in penicillin allergic patients.

PERIODONTAL-ENDODONTIC ABSCESS ~ Signs & symptoms are not always consistent, but include
radiographic involvement of the periodontium and periapex, significant probing depths, percussion and pulpal
sensitivity. Each case mayor may not present with all of these signs and symptoms. In the presence of both
a chronic endodontic and periodontal lesion, both lesions must be treated to achieve complete healing.

• Treatment: RCT (pulp is treated first and after the periodontal condition is re-evaluated 2-3 months
after the completion of endodontic therapy). Antibiotic therapy, SRP, and periodontal surgery if needed,
is performed 2-3 months after the completion of RCT.

PERIODONTAL CYST ~ is usually asymptomatic and without grossly detectable changes, but may
present as a localized tender swelling. Radiographically, an interproximal periodontal cyst appears on
the side of the root as a radiolucent area bordered by a radiopaque line. Its radiographic appearance
cannot be differentiated from a periodontal abscess.

64
APICAL PERIODONTAL CYST - has a predilection for mandibular canine-premolar area. Teeth are
vital, usually asymptomatic, but may be slightly uncomfortable. There are no periodontal pockets, and
radiographs reveal a small, well-defined oval-to-round radiolucency on the lateral surface of the root.
Treatment includes surgical removal without extraction of surrounding teeth.

Periodontal Treatment Planning: Preliminary Phase-treatment of EMERGENCIES ONLY whether a pulpal,

periodontal, or other emergency.

1. Phase I (Initial Therapy)-involves plaque control, extraction of hopeless teeth, mouth

preparation (initial full-mouth scaling, and definitive root-planing). Also includes:
• Oral hygiene instructions (OHI) which is the most important aspect of initial therapy. The
hygienist or dentist teaches, motivates, and guides the patient in the performance of measures
for disease control. During a prophy appointment, the hygienist or dentist can establish a
rapport with the patient and individualize instructions for a particular patient. The patient is
shown proper brushing/flossing techniques, and these techniques are repeated to see if they
understand what you are showing them. If oral hygiene is poor, surgery is CONTRAINDICATED.

• Occlusal adjustments, night guards (if bruxism exists), splinting (stabilizing loose teeth)

• Re-examination that involves charting probing depths.

2. Phase II (Periodontal Surgery)

3. Phase III (Restorative Phase)
4. Phase IV (Maintenance Phase)

ORAL HYGIENE INSTRUCTION

Indications for using Super Floss: plaque removal around isolated teeth, teeth separated by a diastema,
wide embrasures where interdental papillae have been lost, FPD (bridgework), orthodontic appliances,
and implants. Superfloss consists of a nylon floss, ultrafloss, and regular floss.

Toothpaste Ingredients:
1. Polishing (Abrasive Agent)-may be silica, calcium carbonate, or alumina. Polishing agent
REMOVES stain, stained pellicle, and plaque. When selecting a polishing agent to remove
generalized staining, consider tooth sensitivity, type of stain and restorations present, and
the tooth surface condition.
• Factors that REDUCE the abrasive action (effectiveness) of a polishing agent: Using an
agent containing dull and round particles, using a thin, watery mixture of polishing paste,
and/or polishing at a low speed with light pressure.

• Factors that INCREASE a polishing agent's abrasive action (effectiveness): flexing the
polishing cup into proximal areas, or using an agent with nice large particles.

• Contraindications of using abrasive polishing agents and/or a rotary polishing instruments:

• Patients with a communicable disease or respiratory problems due to the production of
aerosols is likely that can disseminate the disease.
• Patients with "green stain" (usually the tooth surface under the stain is demineralized).
• Patients with newly erupted teeth that have not completely mineralized.
• Any patient at risk for dental caries (patients with xerostomia, amelogenesis imperfecta,
rampant caries, or receiving radiation therapy to the head/neck).
• However, the use of a porte-polisher (manual polisher) may be helpful in some of these
cases. Dental tape and finishing strips may be used to polish interproximal tooth surfaces.

2. Binder (Thickener)-may be carrageenates, alginates, or carboxymethylcellulose. The binder

(thickener) gives toothpaste its consistency and flowability when expressed from the tube.

3. Surfactant-detergent like sodium lauryl sulfate that foams to aid in debris removal.

65
 NOTES 4. Humectant-consists of glycerin, sorbitol, or polyethylene glycol. Humectant provides moisture to
the paste, and keeps it from drying out. Serves to retain the paste's moisture.

5. Flavoring-may be spearmint, wintergreen, or peppermint.

6. Active ingredient-may be fluoride (caries protection), triclosan (extremely potent antibacterial

....,
,..., agent found in Colgate's Total Toothpaste), as an antiplaque agent, pyrophosphate (an
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anticaiculus agent), potassium nitrate (a desensitizing agent), or peroxide compounds
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en Toothbrushing Methods: the effectiveness of toothbrushing is BEST measured by the amount and location
of plaque. No matter which brushing method is used , the manual toothbrush should have SOFT, NYLON
bristles and a small head.

1. Bass Method (USulcular Technique")-toothbrush bristles are placed 45° to the tooth surface
at the gingival margin to try and get the bristles into the gingival sulcus. The brush is then
moved in a back-and-forth motion for -20 strokes. This is currently the preferred method of
manual toothbrushing.
• Sulcular technique is theoretically the most effective toothbrushing technique.

2. Modified Stillman Method (URoll Technique)-brush bristles are resting partially on the cervical
area of the teeth and partially on the gingiva pointing toward the gingival margin. Pressure is
applied to the brush to cause the gingiva to blanch. The brush head is then moved in short
back-and-forth strokes with the brush moving coronally simultaneously.

3. Charter's Method-toothbrush is placed against the surface of the teeth with the bristles
pointed away from the gingival margin at a 45° angle. The back-and-forth motion is
a massaging stroke for the gingiva.

Frequent brushing/flossing helps prevent calculus formation by breaking up the plaque matrix. New
plaque growth occurs shortly after brushing and flossing (starts interproximally and works its way around
the tooth). Orange, green, and brown stains on anterior teeth are usually caused by poor oral hygiene.

Other Homecare Aids: Important: NOTHING REPLACES BRUSHING &FLOSSING to disrupt and
remove plaque.
1. Perio-Aid-a homecare aid that consists of a plastic handle that will receive round polished
TOOTHPICKS and permit the patient to cleanse the teeth at gingival margins, where accessible,
and in areas of difficult access. Atapered, round toothpick is inserted into the hole in the carrier,
and is then broken off. The tip is left in and used in a tracing motion along gingival margins. Peri-
Aid is also helpful in cleaning accessible furcations .

2. Stim-U-Dent (balsa wood wedges)-primarily important in gingival massage and good for
patients with interdental recession. These picks are triangular in cross-section and are small
enough to fit into most interdental spaces. As a supplement to brushing, Stim-U-Oents are
useful for dislodging interproximal debris often missed by meticulous brushing, and
for massaging the underlying interproximal gingiva.

3. Interproximal brushes (proxabrush)-replaceable brushes used for interdental cleansing when

the interdental space is wide.

4. Interdental stimulator-consists of a rubber tip of smooth or ribbed conical-shape attached to a

handle or to the end of a toothbrush. Its action massages and stimulates circulation of the
interdental gingiva and may increase tissue tone. It is not recommended for areas where
papillae are normal and fill interproximal spaces. It may cause injury to the gingival tissue.
5. Water-Irrigation devices ("flushing or lavage")-useful around fixed bridgework and orthodontic
appliances where debris tends to accumulate. The water pressure helps remove food debris,
dilutes bacterial by-products and even some plaque, but does not remove all dental plaque.
Water-irrigation devices may be injurious if used forcefully in deep periodontal pockets .
• Oral irrigation devices are CONTRAINDICATED IN PATIENTS WITH PERIODONTAL
INFLAMMATION. Water irrigation devices may be contraindicated in patients requiring
antibiotic premedication prior to dental treatment since these devices have the potential
for causing a bacteremia. The patient's physician should be consulted .
66
 • Oral irrigation devices can remove NON-ADHERENT bacteria from subgingival
&supragingival sites. This can be done at home or in the office.

• Water irrigation is also called "flushing" or "lavage" of periodontal pockets.

• When used with water alone, irrigation can reduce gingivitis, but not as much as if used with
chlorhexidine gluconate 0.12% (works best).

• Oral irrigation devices do not remove acquired tooth pellicle and cannot remove adherent
plaque better than toothbrushes.

Irrigation Benefits: reduce gingivitis, reduce/alter microbial flora, subgingival access (penetrates below
the gingival margin), and delivery of antimicrobial agents (i.e. chlorhexidine gluconate, stannous
fluoride, &sanguinaria) . Fluoride, antibiotics, and chlorhexidine effectively inhibit microbial plaque.

Chlorhexidine Gluconate (0.12%) in an alcohol-containing vehicle:

• Stains teeth, tongue, and resin restorations. The stains are reversible.
• Impairs taste perception, but the taste perceptions are transient.
• Has retention properties that are concentration and time dependent and is not influenced by the
temperature or pH of the rinsing.
• Has a LOW systemic toxicity and is not associated with teratogenic alterations.

Currently, two basic agents have a significant effect on gingivitis over a 6-month period:
Chlorhexidine Gluconate (0.12%) in an alcohol-containing vehicle and phenolic compound/essential
oil-based mouthrinses can be used to help control gingivitis.

• Chlorhexidine kills bacteria in situations when used for 30sec 2x/day.lt is the most effective anti-
microbial agent for reducing plaque and gingivitis over long-term. Its effectiveness may be explained
by the fact that is leaves the greatest residual concentration in the mouth after its use.

• Peridex is rapidly absorbed onto the teeth and pellicle, and is slowly released. It is approved by the
ADA as an antimicrobial and antigingivitis agent (i.e. Peridex &PerioGard).

• Chlorhexidine stains oral tissues if used for a prolonged duration. Chlorhexidine stains impart a
YELLOWISH-BROWN to BROWN color. It does NOT impart a greenish black-to-black color of the
oral cavity tissues.
• Appears in the cervical and interproximal regions of the teeth more commonly.

• The presence of aldehydes & ketones (intermediates of mammalian & microbial metabolism),
are essential for formation of this discoloration. It is not a permanent stain , and can
stain restorations.

Essential oils (thymol, menthol, eucalyptol, and methyl salicylate for flavoring are the active
ingredients in most-phenol-based mouthrinses. These rinses also contain 20-27% alcohol in the
vehicle (i .e. LlSTERINE) .

Other Topical Antimicrobial Agents:

1. Stannous fluoride-its antimicrobial action appears to be related to the stannous (tin) ion rather
than to the fluoride ion. It is available in gel form (i.e. Stop, Gel-Kam). ADA accepts stannous
fluoride in anticaries activity, but NOT for anti -plaque or antigingivitis purposes.

2. Quaternary ammonium compounds-are not as effective as others in reducing plaque or

gingivitis, seem to be best at elim inating bad breath (halitosis) contains cetylpyridinium
(i.e. Scope &Cepacol).

67
 lOCAllY APPlIED ANTIBIOTICS (lAA) TO TREAT PERIODONTAL DISEASE

1. ATRIDOX (Doxycycline Hyclate 1O%)-used to treat periodontal disease. It is a locally applied

antibiotic (LAA) placed gently below the gum line into periodontal pockets where bacteria thrive.
It is bioabsorbable, so it does not have to be removed once placed .
• ATRIDOX is a gel applied with a syringe into the infected tooth pocket. It contains an antibiotic,
..,
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,., doxycycline hyclate which flows to the bottom of pockets and fills even the smallest spaces
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between teeth and gums. After it is applied into the infected pocket, it hardens upon contact with
o oral fluids (saliva) to a wax-like substance. The antibiotic is slowly released into the surrounding
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infected tooth pocket for 21 days. In clinical studies, ATRIDOX has been shown to improve
periodontal pocketing to help arrest the advancement of periodontal disease.

2. ARESTIN (Minocycline Hydrochloride)-an effective antibiotic treatment in a powder form easily

placed inside infected periodontal pockets just after the dental professional completes scaling
and root planing (SRP). ARESTIN contains microspheres (tiny, bead-like particles that are smaller
than grains of sand not visible to the eye). The Microspheres are filled with the antibiotic
minocycline, and they release the drug over time into the infected periodontal pocket, killing
bacteria that live there for up to 21 days.
• In clinical studies, ARESTIN has been proven to be more effective than using SRP alone, and it
significantly reduced the size of periodontal pockets compared to SRP alone, killed the bacteria
most commonly associated with periodontal disease, and reduced bleeding on probing.

3. ACTISITE (Tetracycline Hydrochloride)-peridontal fiber indicated as an adjunct to periodontal

therapy to reduce periodontal pockets and bleeding on probing. Contraindicated in patients
sensitive to tetracycline. Non-bioabsorbable, so must be removed after 10 days.

4. PERIOCHIP (Chlorhexidine Gluconate)-an antimicrobial agent; a small orangish-brown

rectangular chip that is inserted into periodontal pockets as an adjunct to SRP. It is bioabsorbable,
and also contains glycerin and purified water.

ENDOGENOUS INTRINSIC STAIN - stains that originate from inside the tooth. Intrinsic stains
cannot be removed by traditional scaling and polishing because they are incorporated within the tooth
structure (i.e. tetracycline, amelogenesis imperfecta, systemic fluoride).

EXOGENOUS EXTRINSIC STAINS - black line, tobacco, orange, and green stains all begin as extrinsic
stains. After a period of time, both green and tobacco stains may become incorporated with the tooth, at
which point their classification changes and they become exogenous intrinsic stains.

• Exogenous Intrinsic Stains-originates from a source outside the tooth and subsequently
becomes incorporated within the tooth structure (i.e. silver amalgam, green, tobacco stains,
and topical fluoride).

Extrinsic Dental Stains:

1. Brown stain: a thin, translucent, acquired pigmented pellicle. Color is due to TANNIN. Occurs
in patients who do not brush sufficiently or who use a dentrifice with inadequate cleansing.

2. Tobacco stain: dark brown or black resulting from coal tar combustion products and
from penetration of pits & fissures, enamel, and dentin by tobacco juices.

3. Black stain: a thin, black line on the facial and lingual surfaces of teeth near the gingival margin,
and as a diffuse patch on proximal surfaces. Caused by chromogenic bacteria (especially
Actinomyces species). Chromogenic bacteria are also implicated in causing ORANGE STAINS.

4. Green or Green-Yellow stain: common in children. Green discoloration is attributed to

fluorescent bacteria.

5. Metallic stain: common in industrial workers who inhale metal dust or due to orally administered
drugs containing metals or metal salts. Metal stains vary from green due to copper and nickel,
to black stains due to iron, silver, and manganese.

68
$HftPTEH 3

69
 ANATOMY
TRIGEMINAL NERVE (eN V) - the LARGEST of the 12 cranial nerves and principal general sensory
nerve to the head and face. Trigeminal exits the inferolateral pons as a sensory and motor root. The
larger sensory root enters the trigeminal (semilunar, gasserian) ganglion in the middle cranial fossa.

• Trigeminal nerve 3 sensory divisions arise from the ganglion and leave the cranial cavity through
foramina in the sphenoid bone. The smaller motor root passes under the ganglion and joins the
mandibular division (V3) as it exits through FORAMEN OVALE. Mandibular division (V3) innervates
8 muscles.
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Somatic SENSORY bodies of the ganglion's sensory fibers enter the:
-< 1. Ophthalmic Division (V1) supplies general sensation to the ORBIT & SKIN of the face above
the eyes.
2. Maxillary Division (V2) supplies general sensation to nasal cavity, maxillary teeth, palate, &
skin over the maxilla .
3. Mandibular Division (V3) supplies general sensation to the mandible, TMJ, mandibular teeth,
floor of mouth, tongue, and skin of mandible.

The axons of the neurons enter the PONS through the sensory root and terminate in 1 of 3 nuclei of the
trigeminal sensory nuclear complex.
1. mesencephalic nucleus-mediates proprioception (i.e. muscle spindle).
2. main sensory nucleus-mediates general sensation (i.e. touch).
3. spinal nucleus-mediates pain and temperature from the head and neck.

Proprioceptive fibers from muscles & TMJ are found only in trigeminal's mandibular division (V3).
Cell bodies of proprioceptive 1st order neurons are found in the mesencephalic nucleus, not the
trigeminal ganglion. The TMJ (as with all joints), receives no motor innervation, however the muscles that
move the TMJ receive the motor innervation.

Branchiomeric motor fibers-innervate temporalis, masseter, medial & lateral pterygoids, anterior belly
of digastric, mylohyoid, tensor tympani, and tensor veli palatine (palati).

Mandibular Division (V3) of Trigeminal Nerve-passes through FORAMEN OVALE and supplies MOTOR
innervation to tensor veli palatine, tensor tympani, muscles of mastication (temporalis, masseter,
lateral & medial pterygoids), anterior belly of digastric, &mylohyoid muscles.
• V3 Sensory Innervation:
• Long buccal nerve (sensory only) to the cheek and mandibular buccal gingiva.
• Auriculotemporal nerve (sensory only) to TMJ, auricle, and external auditory meatus .
• Lingual nerve (sensory only) to floor of mouth, mandibular lingual gingiva, and anterior
2/3 of tongue .
• Inferior alveolar nerve (sensory & motor) to mandibular teeth, chin skin, and lower lip.

Masseteric Nerve (nerve to the masseter) - branch of mandibular division (V3) that carries a few
sensory fibers to the TMJ's anterior portion.

Auriculotemporal Nerve - a branch of mandibular division (V3) that provides the major SENSORY
innervation to the TMJ's posterior portion. Transmits pain in the TMJ capsule and disc periphery.

Nerve to Mylohyoid Muscle - a branch of the mandibular nerve (V3). Mylohyoid muscle elevates the
hyoid bone, base of tongue, and floor of mouth. The sublingual gland is superior to the mylohyoid muscle.
• When placing the film for a periapical view of mandibular molars, the mylohyoid muscle can obstruct
the view if it is not relaxed.
• When the floor of the mouth is lowered surgically, the mylohyoid &genioglossus muscles
are detached.

70
 N
Anterior Triangle Muscles

Muscle Nerve Innervation

Suprahyoid Muscles
(origin is above the hyoid bone): CN-V3 (anterior belly) CN VII (posterior belly)
• Digastric muscles (anterior & posterior bellies) CN-V3
• Mylohyoid muscle Cl fibers carried via hypoglossal nerve (CN XII)
• Geniohyoid muscle CN VII (facial nerve)
• Stylohyoid muscle
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Infrahyoid Muscles ""

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(origin is below the hyoid bone):
All innervated by Ansa Cervicalis
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• Thyrohyoid muscle ~
• Omohyoid muscle (a loop formed by branches of the
• Sternohyoid muscle cervical plexus C1, C2, C3).
• Sternothyroid muscle

HYPOGLOSSAL NERVE - a motor nerve supplying all intrinsic &extrinsic tongue muscles (except
palatoglossus), which is supplied by the vagus nerve. It leaves the skull through the hypoglossal canal
medial to the carotid canal and jugular foramen. Soon after it leaves the skull through the hypoglossal
canal, it is joined by Cl fibers from the cervical plexus. It passes above the hyoid bone on the lateral
surface of the hyoglossus muscle deep to the mylohyoid muscle. It loops around the occipital artery and
passes between the external carotid artery and internal jugular vein.

• Unilateral lesions of the hypoglossal nerve cause deviation of the protruded tongue towards the
affected side due to the lack of function of the genioglossus muscle on the diseased side. Injury of
the hypoglossal nerve eventually produces paralysis and atrophy of the tongue on the affected side
with the tongue deviated to the affected side. Dysarthria (inability to articulate) may also occur.

• If the genioglossus muscle is paralyzed, the tongue has a tendency to fall back and obstruct the
oropharyngeal airway with risk of suffocation .

• Motor innervation to the tongue comes from the Hypoglossal nerve (CN XII).

CAROTID SHEATH - located at the lateral boundary of the retropharyngeal space at the level of the
oropharynx on each side of the neck deep to the SCM muscle. It extends from the skull base to the first
rib and sternum. It contains the carotid arteries, internal jugular vein, vagus nerve, and deep cervical
lymph nodes.

• During surgical procedures of the neck, structures within the carotid sheath can be retracted (pulled
aside) as a unit (common carotid artery, internal jugular vein, internal carotid artery, & vagus nerve).
However, the cervical sympathetic trunk would remain in place when the carotid sheath is retracted
because it is not within the sheath.

• Facial vein unites with the retromandibular vein below the border of the mandible and empties into
the main venous structure of the neck (internal jugular vein).

• Internal jugular vein descends through the neck within the carotid sheath and unites behind the
sternoclavicular joint with the subclavian vein to form the brachiocephalic vein whose right and left
segments unite in the superior mediastinum to form the superior vena cava (this returns blood to
the right atrium of the heart) .

71
 Maxillary 1st molar is innervated by the MSA & PSA nerves (middle superior and posterior superior
alveolar nerves). To extract the maxillary 1st molar, you MUST numb both the PSA & MAS nerves, and the
greater (anterior) palatine nerve for palatal anesthesia (soft tissue).
• PSA nerve-innervates the DB root of the 1st molar and distal to it (2nd and 3rd molars).
• MSA nerve-innervates the MB root of the 1st molar and the two premolars.
• ASA nerve (anterior superior alveolar nerve)-innervates canines and incisors.

The canine and 1st premolar on the injection side can be removed without pain after administering an
inferior alveolar and lingual nerve block. You must give a long buccal injection to extract all molars and
2nd premolar. For operative procedures, a long buccal injection may not be needed for these teeth.
• Incisors may need local infiltration for extractions.
• Bone of the maxilla is more porous than the mandible, thus it can be infiltrated anywhere.

POSTERIOR SUPERIOR ALVEOLAR (PSA) NERVE BLOCK - provides anesthesia for 1st, 2nd, 3rd
molars, but not mucoperiosteum of the palate. PSA injection does not always anesthetize all roots of
the maxillary 1st molar. Thus, if anesthesia of this tooth for restorative or extraction is required, a local
infiltration injection is given over the second premolar.
• Patients experience few subjective signs of anesthesia after receiving a PSA nerve block, compared
to an IA nerve block (numb lip).
• If the patient's face becomes distended and swollen after a PSA block due to an intravascular
injection, place cold packs and pressure on the affected side, and explain that he/she may become
black and blue on that side.

GREATER (ANTERIOR) PALATINE NERVE - a branch of the maxillary (CN V-2) nerve that provides
soft tissue innervation to the posterior 2/3 of the hard palate. It emerges into the hard palate via the
greater palatine foramen and passes forward halfway between the alveolar crest and midline. Supplies soft
tissues of the palate as far anteriorly as the canine where it overlaps with nasopalatine nerve branches.
It is necessary to anesthetize the GPN if extraction or surgical procedures are contemplated in this area of
the palate. Anesthetize the greater palatine nerve, deposit local anesthetic at the greater palatine foramen
(between the 2nd and 3rd maxillary molars -lcm from the palatal gingival margin toward the midline).

GREATER PALATINE INJECTION - used if extracting any or all of the 3 molars and to anesthetize
mucoperiosteum of the palate.

Cranial Nerve Function

CN I (Olfactory) Sense of smell

CN II (Optic) Sense of sight
CN III (Oculomotor) Eyeball movement, pupil constriction, near vision.
Parasympathetic activity
CN IV (Trochlear) Eyeball movement
CN V(Trigeminal) Sensation to face, scalp, teeth. Contraction of muscles of
mastication & motor innervation for mandible movement.
CN VI (Abducens) Eyeball movement
CN VII (Facial) Sense of taste, contraction of facial muscles, saliva secretion.
Parasympathetic activity.
CN VIII (Vestibulocochlear) Sense of hearing and equilibrium
CN IX (Glossopharyngeal) Sense of taste, sensory for cardiac, respiratory, BP reflexes,
pharynx contraction, saliva secretion. Parasympathetic activity.
CN X(Vagus) Sensory in cardiac, respiratory, & BP reflexes. Sensory and motor
Parasym pathetic Activity to larynx (speaking), decreases HR, contraction of alimentary tube
(peristalsis), increases digestive secretions
CN XI (Accessory) Contraction of neck & shoulder muscles
CN XII (Hypoglossal) Motor to all intrinsic and extrinsic tongue muscles
(except pa latoglossus)
*Cranial nerves III, VII, IX, Xall have PARASYMPATHETIC ACTIVITY.
72
EXTERNAL CAROTID ARTERY - supplies most of the head &neck (except the brain, which gets
its blood supply from the internal carotid and vertebral arteries). External carotid passes through the
parotid salivary gland and terminates as the maxillary & superficial temporal arteries (terminal
branches). The superficial artery supplies the scalp.

Maxillary Artery-supplies maxillary & mandibular teeth, muscles of mastication, palate, and almost the
entire nasal cavity.
1. Inferior alveolar artery-a branch of the maxillary artery that supplies blood to the
mandibular teeth.
2. PSA artery-a maxillary artery branch that supply blood to the POSTERIOR maxillary teeth.
3. ASA & MSA arteries-maxillary arch branches that supply blood to the ANTERIOR maxillary teeth.
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:z,.
VENOUS RETURN of both dental arches is the PTERYGOID PLEXUS of veins. .-
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,...,
'"
GREATER (DESCENDING) PALATINE ARTERY - descends through the greater (descending) palatine ::c
-<
canal to the greater palatine foramen. It supplies the hard palate, gingiva of maxillary teeth, & lateral
nasal wall.

• GPA gives rise to the greater and lesser palatine arteries which pass through the greater and lesser
palatine foramina (respectively), and supply the hard &soft palates. Lesser palatine artery also
helps supply the tonsils (along with the tonsillar arter-a branch of the facial artery).

• GPA sends a branch to anastomose with the nasopalatine branch of the sphenopalatine artery in the
incisive foramen to supply the mucosa of the hard palate anterior to the maxillary canine.

LINGUAL ARTERY - supplies blood to the TONGUE (which also receives blood from the tonsillar
branch of the facial artery &ascending pharyngeal artery).

• Lingual artery arises from the external carotid artery at the level of the tip of the greater horn of
the hyoid bone in the carotid triangle (below the facial artery) . Branches include dorsal lingual artery,
suprahyoid artery, and sublingual artery (supplies the sublingual gland). It terminates as the deep
lingual artery, which ascends between the genioglossus &inferior longitudinal muscles. Floor of the
mouth also receives its blood supply from the lingual artery.

• Lingual artery arises from the EXTERNAL CAROTID ARTERY. It passes deep to the hyoglossus muscle
to supply the tongue, and DOES NOT accompany the corresponding nerve throughout its course.
Lingual artery supplies structures of the mouth floor and posterior and inferior surface of the tongue.

• Lingual Artery Branches:

1. suprahyoid artery: supplies suprahyoid region.
2. dorsal lingual artery: supplies dorsum of tongue (top of the tongue).
3. deep lingual artery: the terminal branch that supplies the anterior 2/3 of tongue.
4. sublingual artery: supplies mouth floor and sublingual gland.

Inferior alveolar nerve & artery, and lingual nerve are found in the PTERYGOMANDIBULAR SPACE
between medial pterygoid muscle and ramus of the mandible. IA nerve passes lateral to the
sphenomandibular ligament.

OPHTHALMIC ARTERY - supplies blood to the orbit and its contents.

Tongue Sensory Innervaton:

• Lingual nerve (branch of V3) supplies anterior 2/3 of tongue.
• Glossopharyngeal nerve (CN IX) supplies posterior 1/3 of tongue (taste & sensation) & vallate
papillae. Also supplies sensory to the tonsil, nasopharynx, and pharynx.
• Vagus nerve (CN Xl via internal laryngeal nerve supplies the area near the epiglottis.
• Facial nerve (CN VII) via chorda tympani supplies taste to anterior 2/3 of tongue.

73
 FACIAL NERVE (CN VII) - originates in the PONS, traverses the facial canal of the temporal bone,
and exits the cranium through the stylomastoid foramen where it then extends laterally around the neck
of the mandible through the PAROTID GLAND. *If you cut the facial nerve just after it exits the foramen,
it causes loss of innervation to the muscles of facial expression. Branches of the facial nerve to muscles
of the face are enmeshed in the parotid gland. Functions:
1. motor innervation: muscles of facial expression, posterior belly of digastric and stylohyoid
muscles, stapedius muscle within the middle ear. Lower motor neuron lesions of CN 7 cause
ipsilateral (same side) flaccid paralysis of the facial muscles.
2. sensory innervation (proprioception): from the same muscles of facial expression that receive
motor innervation.
3. motor (parasympathetic innervation): tear secretion from the lacrimal gland and salivation
from the sublingual and submandibular glands.
4. sensory (taste impulses & sweet sensation): from taste buds on the anterior 2/3 of the tongue,
floor of mouth, and palate.

• Bell's Palsy-facial paralysis (a functional disorder of the facial nerve) caused by nerve irritation or
viral infection, thus is usually temporary.

• Facial Trauma-trauma to the facial nerve destroys the ability to contract facial muscles on the
affected side of the face and distorts taste perception. The affected side of the face sags because
muscle tonus is lost.

PAROTID GLAND - the largest salivary gland and pure SEROUS gland supplied by general visceral
efferent (motor) nerve fibers of the glossopharyngeal nerve. The parotids are located below and just
anterior to the ear, and are divided into deep and superficial lobes with the stylomandibular tunnel (which
encloses the facial nerve) being the dividing line. Thus, a portion of the parotid lies superficial to the
mandibular ramus and another portion lies deep.

• Parotid gland is drained by STENSON'S DUCT which pierces the buccinator muscle and crosses the
masseter muscle where it opens into the vestibule of the mouth opposite the maxillary 2nd molar.

• Von Ebner's glands-the only other adult salivary glands that are PURELY SEROUS. These glands are
located around circumvallate papilla of the tongue. Their main function is to RINSE FOOD AWAY
FROM PAPILLA after it has been tasted by the taste buds.

• Parotid gland receives its parasympathetic secretomotor innervation from the glossopharyngeal
nerve via the lesser petrosal nerve, otic ganglion, and auriculotemporal nerve (branch of V3).

• External carotid artery and its terminal branches within the parotid gland (superficial temporal &
maxillary arteries) supply the parotid gland . Lymphatic drainage of the parotid is through the parotid
nodes to the deep cervical lymph nodes.

• Mumps-a viral disease of the parotid gland. Parotitis-inflammation of the parotid gland.

• An injection into the parotid gland (capsule) when attempting to administer an IA nerve block may
cause Bell's Palsy facial expression (paralysis of the forehead muscles, eyelid, and upper and lower
lips on the same side of the face that the injection was given.

SUBMANDIBULAR GLANDS (FORMELY SUBMAXILLARY GLANDS) - located in the

submandibular triangle (digastric triangle.

• Wharton's Duct (Submandibular Duct)-emerges from the anterior end of the deep part of the
submandibular gland, and passes forward along the side of the tongue, beneath the mucous
membrane of the mouth floor. It opens into the mouth on the summit of a small papilla situated at
the side of the frenulum of the tongue. Clinically, the submandibular duct and deep part of the gland
can be readily palpated through the mucous membrane of the mouth floor alongside the tongue.
Saliva can usually be seen emerging from the duct orifice.

74
• During its course, Wharton's duct is closely related to the LINGUAL NERVE which eventually crosses
over the duct. This is important because if you incise the mucous membranes of the mouth floor, you
NOTES
can expose the lingual nerve, Wharton's duct, and the sublingual gland. To expose the duct intraorally,
only mucous membrane needs to be cut through.

• Submandibular glands are innervated by parasympathetic secretomotor fibers from the FACIAL
NERVE, which runs in the chorda tympani and lingual nerve (V3 branch) and synapse in the
submandibular ganglion (this is the same as the sublingual glands). Blood supply to the glands
comes from the FACIAL ARTERY (a branch of external carotid artery).

• Lymphadenopathy is the most common cause of swelling of the submandibular triangle tissues
(not cysts or sialoliths) .

SUBLINGUAL GLAND - the smallest salivary gland that contains mostly MUCOUS ACINI . Sublingual
glands are in the floor of the mouth below the tongue, close to the midline. Mylohyoid muscle supports
the individual sublingual glands inferiorly. They have many small ducts (Rivian Ducts) that open onto
the mouth floor. Most of its secretory units are mucous-secreting with serous demilunes.

• Innervated by parasympathetic secretomotor fibers from the FACIAL NERVE, which run in the chorda
tympani and lingual nerve (V3 branch) and synapse inthe submandibular ganglion. Blood supply is from
the SUBLINGUAL ARTERY (branch of the lingual artery, which is a branch of the external carotid artery).

• Lymphatic drainage from the sublingual &submandibular glands goes to the submandibular and
deep cervical lymph nodes.

• Sometimes the numerous sublingual ducts join to form a single main excretory duct (Bartholin's
Duct) that usually empties into the submandibular duct.

In the head and neck, all lymph ultimately drains into the DEEP CERVICAL LYMPH NODES which form
a chain along the course of the internal jugular vein, from the skull to the root of the neck. These nodes
receive lymph from neighboring structures and from all other regional lymph nodes in the head and neck.
The efferent lymph vessels join to form the jugular lymph trunk (this vessel drains into either the thoracic
duct or right lymphatic duct).

Regional Lymph Nodes:

1. Parotid lymph nodes-receive lymph from a strip of scalp above the parotid salivary gland,
anterior wall of the external auditory meatus, and from lateral parts of the eyelids and middle
ear. Efferent lymph vessels drain into the deep cervical lymph nodes.
2. Submandibular lymph nodes-receive lymph from the front of the scalp, nose, and adjacent cheek,
upper and lower lips (except the center part), paranasal sinuses, maxillary &mandibular teeth
(except mandibular incisors), anterior 2/3 of the tongue (except the tip), floor of the mouth
and vestibule, and gingiva. Efferent lymph vessels drain into the deep cervical lymph nodes.
• Paranasal Sinuses-a series of mucous membrane-lined air spaced that lighten the skull and
enhance voice resonance. Located within the frontal , ethmoid, maxillary, & sphenoid bones.
3. Submental lymph nodes-receive lymph from the tip of the tongue, floor of the mouth below the
tip of the tongue, mandibular incisors and associated gingiva, the center part of the lower lip,
and skin over the chin. Efferent lymph vessels drain into the submandibular and deep cervical
lymph nodes.

MAXILLARY SINUSES - open into the HIATUS SEMILUNARIS (groove in the middle meatus of the
lateral nasal cavity that conta ins openings of the frontonasal duct & anterior ethmoid air cells). The
maxillary sinuses develop after the permanent teeth have erupted, and growth continues throughout
adulthood . Maxillary sinus is innervated by the maxillary division of the trigeminal nerve (CN V-2
which includes ASA, PSA, MSA, &infraorbital nerves).

• Clinical signs of Acute Maxillary Sinusitis: severe, constant, localized pain (any unusual motion or
jarring accentuates the pain). Tenderness to percussion of the maxillary posterior teeth and
tenderness over the anterior sinus wall , and mucopurulent exudates also manifest.

75
 • Antibiotics that treat sinus infections:
• Ampicillin: treats sinusitis due to upper respiratory infections.
• Penicillin & Amoxicillin: treats sinusitis caused by odontogenic foci.

Maxillary Sinus Communication: if a small communication is made with the maxillary sinus while
extracting a maxillary 2nd molar, no additional surgical treatment is needed, simply allow a blood clot
to form. Advise the patient to avoid vigorous mouth washing, frequent nose blowing, smoking, sucking
on a straw, and violent coughing or sneezing.
• Medications that can be prescribed for 1 week: antibiotics (penicillin or erythromycin), decongestant
nasal spray, and/or an oral decongestant.
• If the communication opening is moderate sized (2-6mm), a figure-eight suture is placed over the
CI
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tooth socket.
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.-- • If the communication opening is large (7mm or larger), the opening is closed with a flap.
en
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::c • If a tooth or large fragment is displaced into the maxillary sinus, it should be removed. If the
,..,
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tooth fragment is irretrievable through the socket, it should be retrieved using a "Caldwell-luc"
::c
-< approach ASAP. However, only perform this technique if you know what you are doing. If not, refer the
patient to an OMS.
• The integrity of the maxillary sinus floor is at greater risk with surgery involving removing a single
remaining maxillary molar due to possible ankylosis.

PTERYGOPALATINE FOSSA - a small space behind and below the orbital cavity that lies between
sphenoid bone's pterygoid plates and palatine bone below the orbit apex. Maxillary nerve (V-2) & artery
pass through the pterygopalatine fossa.
• communicates laterally with the infratemporal fossa through the pterygomaxillary fissure.
• communicates medially with the nasal cavity through the sphenopalatine foramen.
• communicates posteriorly with foramen lacerum through the pterygoid canal.
• communicates superiorly with the skull through foramen rotundum.
• communicates anteriorly with the orbit through the inferior orbital fissure.
• openings into pterygopalatine fossa: pterygomaxillary fissure, inferior orbital fissure, sphenopalatine
foramen, pterygoid canal, pharyngeal canal, and foramen rotundum.
• Pterygopalatine Ganglion-lies in the pterygopalatine fossa just below the maxillary nerve (V2). It
receives preganglionic parasympathetic fibers from the facial nerve (eN VII) via the greater petrosal
nerve. It sends postganglionic parasympathetic fibers to the lacrimal gland and glands in the palate
and nose.

BUCCINATOR MUSCLE - a muscle of mastication that forms the muscular substance of the cheek
just lateral to the teeth. The maxillary & mandibular alveolar processes, and pterygomandibular raphe
are the buccinator attachments.

Buccinator muscle originates from 3 areas:

1. pterygomandibular raphe-a thin, fibrous band or tendon running from the hamulus of the
medial pterygoid plate down to the mandible. Pterygomandibular raphe lies between
the buccinator and superior constrictor muscles.
2. maxillary & mandibular alveolar processes.

Buccinator muscle INSERTS at orbicularis oris and skin at the angle of the mouth. Facial and maxillary
arteries supply blood to the buccinator muscle. The buccinator's action is to compress the cheeks
against the molar teeth for sucking and blowing.

When draining purulent exudates from an abscess of the pterygomandibular space from an intraoral
approach, the buccinator muscle is most likely to be incised.

LATERAL PTERYGOIDS (RIGHT & LEFT) - acting together are the PRIMARY PROTRACTORS of the
mandible. *In addition to opening and protruding, they move the mandible from side-to-side (lateral
excursions). For right lateral excursive movements, the LEFT lateral pterygoid is the primary mover (and
vice versa). Thus, when a patient attempts PROTRUSION, the mandible deviates markedly to the right
causing the buccinator, temporalis, and left lateral pterygoid to contract. However, the right lateral
pterygoid cannot contract during protrusion.

76
• Mandible deviates toward the injury side in cases of: condlyar ankylosis (the most common cause NOTES
of TMJ ankylosis is TRAUMA), and with a unilateral condylar fracture. Also, with a lateral pterygoid
injury, the mandible deviates toward the side of injury).
• Apatient who sustained a subcondylar fracture on the left side is unable to deviate the
mandible to the right. This is usually treated by a closed procedure involving intermaxillary
fixation which immobilizes the concomitant fractures and corrects jaw displacement
associated with the condylar fracture. This corrects the shift of the midline toward the side
of the fractured condyle and slight premature posterior occlusion on that side.

• Mandible deviates away from the affected side of injury in cases of: condylar hyperplasia
(malocclusion is a common occurrence with this injury).

• Lateral pterygoid muscles form the ROOF of the PTERYGOMANDIBULAR SPACE.

Masseteric, Pterygomandibular, &Temporal spaces =Masticator Space. These spaces are bound by
the muscles and fascia of mastication. Masticator space infections are almost always of dental origin,
especially from the mandibular molar region. *Needle tract infections after and IA block initially involve
the pterygomandibular space.
• Masticator Space is formed by the splitting of the superficial layer of cervical fascia to enclose the
ramus, masseter, medial pterygoid , and lower portion of the temporalis muscle. It lies largely among
the muscles of mastication.
• It is traversed by the mandibular nerve (V3) and maxillary blood vessels.
• Infections of the zygomatic or temporal bones may pass to the masticator space, and so may
abscesses from mandibular molars.
• Abscesses within the masticator space may point at the anterior aspect of the masseter muscle,
either into the cheek or mouth, or they may point posterior below the parotid gland.
• Amasticator space infection is dominated by TRISMUS, PAIN, SWELLING occurring within a few hours
after a molar extraction, or mandibular trauma. These signs increase rapidly and peak in 3-7 days.
Spontaneous intra-oral drainage usually occurs between 4-8 days. If intra-oral dra inage does not
occur, then surgical drainage is indicated.
• The MOST definite clinical sign indicating extension of an odontogenic infection into the
masticator space is TRISMUS (difficulty opening the mouth due to a tonic spasm of the muscles of
mastication). Trismus is also caused by passing the needle through the medial ptereygoid muscle
during an inferior alveolar nerve block.

TEMPOROMANDIBULAR JOINT (TMJ)

TEMPOROMANDIBULAR JOINT (TMJ) - articulation between mandibular condyle and squamous
portion of temporal bone.

TMJ Components:
1. Mandibular Condyle (Condyloid Process)-elliptically shaped with its axis oriented mediolaterally.
The articulating surface or functioning part of the condyle is on the superior and anterior surfaces
of the head of the condyle. This surface is covered with a VASCULAR LAYER of fibrous C.T.
Each condyle is elliptically-shaped with their long axis oriented mediolaterally (they are not
symmetrical or identical).
2. Articular Fossa (Mandibular or Glenoid Fossa)-a CONCAVE fossa that is the anterior %of the
larger mandibular fossa (a depression in the temporal bone just anterior to the auditory canal).
*This part of the mandibular fossa is a NON-FUNCTIONING portion of the TMJ. Helps make up
the articular surface of the temporal bone.
3. Articular Eminence (Articular Tubercle)-a CONVEX ridge linked with a thick layer of fibrous
C.T. that extends mediolaterally just in front of the mandibular fossa. *The FUNCTIONAL
and articular portion of the TMJ lined or covered with dense fibrocartilage (C.T.) and helps
make up the articular surface of the temporal bone.

77
 NOTES 4. Articular Disc (Meniscus)-a BIOCONCAVE fibrous saddle-shaped structure composed of dense
fibrous C.T. positioned between the condyle and fossa. The disc separates the condyle and
temporal bone (dividing the TMJ into superior &inferior joint spaces). Meniscus varies in
thickness. Central intermediate zone-thin area that separates the thicker portions called
anterior and posterior bands).
• Posterior band of Articular disc-thickest band attached with the posterior loose C.T.
(Retrodiscal tissues or bilaminar zone/posterior attachment). Retrodiscal tissue is highly
vascularized & innervated. Only the articular disc's extreme periphery is SLIGHTLY innervated.
• Thinner anterior band of the articular disc is contiguous with the capsular ligament,
condyle, &superior belly of the lateral pterygoid muscle.

Muscles Acting on the TMJ: masseter, temporalis, pterygoids (medial &lateral), and digastric.

3 TMJ Ligaments support and reinforce the TMJ, and are involved in complex jaw movements:
1. Temporomandibular ligament (Lateralligament}-the major ligament that runs from the
articular eminence to the mandibular condyle to provide direct support to the capsule (the
only ligament that gives direct support to the TMJ capsule). Prevents posterior and
inferior displacement of the condyle.
2. Stylomandibular ligament-an accessory ligament that separates the infratemporal region
anteriorly from the parotid region behind. It runs from the styloid process of the sphenoid
bone to the angle of the mandible (posterior border of the mandible).
3. Sphenomandibular ligament-an accessory ligament attached to the spine of the sphenoid
bone and lingula of the mandible (located on the medial surface of the mandible).

Arteries that vascularize the TMJ:

• Middle meningeal artery (branch of maxillary artery (a terminal branch of external carotid artery).
• Ascending pharyngeal artery (branch of the external carotid artery).
• Oeep auricular artery (branch of maxillary artery).
• Superficial temporal artery (terminal branch of the external carotid artery).

TMJ Syndrome is Divided into 3 Categories:

1. Myofascial Pain Oysfunction (MPD) Syndrome-the most common cause of TMJ pain. It is
a disease primarily involving the muscles of mastication.
• MPD is believed to be a stress-related disorder. An increase in stress produces an increase
in mandibular muscle tension and in combination with teeth clenching causes muscle spasm,
pain, and dysfunction.
• MPD often responds to an acrylic night guard (occlusal separator or occlusal appliance)
along with a soft diet, limited talking, and elimination of gum chewing. Moist heat applied to
the face and non-steroidal anti-inflammatory agents are also helpful during the acute phase.
2. Internal Derangement (Disc Displacement}-an abnormal relationship of the articular disc to
the mandibular condyle, fossa, &articular eminence (or tubercle). The most common direction
the TMJ's articular disc can become displaced is ANTERIORLY. Internal derangement is present
when the posterior band of the articular disc is anteriorly displaced in front of the condyle. As the
articular disc translates anteriorly, the posterior band remains in front of the condyle and the
retrodiscal tissue (bilaminar zone) becomes abnormally stretched. Often the displaced
posterior band returns to its normal position when the condyle reaches a certain point (this is
anterior displacement with reduction). When the articular disc reduces the patient often feels
a pop or click in the joint.
• Subluxation (Dislocation or Open Lock): patient opens wide or maintains open mouth for a
long time, causing the posterior band to stretch and the joint to travel beyond the articular
eminence (condyle is in front of the eminence). Patient cannot close (mouth is stuck open)
after keeping mouth open for a long time in the dental chair.
• Disc Displacement WITH Reduction: "clicking joint" disc is out of place. If painless with no
dysfunction (no treatment necessary) , patient has normal opening or an "S" shaped opening.
TMJ is only ROTATING (not translating). Recipricol clicking on opening and closing is a sign.
A reproducible reciprocal click. On closing, the disc is forward to the condyle. Disc should be
between the condyle &articular eminence.

78
 • Disc Displacement WITHOUT Reduction (Closed Lock): rarely clicking with occasional locking.
Clicking and popping has disappeared with limited opening &pain « 35mm). These patients
have a consistent limited opening ("hard-end feel"). Patient deviates on opening to affected
side (jaw goes to the affected side) . Treatment: always treat conservative (4-6 weeks first)
before considering surgery (95% improve without surgery). Surgery is mainly done to restore
disc position and increase opening (normal opening is 50mm). There is NOT a REPRODUCIBLE
reciprocal click. Most disc displacements are ANTERIOR &MEDIAl.
• In some patients, the articular disc remains anteriorly displaced at full mouth opening
(anterior displacement without reduction). The articular disc is reduced by inducing
downward pressure on the posterior teeth and upward pressure on the chin, accompanied
by posterior displacement of the entire mandible.
• The most common cause of restricted mandibular movement is DISC INTERFERENCE
DISORDERS, which change the relationship of the disc and condyle.
3. Degenerative Joint Disease (Osteoarthritis)-organic degeneration of the TMJ's articular surfaces.

The best way to palpate the posterior aspect of the mandibular condyle is EXTERNAllY over the
posterior surface of the condyle with the mouth open. The TMJ should be evaluated for tenderness and
noise. When checking for joint noises (clicking and crepitus), the joint is palpated laterally (in front of
the external auditory meatus) while the patient opens and closes the mandible.
• Tenderness is assessed by palpating the lateral aspect of the joints when the mouth is closed and
during opening of the mouth . The joint should also be palpated for tenderness while the patient
opens maximally, and the fingertip should be positioned slightly posterior to the condyle to apply
force to determine if there is inflammation of the retrodiscal tissue.
• By placing the fingertips in the patient's external auditory meatus, this technique can produce false
joint sounds during mandibular function because of pressure against the thin ear canal cartilage.

TMJ Surgical Approaches:

1. Preauricular-the best incision to expose the TMJ. A perpendicular incision is made just anterior
to the external ear parallel to the superficial temporal artery. The incision extends from 1 inch
above the zygomatic arch to the lower extremity of the ear. The condyle is approached from behind.
With this approach, care must be taken not to damage the facial nerve or the vessels that
richly supply this area.
2. Submandibular Approach (Risdom Approach)-this is the standard surgical approach to
the mandibular ramus and neck of the condyle. Not the best approach for procedures within
the joint space itself.

Most common cause of TMJ ankylosis is TRAUMA. Ankylosis is the most common complication of
rheumatoid arthritis.

FRACTURES
Radiographic views helpful to evaluate mandibular fractures: posteroanterior view, lateral oblique view,
Towne view, and panoramic view. Control of airway is vital to treating any patient with a facial fracture.
The maxilla and mandible are in a critical relationship to the upper airway. Thus, displacement of fractures
can cause airway obstruction and cause respiratory arrest.
• The highest incidence of fractures occurs in YOUNG MALES ages 15-24 usually from trauma
(i.e. car accidents).

3 Muscle Groups Displace the Mandibular Condyles:

1. Masseter, medial pterygoid, &temporalis ELEVATE the mandible during mastication and cause
upward displacement of the proximal segment.
2. Digastric, mylohyoid, geniohyoid, &lateral pterygoid DEPRESS the mandible and displace
the distal fractured segment inferiorly and posteriorly.
3. Lateral pterygoid is responsible for forward displacement of the condylar head when the
condyle neck is fractured.

79
 Anatomic Distribution of Mandibular Fractures:
• Angle-the most common anatomic site of fracture of the mandible (30% of fractures). Frequently,
impacted 3rd molars are located in this region and further add to the weakness of the mandible in
this area.
• Condylar neck-represents 25% of fractures. It is a safety feature that allows the blow to the jaw to
be dispersed at this point rather than driving the condyle into the middle cranial fossa.
• Bilateral dislocated fractures of the condylar necks cause an anterior open bite and inability
to protrude the mandible.
• Unilateral fracture through the neck may cause forward displacement of the head of the
condyle due to pull of the lateral pterygoid muscle.
• Symphysis area (chin)-represents 22% of fractures, and is usually where blows are sustained.
CI These blows often result in fractures of the subcondylar region.
=
:.- • Body of mandible (17%), Ramus (2%), & Coronoid Process (1 %)-Ieast common fracture site.
r-
(I)
c:::
=
C')
I'T'I Weak points in the mandible where fractures are most common are the angle of the mandible,
=
-< condylar neck, and symphysis area. The location and extent of mandibular fractures are determined
by the direction and intensity of the blow and specific points of weakness in the mandible.
• Patient's mandible deviates to the side of injury upon opening.
• Coronoid process is NOT a weak point in the mandible where fractures are common.

Most common pathognomonic sign of a mandibular fracture is MALOCCLUSION. Other signs and
symptoms of a mandibular body or angle fracture are lower lip numbness, mobility, pain, or bleeding at
the fracture site. In a fracture involving the angle of an edentulous mandible, the proximal segment
is usually displaced anteriorly & superiorly.

OPEN REDUCTION - the reduction of a fractured bone by manipulation after incision into skin and
muscle over the fracture site. The most common site for open reduction is at the angle of the mandible.
Once the incision is made, an intraosseous wire is placed through holes made on either side of the
fracture. Reduction is accomplished under direct vision, and immobilization is obtained by tightening the
wires. This procedure is usually reserved for fractures that cannot be reduced and immobilized adequately
by closed methods. Best used to reduce a fracture when teeth are missing in one or more of the
fractured segments.
• Indications for open reduction are continued gross displacement of the bony segments and an
unfavorable fracture that is likely to cause further displacement of the fractured segments caused
by muscle pull. This type of reduction is commonly performed for displaced angle or body fractures.
*Condylar neck fractures are usually treated by closed reduction.

CLOSED REDUCTION - the reduction of a fractured bone by manipulation without incision into the
skin. It is the simplest method of reduction and is used most often when both fractured segments contain
teeth. After manipulation of the bone, it is usually maintained in place by intermaxillary fixation (IMF).
• Intermaxillary Fixation-fixation obtained by applying wires or elastic bands between the upper and
lower jaws in which suitable anchoring devices have been attached. The most common technique
for IMF is the use of pre-fabricated arch bars.
• Treatment of a mandibular fracture using only intermaxillary fixation (lMF) is a closed reduction
because it does not involve direct opening, exposure, and manipulation of the fractured area.

BILATERAL SAGITTAL SPLIT OSTEOTOMY - the most commonly performed mandibular

orthognathic procedure to correct mandibular retrognathia (Class II malocclusion). When performed
correctly, this technique allows for versatile, accurate, expeditious corrections of mandibular
disharmonies. The mandible is split sagitally and can be used to either advance the mandible (i.e.
retrognathia) or to set back the mandible (i.e. prognathia). It is the standard procedure used today.
*Position of the condyle is unchanged when correcting mandibular prognathism or retrognathism.

VERTICAL RAMUS OSTEOTOMY - used to correct mandibular prognathism. By vertically sectioning

the ramus in a line from the lower aspect of the mandibular notch vertically downward over the
mandibular foramen, or just posterior to the lower border of the mandible at the angle.

80
BODY OSTEOTOMY - a procedure that involves extracting mandibular teeth bilaterally (usually NOTES
premolars), a piece of bone is removed from the mandible, and everything slides back. Corrects
mandibular prognathism (Class III malocclusion).

Ways to Immobilize a Fracture:

1. Barton Bandage-the simplest form of immobilization . Primarily a first aid measure until
definitive therapy can be instituted.
2. Intermaxillary Fixation (lMF}-establishing a proper occlusal relationship by wiring the teeth
together. The method successfully treats most mandibular fractures. The main methods for IMF
are wiring, arch bars, and splints. This is the classical way to immobilize the fracture after
closed reduction .
3. External Skeletal Fixation-used in most cases in which the management of a fractured bone
segment is not satisfactorily accomplished by intermaxillary fixation. It involves placing screws
or pins through the skin on each side of the fracture and a cold cure acrylic bar that holds the
screws in proper relationship with the fracture in the reduced position . It is cumbersome
and esthetically displeasing.
4. Direct Intraosseous Wiring combined with a period of IMF-the traditional method of bone
stabilization after open reduction. This method of stabilization can be accomplished through
various wiring techniques. The wire is placed through holes on either side of the fracture
and immobilization is accomplished by tightening the wires.

GREENSTICK FRACTURE - a mandibular fracture that extends only through the cortical portion of
bone without complete fracture of the bone. It is a closed fracture involving incomplete fractures with
flexible bone, most common in children.

Mandibular fractures are classified based on condition of the bone fragments at the fracture site, and
possible communication with the external environment:
1. Simple fracture-divides a single bone into two distinct parts with no external communication
(closed fractures with no lacerations of the oral mucosa or facial tissues) .
2. Compound fracture-fracture that communicates with the outside environment (open fracture).
This may occur by laceration of the oral tissues exposing the bone fragments, fracture of the
maxilla into the sinuses, or via skin lacerations that would expose the fracture segments.
The most common complication of an open fracture is INFECTION.
3. Comminuted fracture-multiple fractures of a single bone that can be simple or compound.

The line of fracture determines if muscles will be able to displace the fractured segments from their
original position.
• unfavorable fracture-occurs if the fracture line results in a muscle pull displacing the
fracture segment.
• favorable fracture-occurs if the fracture line prevents displacement of the fracture by
muscle pull.

MIDFACIAL FRACTURES - fractures affecting the maxilla, zygoma, & nasoorbital ethmoid complex.
Types of midfacial fractures:
1. LeFORT I (Horizontal Fracture}-a horizontal segmented fracture of the alveolar process of the
maxilla in which the teeth are usually contained in the detached portion of the bone, causing
an OPEN BITE. A LeFort I osteotomy is most commonly used to correct maxillary retrognathia.
2. LeFORT II (Pyramidal Fracture)-a unilateral or bilateral fracture of the maxilla in which the
body of the maxilla is separated from the facial skeleton and the separated portion is pyramidal-
shaped . Signs: periorbital edema, ecchymosis, subconjunctival hemorrhage, and nose bleeding.
Acommon finding is paresthesia over the distribution of the infraorbital nerve.
3. LeFORT III (Transverse Fracture or Craniofacial Oysfunction)-a fracture in which the entire
maxilla and one or more facial bones are completely separated from the craniofacial skeleton .
These patients have restricted mandibular movement.

81
 NOTES 4. Zygomatic complex fractures (most common midfacial fracture). Fractures of the facial bones
(especially the zygomatic complex) may on rare occasions be complicated by damage to the
contents of the superior orbital fissure. Other possible complications of the zygomatic
complex fractures:
• Paresthesia-the most common complication, but usually subsides.
• Antrum (sinus) may be filled with a hematoma, which usually evacuates itself.
• Ocular muscle balance may be impaired because of fracture of the orbital process.
5. Zygomatic arch fractures-are nicely demonstrated by the submental vertex view. This fracture
may not cause any problem other than a possible slight sinking of the cheekbone area . There
may be some encroachment and impairment in closure of the jaw if it comes down and entraps
the coronoid process of the mandible.
o 6. Nasoorbital Ethmoid fractures.
::a
:...
,.....
en
c:::
::a
The first step to treat mid-facial fractures that affects the occlusal relationship is similar to treating
,..,
en
mandibular fractures (re-establish a proper occlusal relationship by placing the maxilla into proper
::a
-< occlusion with the mandible.

Zygomatic bone fractures is the 2nd most common fracture of facial bones behind nasal bone
fractures (most common facial bone fracture). The mechanism of injury usually involves a blow to the
side of the face from a fist, object, or secondarily to motor vehicle accidents (studies show 80% of these
injuries are due to motor vehicle accidents).

Signs &Symptoms of a zygomatic fracture:

• Binocular diplopia (can be secondary to muscle entrapment, neuromuscular injury, or
intramuscular hematoma).
• Difficulty with mastication (trismus) due to masseter spasm or bony impingement of the
coronoid process.
• Ipsilateral epistaxis occurs in some patients to a lacerated maxillary sinus mucosa.

Fracture of the infraorbital rim presents with the symptoms of numbness of the upper lip, cheek, and
nose on the affected side. *Water's view is best to evaluate orbital rim areas.

Water's view, PA skull view, & submental vertex view are radiographic views helpful to evaluate
midfacial fractures.

Maxillary fractures have a greater tendency to produce facial deform ities than mandibular fractures. Due
to the slope of the sphenoid bone comprising the cranial vault floor, blows to the maxilla drive the maxilla
backwards and downwards, resulting in a potential open bite or impingement of the airway.

Segmental Osteotomy-a maxillary procedure where the maxilla is sectioned into two or more pieces.
Bone mayor may not be removed .

Fracture Healing:
• Endosteal Proliferation-occurs within a bone.
• Periosteal Proliferation-occurs within the C.T. covering all pones (periosteum).
• Primary (Bone-to-Bone) Healing-involves both endosteal and periosteal proliferation.
• Secondary Bone Healing-involves mostly endosteal proliferation into the void/space between 2
pieces of bone). The space fills in with callus.

Healing of Bone occurs in 3 overlapping phases:

1. Hemorrhage: occurs first and is associated with clot organization &proliferation of blood
vessels. This non-specific phase occurs during the first 10 days of healing.
2. Callus Formation: a primary callus is formed in the next 10-20 days. Asecondary callus forms
in 20-60 days.
3. Functional Reconstruction: mechanical forces are important in this phase. Haversian systems
are lined up according to stress lines and excess bone is removed . The shape of the bone is
molded to conform with functional usage so that bone can be added to one surface, and
removed from another surface. It takes 2-3 years to completely reform a fracture.

82
4 Reasons Fractures Do Not Heal:
1. Ischemia: navicular bone of the wrist, femoral neck, and lower third of the tibia are all poorly
vascularized, thus are subject to ischemic necrosis after a fracture .
2. Excessive Mobility: healing is prevented and pseudoarthrosis or a pseudo-joint may occur.
3. Interposition of soft tissue: occurs between the fractured ends.
4. Infection: compound fractures have a tendency to become infected.

*A FAT embolism is most often a sequela of fractures.

3 Types of Inappropriate Healing:

1. Delayed-union: satisfactory healing that requires greater than the normal 6-week period. May
be caused by infection, interposition of soft tissue, or muscle between the fractured segments. CI
::c
2. Non-union: failure of the fracture segments to unite properly. May be caused by infection , .--
l>
VI
improper immobilization, or interposition of soft tissue.
3. Mal-union: can be delayed or complete union in an improper position. May be caused ...,...,
c::
::c
::c
by improper immobilization or imperfect reduction. -<

ANESTHESIA
Geudel's Stages of General Anesthesia:
1. Stage 1 (Amnesia & Analgesia): describes conscious sedation that begins with the
administration of anesthesia and continues until the loss of consciousness. Respiration is quiet,
though sometimes irregular, and reflexes remain present. Patient has decreased awareness of
pain, sometimes with amnesia . Consciousness may be impaired, but is not lost. The best
monitor of the level of analgesia is the verbal response. Altered consciousness, loss of
sensory from cerebral cortex occurs.
2. Stage 2 (Delirium/Disinhibition &Excitement): begins with loss of consciousness and includes
the onset of total anesthesia. The patient may move their limbs, chatter incoherently, hold their
breath, or become violent. Vomiting with the attendant danger of aspiration may occur. Patient
appears delirious and excited, amnesia occurs, reflexes are enhanced, and respiration is typically
irregular; retching and incontinence may occur. The patient is brought to Stage 3 as quickly and
smoothly as possible. Loss of consciousness-motor centers.
• Respirations irregular, lateral nystagmus, pupillary reflex intact, muscle tonus decreases as
this stage progresses. Laryngeal and pharyngeal reflexes become obtunded.
3. Stage 3 (Surgical Anesthesia): begins with establishing a regular pattern of breathing, total
loss of consciousness, and is the period when signs of respiratory or cardiovascular failure first
appear. Patient is unconscious with no pain reflexes. Respiration is very regular and BP is
maintained. This stage has 4 planes. Spinal reflexes are depressed and skeletal muscle
relaxation occurs. Agents Useful for Surgical Anesthesia:
• Cyclopropane: 20-35% for Stage 3 causes rapid induction and recovery, good muscle
relaxant, and sensitizes the heart to catecholamines.
• Halothane: 3% induction and 1-2% maintenance causes relatively slow induction and
recovery. Not a good muscle relaxant. Side effects: sensitizing heart to the catecholamines,
hypotension, and cardiac arrhythmias. Not a good analgesic, so used as an adjunct.
Halogenated hydrocarbons are associated with liver damage if toxic doses are used.
• Methoxyflurane: 1-3% causes slow induction and recovery, good muscle relaxant, sensitizes
the heart to catecholamines, a respiratory depressant, and good analgesic.
4. Stage 4 (Premortem or Medullary Depression)-signals danger (characterized by maximally
dilated pupils and cold, ashen skin). BP is extremely low and often un-measurable. Cardiac
arrest is imminent. *Eyes are greatly enlarged in size and do not react to bright light when
functional circulation to the brain has stopped . Patient experiences severe respiratory
and cardiovascular depression/paralysis requiring mechanical & pharmacologic support.

83
 American Society of Anesthesiologists (ASA) Classification of Patient Physical Status:
1. ASA-I: a normal, healthy young patient with an unremarkable medical history and no
systemic disease.
2. ASA-II: patient with mild systemic disease or significant health risk factor (smoking, excessive
alcohol use, obesity).
3. ASA-III: patient with severe disease that is not incapacitating.
4. ASA-IV: patient with severe systemic disease that is a constant threat to life.
5. ASA-V: a moribound patient who is not expected to survive without the operation.
6. ASA-VI: patient is declared "brain-dead" and their organs are being removed for donor purposes.

Elements of General Anesthesia: analgesia, relaxation, hyporeflexia, and narcosis

o (not hyperpyrexia = elevated body temperature).
::0:1
:co • Medulla-the last area of the brain depressed during general anesthesia. This area is the most
r-
en
vital part of the brain and contains the cardiac, vasomotor, and respiratory centers of the brain.
...,...,
c::
::0:1

::0:1
• The most reliable sign of "oxygen want" while monitoring a patient during general anesthesia is
-< increased pulse rate. Cyanosis may also be present.
• The emergency most often experienced during outpatient general anesthesia is
respiratory obstruction.
• The best anesthetic technique used in oral surgery to avoid aspiration of blood or other debris when
a patient is under general anesthesia is endotracheal intubation with pharyngeal packs.
• A patient with an acute respiratory infection is contraindicated for general anesthesia.
• The eyes are taped shut prior to draping a patient before surgery to prevent corneal abrasion.

INDUCTION - phase of anesthesia that begins with the administration of anesthetic and continuing
until the desired level of patient unresponsiveness is reached. The depth of general anesthesia by
inhalation varies with the partial pressure (tension) of the anesthetic agent in the brain, and the rates
of induction and recovery depend on the rate of change of tension in this tissue, blood supply to the
lungs, pulmonary ventilation, and concentration of the anesthetic influence the induction rate. The
signs and stages of anesthesia are most likely seen with an anesthetic with a slow rate of induction.

MAINTENANCE - process of keeping a patient in surgical anesthesia.

RECOVERY - phase of anesthesia commencing when surgery is complete and delivery of the
anesthetic is terminated, and ending when the anesthetic has been eliminated from the body.

DISSOCIATIVE ANESTHESIA - a unique method of pain control that reduces anxiety and produces
a trance-like state where the person is not asleep, but feels separated from their body. Used in
emergency situations (i .e. injury/trauma) and can be used for short, painful procedures (i.e. changing
bandages). This method is safe and lasts only a short time. Since the person does not usually remember
the procedure, dissociative anesthesia is useful in CHILDREN . Aperson who received dissociative
anesthesia usually does not remember the procedure, especially if a sedative was given with the pain
medication. Most people feel normal within a few hours. As the medication wears off, an individual may
have intense dreams or hallucinations.

• KETAMINE is the primary medication used in dissociative anesthesia, but a sedative is often given
before the Ketamine to reduce anxiety. Asingle dose of ketamine produces a trancelike state for 10-
30 minutes, and pain control for 30-45 minutes. The patient's eyes are open during the procedure,
but he/she is in a daze and feels no pain.
• Ketamine secretions of salivary and bronchial glands, BP, HR, and muscle tone
(not respirations).
• Side Effects: hypertension, increased pulse, delirium.

Local anesthetics are MOST EFFECTIVE in tissues above a pH 7 (alkaline). Local anesthetics are
alkaloid bases combined with acids to form water-soluble salts. A pH > 7 causes hydrolysis of the
anesthetic salts. The potential action of all local anesthetics depends on the anesthetic salt's ability
to liberate the free alkaloidal base (the non-ionic lipophilic molecule). The potency of local anesthetics
increases with increasing lipid solubil ity.

84
• As the pH of the tissue decreases and [H+1increases, the cationic (water-soluble) form rises and free NOTES
base decreases. Conversely, as pH is increases and [H+l is decreased, the free base (fat-soluble) form
increases and the cationic form decreases. This free base form readily penetrates the lipid-rich nerve.
• Inflammation and infection cause tissues to become acidic. The cationic (water-soluble) form of
the anesthetic predominates (there is less free base available). Thus, the penetration through the
membrane is decreased, giving the anesthetic poor effectiveness.
• Local anesthetics affect the nerve membrane by DECREASING the membrane's permeability to
Na+ and DECREASING the membrane's excitability. Local anesthetics bind to inactivation gates of
fast voltage gated sodium channels, stabilizing them in closed position, effectively prolonging the
absolute refractory period . This decreases Na+ membrane permeability, thus reducing membrane
excitability. When membrane excitability is reduced below a critical level, a nerve impulse fails to pass
through the anesthetized area. o
::a
• K+, Ca2+, &CI- conductances are unchanged. ,....
:.>0
en
• Local anesthetics "reversibly block" nerve impulse conduction and produce reversible c:
::a
loss of sensation at their administration site. The action site of local anesthetics is at the ...,
."

::a
lipoprotein sheath of nerves. -<
• Small, NONmyleinated nerve fibers that conduct pain and temperature sensations are affected
first, then touch, proprioception and lastly skeletal muscle tone.

MAXIMUM allowable dose of 2% lidocaine with 1: 100,000 EPI is 3.2mg lidocaine/ per lb. (or 7mglkg).
*lkg = 2.2 Ibs.
• Ex: 701b patient x 3.2mg = 224mg (maximum allowable dosage) / 36mg (amount of lidocaine in 2%
carpule) = 6.2 carpules (-6).
• For Carbocaine without EPI, the maximum allowable dose is 3.0mg/lb.
• Maximum allowable dose of EPI that can be administered to a cardiac-risk patient is 0.04mg. In
terms of local anesthetics, this is equivalent to either:
• 1 cartridge (1.8cc) with anesthetic concentration of 1:50,000.
• 2 cartridges (3.6cc) with anesthetic concentration of 1: 100,000.
• 4 cartridges (7.2cc) with anesthetic concentration of 1:200,000.

0.018mg of EPI are in each cartridge/carpule (1.8cc) of 2% lidocaine with 1:100,000 EPI. 0.018mg
= 1.8cc x .Olmg EPI.
• 1cc of 2% lidocaine with 1: 100,000 EPI contains:
• 20mg of lidocaine, O.Olmg EPI, 6mg NaCI, 0.5mg sodium-metabisulfate (preservative
to stabilize EPI).
• Img of methylparaben (a preservative) and NaOH to stabilize the pH.

• 1.8cc of 2% lidocaine (1 carpule) with EPI 1:100,000 contains:

• 36mg lidocaine (1.8 x 20mg), 0.18mg EPI (1.8 x .Olmg), 10.8mg NaCI (1.8 x 6mg).
• .90mg sodium-metabisulfate (1.8 x 0.5), 1.8mg of methylparaben (1.8 x Img), and NaOH
to stabilize the pH.

ESTERS - potent local anesthetics slightly different in chemical structure from amides. Allergic reactions
are much more common with esters. Allergic reactions to local anesthetics are usually caused by an
antigen-antibody reaction.

• PABA Esters: Procaine (Novocain), Tetracaine/Pontocaine (most commonly used), Propoxycaine

(Ravocaine), Benzocaine (Monocaine), Cocaine. *Procaine was the prototype ester local anesthetic used.

• Ester local anesthetics undergo rapid biotransformation in BLOOD PLASMA. The major portion of
this inactivation process occurs in the blood through hydrolysis to paraaminobenzoic acid by the
enzyme "pseudocholinesterase". Patients with pseudocholinesterase inactivity are unable to detoxify
ester-type agents at a normal rate. Thus, amide anesthetics are recommended in these patients.

85
 AMIDES - safe, versatile, and effective local anesthetics. If hypersensitivity to a drug in this group precludes
its use, one of the ester-compound local anesthetics may provide analgesia without adverse effect.

• Amide local Anesthetics: Prilocaine (Citanest), Bupivacaine (Marcaine), lidocainelXylocaine (the

most common), Mepivacaine (Carbocaine), Etidocaine (Duranest).

• Allergic reactions to amide local anesthetics are rare, but may occur as a result of hypersensitivity
to the local anesthetic agent or due to an allergy to methylparaben or other preservatives used in many
solutions. These reactions are characterized by cutaneous lesions of delayed onset or urticaria, edema,
and other manifestations of allergy. For patients allergic to ester and amide local anesthetics,
DIPHENHYDRAMINE is a safe and effective alternative.

• Amide local anesthetics undergo biotransformation in the LIVER by microsomal enzymes, but 10-
20% is excreted unchanged.

local anesthesia works by reducing anxiety and sensitivity during the procedure. Local anesthesia acts
by reducing sensitivity which thus reduces anxiety and stress related to treatment. Salivation is also
decreased.

LIDOCAINE is the local anesthetic that may manifest its toxicity clinically by initial depression and
drowsiness (rather than stimulation and convulsion).
• The initial effect on the brain for local anesthetics is usually stimulation, then depression. However,
it is possible that the excitatory phase of the reaction may be extremely brief, or may not occur (this
is true especially with lidocaine and mepivacaine) causing patients to feel drowsiness. *lidocaine
& Mepivacaine can also show cross-allergenicity.
• Usually, the FIRST clinical sign of mild lidocaine toxicity is NERVOUSNESS. Mild toxicity can be
caused by an intravascular injection, unusually rapid absorption, or too large a total dose of the local
anesthetic. Clinical manifestations of a mild lidocaine toxicity related to CNS excitation:
• Nervousness (increased anxiety), talkativeness, muscular twitching, perioral numbness, l'HR, BP, RR.
• Lidocaine can skip the excitatory phase and go straight to the depression phase (drowsiness).
• If the clinical manifestations do not progress beyond these signs with retention of consciousness,
no definitive therapy is needed. The lidocaine will undergo redistribution and biotransformation, and
the blood level will fall below the toxic level in a short time.
• Treatment of a sustained convulsive reaction to a local anesthetic includes oxygen and Diazepam
IV. If proper equipment and adequately trained staff are unavailable, do not attempt injections.
• Possible side effects of lidocaine systemic absorption (not necessarily toxic levels) are tonic-clonic
convulsions, respiratory depression, and decreased CO.

Inadvertent intravascular injection of a local anesthetic with a vasoconstrictor (EPI) may cause clinical
signs of nervousness, tremors, dizziness, blurred vision, and excitation and/or depression of the CNS. These
signs may be followed by drowsiness, convulsions, unconsciousness, and possible respiratory arrest.
• Injections should always be made slowly with aspiration to avoid intravascular injection and prevent
a systemic reaction to the local and vasoconstrictor used in many solutions. The presence of a
vasoconstrictor does not prevent an intravascular injection or systemic absorption. The acute
intravenous toxicity of a local anesthetic with a vasoconstrictor may be higher than that of the
anesthetic agent alone. If drowsiness is apparent after administration of a local anesthetic, then the
reaction is probably due to the toxic effect of the anesthetic, rather than a psychogenic reaction.
• In local anesthesia, depression of respiration is a manifestation of the toxic effects of the solution.

Reasons Vasoconstrictors (EPI) are placed in local Anesthetics:

1. Prolong the duration of action of the local anesthetic (most important reason).
2. Reduce the toxicity because less local anesthetic is necessary
3. Reduce the rate of vascular absorption by causing vasoconstriction.
4. Help make the anesthesia more profound by increasing the concentrations of the local
anesthetic at the nerve membrane.

Vasoconstrictors do NOT reduce the chance of developing an allergic reaction to the local anesthetic.

86
 NOTES
Vasoconstrictors Used in Local Anesthetics

Vasoconstricto Concentrations Available Anesthetics that contains this vasoconstrictor

Epinephrine 1:50,000 or 1:100,000 Lidocaine 2%
1:200,000 Prilocaine 4%
1:200,000 Marcaine .5%

Levonardefrin
(Neo-Cobefrin) 1:20,000 Mepivovaine 2%
Norepinephrine (NE) 1:30,000 Procaine 2%

Vasoconstrictors act at ALPHA RECEPTORS to produce constriction of arterioles. Cocaine acts as an

intrinsic vasoconstrictor that increases the PRESSOR ACTIVITY of both EPI &NE.

Local anesthetics depress small, non-myelinated nerve fibers FIRST, and depress large, myelinated
nerve fibers LAST. Variations in susceptibility of nerve fibers to local anesthetics depend on nerve
diameter and distance between the nodes of Ranvier. Clinically, the general order of loss of nerve
function from a local anesthetic is:
1. pain
2. temperature (cold and warmth).
3. touch &pressure.
4. proprioception.
5. skeletal muscle tone (motor).

Nerves regain their function in the reverse order.

EPINEPHRINE - drug of choice for managing an acute allergic reaction involving bronchospasm
(acute narrowing of the respiratory airway) and hypotension.

NITROUS OXIDE - the inhalation anesthetic with the FASTEST ONSET of action. It is a colorless, non-
irritating gas with a pleasant, mild odor and taste. It has a blood/gas partition coefficient of 0.47, thus is
poorly soluble in blood . It is excreted unchanged by the lungs. N20 is stored under pressure in steel
cylinders painted blue (oxygen is stored in green tanks). N20 is the oldest gaseous anesthetic used today,
and the only inorganic substance used as an anesthetic. Nitrous oxide is a great drug to reduce anxiety.

Nitrous oxide is a gas used as an ANESTHETIC in SURGERY to provide light anesthesia and is delivered
in various concentrations with oxygen. Nitrous oxide alone does NOT provide deep enough anesthesia for
major surgery, so it is supplemented with other anesthetic agents. It is often given for induction of
anesthesia, preceded by the administration of a barbiturate or analgesic narcotic. Induction and recovery
are rapid. *Sedation can be reversed rapidly when using inhalation as the route of administration of drugs.
• Advantages of N20 Analgesia: good analgesia , nonflammable, suitable for all ages and therapeutic
for many medically compromised patients, has virtually no adverse effects in the absence of hypoxia,
titratable, and produces euphoria.
• Disadvantages of N20 Analgesia: misuse potential with patients and dentists, is not a complete
pain reliever (a local anesthetic is still required for most dental procedures) , nausea is the most
common patient complaint, and diffusion hypoxia can occur (so give 100% oxygen at the end of
dental procedures to prevent it). *Inhalation of 100% oxygen is contraindicated in a patient with
COPD (chronic obstructive pulmonary disease).
• Nausea is the most common SIDE EFFECT of nitrous oxide analgesia .
• Primary disadvantage of N20 as a general anesthetic is its LACK OF POTENCY.
• The most common complication of N20 sedation is a behavioral problem (laughing, giddy) .
• N20 inh ibits methionine synthetase which is required for vitamin B12 production
(can cause fatigue).

87
 • N20 Contraindications:
• Hypoxemia: abnormal deficiency of oxygen in arterial blood.
• Respiratory disease: emphysema, asthma, upper respiratory obstruction.
• Emotional instability and contagious diseases because cannot sterilize the entire tube.
• N20 is acceptable for a pregnant patient, but from a risk management point it may
be prudent not to use nitrous oxide on any pregnant patient.
• N20 works on the CNS, and is the only INORGANIC gas used by the anesthesiologist. Room air
contains 21 % oxygen (so the patient MUST receive at least this much oxygen). Maximal safe
concentrations of N20 (70% nitrous &30% oxygen) produce intoxication, analgesia, and amnesia.
• N20 is carried in the bloodstream in physical solution . There is no metabolism or degradation of N20
in the body. Rather, it is excreted solely by the lungs, unchanged. High blood levels of N20 can be
C) achieved Quite Quickly. N20 is non-toxic to body tissues (the only toxicity using N20 is the lack of
:::<:I
,....
> oxygen that can result from operator error) . The gag reflex is only slightly obtunded with N20
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analgesia.
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• N20 has its main effects on the RETICULAR ACTIVATING and LIMBIC SYSTEMS .
:::<:I
-< • First symptom of nitrous oxide analgesia is TINGLING OF THE HANDS.
• Correct total liter flow of nitrous oxide/oxygen is determined by the amount needed to keep the
reservoir bag 1/3-213 full.
• Nitrous oxide is very appropriate for children who are fearful and timid.
• The difference between conscious sedation vs. general anesthesia with respect to patient response
is the patient retains all reflexes under conscious sedation, but not under general anesthesia.

Neuroleptic + Narcotic analgesic + N20 Neurolept Anesthesia (a state of neurolept anesthesia &
unconsciousness produced by combined administration of a narcotic analgesic and neuroleptic agent
with inhalation of N20 &oxygen).
• The induction of anesthesia is slow, but consciousness returns Quickly after nitrous oxide inhalation
is stopped.

Neuroleptic agent (Droperidol) + Narcotic analgesic (Fentanyl) Neurolept Analgesia (conscious). Under
the influence of this combination, the patient is sedated and demonstrates psychic indifference to the
environment, but remains conscious and can respond to Questions and commands. Neurolept analgesia
only produces an unconscious state if nitrous oxide is also administered.

Nitrous Oxide &Ethylene are useful ONLY for sedation &analgesia.

1. N20: 10-20% (maximum 35%) causes rapid induction and recovery. *Ventricular fibrillation is
LEAST LIKELY to occur during anesthesia with nitrous oxide. The primary danger associated
with using N20 anesthesia in concentrations exceeding 80% is HYPOXIA.
2. Ethylene: 25-35% causes rapid induction & recovery, not often used due to explosiveness and
disagreeable odor.

Agents currently used in INHALATION ANESTHESIA are nitrous oxide (a gas) and several easily
vaporized liquid halogenated hydrocarbons (Halothane, Desflurane, Enflurane, Isoflurane, Sevoflurane,
& Methoxyflurane). These anesthetics are liquid at room temperature and are vaporized in precisely
controlled concentrations in a metered stream of oxygen and N20. Inhalation anesthetics are absorbed
and primarily excreted through the lungs.
• Desflurane-an inhalation anesthetic with a low blood: gas partition coefficient, but is not used to
induce anesthesia because of its pungency (irritates the airway) which causes patients hold their
breath. The pungency of desflurane leads to a high incidence of coughing, bronchospasm, and can
cause centrally mediated tachycardia and l'BP.
• They are administered as GASES (their partial pressure or "tension" in the inhaled air or in blood or
tissue is a measure of their concentration). Since the standard pressure of the total inhaled mixture
is atmospheric pressure (760mm Hg at sea level), the partial pressure can also be expressed as a
%. Thus, 50% N20 in the inhaled air would have a partial pressure of 380mm Hg.
• SPEED of inhalation induction of anesthetic effects depends on:
1. Gas solubility (the primary factor). The more soluble the gas in blood, the slower rate of induction.
2. Inspired gas partial pressure.
3. Ventilation rate.
4. Pulmonary blood flow.
5. Arteriovenous concentration gradient.

88
Administration of an inhalation anesthetic (except N20) is usually preceded by IV or intramuscular
administration of a short-acting sedative hypnotic drug (often a barbiturate). The procedure almost
NOTES
always requires endotracheal intubation.

Barbiturates DEPRESS the CNS, which lasts 3-8 hours depending on the dose. The barbiturates of
choice for the dentist are usually the short-acting drugs because the onset of sedation is short (-30
minutes to 1hr), and the duration of effect (3-4 hours) is more than sufficient for most dental procedures.
• Barbiturates have two major effects: sedative (decreases anxiety) and hypnotic (helps sleep).
• Drugs to avoid in patients taking barbiturates: phenothiazines, alcohol, antihistamines, &
antihypertensives. These drugs enhance the CNS depression of barbiturates.
• After IV administration of an ultra-short acting barbiturate (i.e. Brevital or Pentothal), the last tissue
to become saturated as a result of redistribution is FAT (because it is not as vascular as liver, Q
:::a
brain, and muscle tissue). :D-
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en
• In low doses barbiturates reduce anxiety, respiration, BP, HR, and REM sleep. c:

• In higher doses, barbiturates can increase some types of behavior and act like a stimulant. These
..,
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,.."

effects may be caused by depression of inhibitory brain circuits (barbiturates at these doses act to =:l
remove inhibitory behavior).
• Barbiturates can lead to excessive sedation and cause anesthesia, coma, even death. Barbiturate
overdoses may occur because the effective dose of the drug is not too far away from the lethal dose.
• Properties of Barbiturate Hypnotic Agents: respiratory depression, induction of liver microsomal
enzymes, tolerance development, &suppression of REM sleep. Barbiturates can cause hyperanalgesia
(l'sensitivity to pain).

General Anesthetics most commonly used are inhalation alone, barbiturates alone, barbiturates with
oxygen, and nitrous in combination with a more potent agency like Halothane. Also, a local anesthetic is
sometimes used for vasoconstriction and to decrease the amount of barbiturate used in lengthy procedures.
• The most effective agent in initial treatment of respiratory depression due to overdose of
barbiturates is OXYGEN under positive pressure.
• The behavior of patients under GENERAL anesthesia suggests that the most resistant part of the
CNS is the MEDULLA OBLONGATA (cardiac, vasomotor, and respiratory centers of the brain) . The most
controllable route of administration of a general anesthetic is inhalation.

BREVITAL (METHOHEXITAL) - the drug most commonly used to attain GENERAL anesthesia
(an IV barbiturate prescribed to induce anesthesia in short surgical procedures as a supplement
to other anesthetics.
• Brevital is metabolized in the liver and excreted by the kidney.
• General anesthesia induction and recovery using Brevital is rapid.
• Hiccoughs is the most common side effect due to rapid injection of Brevital.
• A primary advantage of IV sedation is the ability to titrate individualized dosages.

MALIGNANT HYPERTHERMIA - an autosomal dominant inherited condition and life-threatening,

acute pharmacogenetic disorder occurring in patients undergoing general anesthesia. Classic MH
usually manifests in the operating room, but can also occur within the first few hours of recovery from
anesthesia. Characterized by a sudden, rapid rise in body temperature associated with signs of
increased muscle metabolism (Le. tachycardia, tachypnea, sweating, and cyanosis, increased C02
production, and muscle rigidity).
• Usually occurs in apparently healthy children and young adults at an average age of 21 years (equally
in males &females).
• When MH is diagnosed early and treated promptly, the mortality rate should be near zero. Whenever
anesthesia is administered, Dantrolene should be readily available and the protocol for MH
management (100% oxygen, cooling procedures, and correcting acidosis and hyperkalemia).
Dantrolene is currently the only known drug that treats MH by impairing calcium-dependent
muscle contraction, and controlling hypermetabolism manifestations.
• People with MH are informed of their condition and advised that 50% of their first-degree relatives
are likely to have the trait.

89
 N Sedation Indications: apprehensive or scared patients, decrease stress in a medically compromised
patient, or to perform several procedures on a patient who is extremely anxious. The optimum site for IV
sedation for an outpatient is the MEDIAN CEPHALIC VEIN which lies in the lateral aspect of the
antecubital fossa (anterior to the elbow). Avoid entering the brachial artery to avoid immediate burning
at the injection site (arm appears blotchy, and the arm pulse is weak compared to the other arm).
• IV sedation is usually done with a 21-gauge needle with a Valium (Diazepam). The rate of injection
of va lium is Imllminute (lml of injectable valium contains Smg of valium . The injection is
discontinued when the eyelids droop (ptosis).
• 3 common signs that indicate the correct level of sedation has been reached with Valium are
blurring of vision, slurring of speech, and 50% ptosis of the eyelids (Verrill's sign).

Phlebitis (Thrombophlebitis) of a vein after administration of IV valium is usually attributed to the

presence of propylene glycol in the mixture. Phlebitis is irritation or inflammation of a vein sometimes
seen after IV administration of valium due to the propylene glycol in the mixture. Phlebitis is more likely
to occur if a vein in the hand or wrist is used and may be more common after repeated injection, especially
in heavy smokers, elderly, and women taking oral contraceptives. Treatment: elevate the limb, apply
moist heat, and possibly use anti-coagulants.

Clinical Observations of Phlebitis:

• Vessels feel hard, thready, or cord-like.
• It is extremely sensitive to pressure.
• The surrounding area may be erythematous and warm to touch.
• The entire limb may be pale, cold, and swollen.

SCOPOLAMINE - a drug structurally similar to Acetylcholine. Scopolamine acts by interfering with

the transmission of nerve impulses by acetylcholine in the PNS and produces symptoms typical of
parasympathetic system depression (dilated pupils, rapid heartbeat, dry skin and mouth, and dry
respiratory passages).

• Scopolamine is very effective for preventing MOTION SICKNESS and this indication is its most
common clinica l use. Since scopolamine depresses the eNS, it is used as a sedative before
anesthesia and as an anti-spasmodic in certain disorders characterized by restlessness and
agitation (i.e. delirium , tremors, psychosis, mania , and Parkinsonism).

• Premedication with Scopolamine prolongs certain effects (similarto premedication with Morphine)
like amnesia, psychic sedation, and decreased salivation.

• Reduction of secretions occurs by competitive blockade of acetylcholine and other cholinergic

stimuli at cholinergic receptor sites on salivary and bronchial glands. Antagonism of acetylcholine
on the sphincter and ciliary body in the eye causes mydriasis (dilation of pupils) .

ANTICHOLINERGIC DRUGS - interfere with binding of acetylcholine at its receptor. The most common
method for categorizing anti-cholinergic drugs is to identify the ionization state of nitrogen (i.e. tertiary
or quaternary) because this affects the drug's ability to penetrate the eNS.

• Atropine, Benztropine, Scopolamine, Dicyclomine, Trihexyphenidyl are tertiary compounds (these

penetrate the eNS more readily than quaternary (Le. ionized) compounds. However, at normal doses
Atropine penetrates the eNS poorly. Atropine is contraindicated for nursing mothers and patients
with glaucoma.

• Scopolamine, Atropine, and Benztropine decrease saliva flow and secretion from respiratory
glands during general anesthesia.

• Glycopyrrolate, Ipratropium, & Probanthine are quaternary compounds that cannot penetrate the CNS.

• Principal therapeutic uses of anti-cholinergic drugs in dentistry:

90
• Decrease saliva flow during dental procedures (anti-sialogue) and the secretion from respiratory
glands during general anesthesia . Atropine is the most commonly used anti-cholinergic drug for
these purposes. Scopolamine penetrates the eNS more readily than Atropine, but is rarely used .

• A patient pre-medicated with Atropine will exhibit mydriasis (dilated pupils).

Air Volumes:
1. Tidal Volume (TV}-volume of air normally inhaled or exhaled by quiet breathing.
2. Residual Volume (RV}-volume of gas in the airway that does not participate in ventilation.
3. Expiratory Reserve Volume (ERV}-amount of air that can be exhaled in addition to the TV.
4. Inspiratory Reserve Volume (lRV}-amount of air that can be inhaled in addition to the TV.
5. Vital Capacity (VC}-totallung capacity. VC = TV + ERV + IRV.
6. Functional Residual Capacity (FRC}-the amount of air remaining in the lungs at the end of a
normal expiration. This air is used to provide air to alveoli to aerate the blood evenly between
breaths. A larger than normal functional residual capacity (FRC) causes N20 sedation to
take longer. FRC = ERV + RV.

Pulmonary volumes and capacity are 20-25% less in females than males, and are greater in large and
athletic people. N20 sedation varies accordingly.

LARYNGOSPASM - sudden acute spasm of the vocal cords and epiglottis that can result in airway
occlusion and death. Apatient under general anesthesia loses the laryngeal reflex. If blood and saliva collect
near the vocal cords, this stimulates the patient to go into spasm (laryngospasm) and the vocal cords close.
When this happens, air cannot pass through. The two most important steps in initial management of a
laryngospasm are applying oxygen under positive pressure and administering succinylcholine (a skeletal
muscle relaxant used when performing endotracheal intubation and endoscopies).

UNIVERSAL sign of laryngeal obstruction is STRIDOR (crowing sounds). Stridor is a high-pitched, noisy
respiration, like blowing of the wind. It is a sign of respiratory obstruction, especially in the trachea or larynx.
• Because total airway obstruction usually occurs during inspiration, there is usually adequate oxygen
left in the cerebral blood to permit up to 2 minutes of consciousness. If the obstruction is not
recognized, managed, and oxygen is not delivered to the victim's lungs, blood, and brain, permanent
neurologic damage occurs in 3-5 minutes.
• Non-invasive Procedures for Obstructed Airway: back blows, manual thrusts, Heimlich maneuver,
chest thrust, and finger sweep.
• Invasive Procedures for Obstructed Airway: these procedures are only performed by people trained
in these techniques and with the proper equipment:
• Tracheotomy-used more for long-term airway maintenance, not for emergency airway.
• Cricothyrotomy-a procedure to establish EMERGENCY AIRWAY when other methods are
unsuitable or impossible. The access site is the cricothyroid membrane of the trachea,
located on the anterior neck between the cricoid and thyroid cartilages.
• Acricothyrotomy may be life-saving in an anaphylactic reaction where a patient shows
signs of laryngeal obstruction. If a patient shows signs of laryngeal obstruction
(stridor/crowing sounds), epinephrine and oxygen is administered.
• If a patient loses consciousness and is unable to breathe, an emergency cricothyrotomy
may be required to bypass the laryngeal obstruction.

During an inferior alveolar nerve block injection, the needle passes through the mucous membrane &
buccinator muscle, and lies lateral to the MEDIAL PTERYGOID MUSCLE.
• If the needle accidentally passes posterior at the level of the mandibular foramen, it penetrates the
parotid gland causing the patient's cheek to feel numb (patient may develop paralysis of muscles
of facial expression CN VII).
• If the needle tip is resting well below the mandibular foramen, it penetrates the medial pterygoid
muscle.
• Trismus is most likely caused by irritation of the medial pterygoid muscle during an inferior
alveolar nerve block.

91
 N • After an inferior alveolar nerve block or mental nerve block, a prickly or tingling sensation
(paresthesia), or complete numbness in the lower lip may result and persist for a considerable time
due to direct trauma or piercing of the nerve trunk by the needle. This happens more often in a
mental nerve block injection. The paresthesia symptoms gradually diminish (may last from two weeks
to 6 months), but there is usually a complete recovery.
• The most common cause of paresthesia of the lower lip is extracting a mandibular 3rd molar
(especially horizontally impacted 3rd molars).

Post-operative Hypotension may be due to the effect of transfusion reactions, fat embolism, anesthetic
or analgesics on the myocardium (the most common cause), liver failure, or anaphylaxis. Treatment:
Narcan (narcotic antagonist) if hypotension is due to narcotics. Use Atropine (anti-cholinergic) if
c bradycardia is present.
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en
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Post-operative Hypertension-most often due to post-operative pain, so treat with narcotics and
....,
."
sedatives. It is also caused by hypercarbia (> normal C02 amounts in the blood), or administration of
:::a
-< a vasopressor or catecholamine agents.

PSYCHOGENIC REACTION - caused by psychological factors (ratherthan physical factors like drugs).
Signs: nausea, pallor and cold perspiration, widely dilated pupils, eyes rolled up, and brief convulsions.
• Vasovagal syncope-a psychogenic reaction and the most commonly experienced complication
associated with using local anesthetic solutions. The clinical signs closely resemble shock. These
psychogenic reactions readily respond to placing the patient in a supine position.

Actions that may prevent a patient from developing a vasovagal syncopal reaction after a
local anesthetic:
• Slowly injecting the anesthetic solution.
• Watching the patient's color change during the injection.
• Using a topical anesthetic prior to administration of the local anesthetic.
• Using a low concentration of vasoconstrictor.
• Premedicating extremely anxious patients.
• Sympathetic, but confident handling of the patient.
• Proper patient preparation.

The most common cause of transient loss of consciousness in the dental office is vasovagal syncope
due to a series of cardiovascular events triggered by emotional stress brought on by the anticipation of
or delivery of dental care. Any signs of an impending syncopal episode should be quickly treated by
placing the patient in a FULLY SUPINE POSITION, or a position where the legs are elevated above the
level of the heart (TRENDELENBURG POSITION), and by placing a cool, moist towel on the forehead .
The most common early sign of syncope is PALLOR (paleness).

TRENDELENBURG'S POSITION - a position where the patient is on an elevated and inclined plane
(_45°) with the head down and legs and fee over the edge of the table. It is used in abdominal
operations to push abdominal organs toward the chest, and is usually used to treat shock (i.e.
anaphylaxis reactions). However, if there is an associated head injury, the head should not be kept lower
than the trunk.

Drugs that when administered 1 hour prior to the dental appointment are safe and effective ways to
allay fears of an apprehensive ADULT dental patient and avoid a psychogenic reaction in the dental
chair include:
• Diazepam (Valium): 5-10mg orally (PO).
• Promethazine (Phenergan): 25mg orally (PO).
• Pentobarbital (Nembutal) or Secobarbital (Seconal): 50-100mg orally (PO).

• These drugs are NOT recommended unless the dentist has experience with them and can handle any
complications from their use. For a dentist to use "enteral sedation" (use of a pharmacological
method that produces a minimally-depressed level of consciousness), some states require special
training and registration with the state.

92
The most common emergency seen after using local anesthetics is SYNCOPE (fainting). Syncope often
occurs when upright, but can also occur while sitting. Syncope never occurs when lying down. The
patient may complain of feeling generalized warmth with nausea and palpitations.
• The initial event in a vasovagal syncope episode is the stress-induced release of increased amounts
of catecholamines that cause peripheral vascular resistance, tachycardia, and sweating.
• As blood pools in the periphery, ~BP and cerebral blood flow occurs, causing the patient to complain
of feeling dizzy or weak. Compensatory mechanisms attempt to maintain adequate BP, but they soon
fatigue, causing vagally-mediated bradycardia. Once BP drops below levels necessary to sustain
consciousness, syncope occurs.
• Placing the patient in the supine position while administering 100% oxygen is often all that is
required. Additional treatment is based on symptoms.
• The primary airway hazard for an unconscious dental patient in a supine position is tongue
obstruction (so head tilt and lift the chin).

After receiving injecting a local anesthetic containing 2% lidocaine with 1:100,000 EPI, the patient loses
consciousness. The most probable cause is SYNCOPE, caused by transient cerebral hypoxia. Proper
Management of Syncope:
1. Place the patient in the supine position with their feet slightly elevated .
2. Establish airway (head tilt/chin lift) and administer 100% oxygen via a face mask (02 is
indicated for treating all types of syncope EXCEPT hyperventilation syndrome).
3. Monitor vital signs and support the patient. Pupils may dilate from lack of oxygen to the brain.
4. Maintain your composure. Apply a cool, wet towel on the patient's forehead.
5. Follow-up treatment. Determine factors causing the unconsciousness.

*Hyperventilation in an anxious dental patient leads to CARPODEDAL SPASM (spasm of hand, thumbs,
foot, or toes).

SOMATOGENIC REACTION - the development of a reaction from an organic pathophysiologic cause.

Shock Symptoms: tiredness, sleepiness, confusion. Skin is cold, sweaty, bluish, and pale. Pulse is
weak & rapid, and BP drops. Reduces cardiac output (CO) is the MAIN factor in all types of
shock. Stages of Shock:
1. compensatory stage-the early stage where compensatory mechanisms (l'HR and peripheral
resistance) maintain perfusion to vital organs.
2. progressive stage-metabolic acidosis occurs and compensatory mechanisms are no
longer adequate.
3. irreversible/refractory stage-organ damage occurs and survival is impossible.

Major Types of Shock:

1. Cardiogenic Shock-most commonly caused by MYOCARDIAL INFARCTION. Shock consists of a
set of hemodynamic changes that diminish blood flow below a level that provides adequate
oxygen for the metabolic needs of organs and tissues. Shock is circulatory collapse resulting
from pump failure of the LEFT VENTRICLE, most often caused by a massive myocardial infarction.
2. Hypovolemic Shock-produced by a reduction in blood volume due to severe hemorrhage,
dehydration, vomiting, diarrhea, or fluid loss from burns.
3. Septic Shock-due to severe infection caused by endotoxin from gram (-) bacteria.
4. Neurogenic Shock-results from severe injury or trauma to the CNS.
5. Anaphylactic Shock-occurs from a severe allergic reaction.

A patient who fractured his jaw in a car accident received an 1M injection of 60mg of Meperidine, then
subsequently developed a severe reaction characterized by tachycardia, hypertension, hyperpyrexia, and
seizures. When questioned, the uninjured father revealed his son takes a drug for a psychiatric condition.
The psychiatric drug most likely responsible for this untoward reaction with Meperidine is PHENELZINE.
Concomitant administration of Meperidine and MAO inhibitors can cause life-threatening hyperpyrexic
reactions that may culminate into seizures or coma.

• Meperidine (Demerol)-a potent narcotic analgesic prescribed to relieve moderate-to-severe pain,

and as a cough suppressant. Demerol is probably the most widely used narcotic in U.S. hospitals.
It compares favorably with morphine (the standard for narcotic analgesics). Meperidine is the most
abused drug by health professionals.
93
 • Morphine-the standard drug to which all analgesic drugs are compared. It causes euphoria,
analgesia, drowsiness, miosis, and respiratory depression.

Complete Blood Count (CBC) & Urinalysis are two tests that should be done before using a genera I
anesthetic for surgical procedures. If a bleeding problem is suspected, PIT (partial thromboplastin time)
is also evaluated. A CBC test includes:
1. Hematocrit: the volume % of RBC in whole blood. Normal male (45-50%), normal female
(40-45%). Hematocrit is the amount of your blood that is occupied by red blood cells (its like
chocolate milk; how much is chocolate vs. milk). Hematocrit is the volume % of RBC in whole
blood. Normal male (45-50%) & normal female (40-45%). *The minimal acceptable value of
hematocrit is 30% for elective surgery.
o
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2. Hemoglobin: normal men (14-18g/dU and normal women (12-16g/dU.
~
.-- 3. Total Leukocytes (WBC): normal (5000-1O,000/mm3); dental infection (15,000-20,000/mm3).
en
c:::
:::a 4. Total Erythrocytes (RBC): normal men (4.5-6.0) x 106/mm3; normal women (4.3-5.5) x 106/mm3.
,..,
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-< Normal Values for Coagulation:
• Template Bleeding Time: 1-9 minutes.
• Prothrombin Time (PTl: 11-16 seconds (compared to normal control).
• Partial Thromboplastin Time (PIT): activated, 32-46 seconds (compared to normal control).
• Platelets: 140,000-440,000/ml.

Urine Values: pH 6 (4.7-8.0); specific gravity (1.005-1.025).

EXODONTIA
General Concerns of Surgery: patient's nutritional status, body fluids and electrolytes, pre-operative and
post-operative information, wound healing (primary and secondary), and most important-infection.
*The difference between acceptable and an excellent surgical outcome depends on how the surgeon
handles the tissue.

Discipline of oral surgery is "the diagnosis and surgical treatment of injuries, disease, and malformation
of the mouth and jaws".

Major Oral Surgical Procedures:

• Treatment of maxillary and mandibular fractures.
• Pre-prosthetic surgery (tuberosity reductions and vestibuloplasty).
• Reconstructive surgery (orthognathic surgery and facial deformities).
• Traumatology (treatment of wounds, injuries, and resulting disabilities).
• Exodontia (including routine, multiple, & surgical extractions) is NOT a major oral
surgery procedure.

Minor Oral Surgical Procedures:

• Exodontia (routine extractions, multiple extractions, surgical extractions)
• Treatment of dental infections (periapical, periodontal, pericornitis, facial infections (cellulitis).
• Treatment of hard tissue (alveoplasty) and soft tissue (biopsy, benign lesions) pathologies.

Local Contra indications to Tooth Extractions:

• ANUG, irradiated jaws, and malignant disease.
• Acute infection with uncontrolled cellulitis.
• Acute infectious stomatitis.

94
Systemic Contraindications to Tooth Extractions:
• Uncontrolled diabetes mellitus
• Uncontrolled cardiac disease and dysrythmias.
• Uncontrolled leukemias and lymphomas.
• Debilitating diseases.
• Severe bleeding disorders.
• Patients taking certain medications (i.e. immunosuppressives, corticosteroids, & cancer
chemotherapeutic agents).

An acute dentoalveolar abscess should NOT be a contraindication to extraction because infections

can resolve very quickly when the affected tooth is removed. However, it may be difficult to extract the
tooth either because the patient cannot open sufficiently wide enough , or because adequate local
anesthesia cannot be obtained.

Conditions that require Antibiotic Prophylaxis prior to oral surgery:

1. Prosthetic hea rt va Ive
2. Rheumatic valve disease
3. Most congenital heart malformations

Patients with cardiac pacemakers do not require antibiotic prophylaxis since the endocardium is not
involved.

If antibiotic prophylaxis is necessary, these medications & dosages are recommended by the American
Heart Association:

Situation Medication Dosage

Standard prophylaxis Amoxicillin Adults: 2g

Children: SOmg/kg orally Ihr prior

Unable to take oral Ampicillin Adults: 2g 1M or IV

medications Children: SOmg/kg 1M or IV 30min prior

Penicillin Allergy Clindamycin Adults: 600mg

Children: 20mg/kg orally Ihr prior

Cephalexin or Cefadroxil Adults: 2g

Children: SOmg/kg orally 1 hr prior

Azithromycin or Adults: SOOmg

Clarithromycin Children: lSmg/kg orally Ihr prior

Penicillin Allergy & Clindamycin Adults: 600mg

cannot take oral Children: 20mg/kg IV 30m in prior
medications
Cefazolin Adults: 19
Children: 2Smg/kg 1M or IV 30min prior

The most frequently IMPACTED teeth are MANDIBULAR 3rd MOLARS (followed by maxillary 3rd molars
and maxillary canines). One system describes the angulation of the long axis of the impacted 3rd molar
wlr/t the 2nd molar's long axis:
• Mesioangular = 43% of all impacted teeth.
• Vertical = 38% of all impacted teeth.
• Oistoangular = 6% of all impacted teeth.
• Horizontal = 3% of all impacted teeth .

Additionally, teeth can be angled buccally or lingually (*most mandibular 3rd molars are angled
toward the LINGUAL) .
95
 Impacted teeth are also classified based on their relationship to bone and tissue:
• Soft tissue impaction = tooth is impacted only by soft tissue.
• Partial bony impaction = crown is partially covered by bone.
• Full bony impaction = tooth is completely covered by bone.

The ideal time to remove impacted 3rd molars is when the root is approximately 2/3 formed . The
patient is around 17-21 years old. At this time, bone is more flexible and the roots are not formed well
enough to have developed curves and rarely fracture during extraction.
• When the root is fully formed, the possibility increases for abnormal root morphology and fracture of
root tips during extraction.
• If root development is insufficient (1/3 or less), the tooth is more difficult to remove because it
tends to roll in its crypt (like a ball in a socket), preventing easy elevation .
• Young patients tolerate surgery very well, with minimal post-operative complications. Older
patients have the most post-operative difficulties, as the bone is more dense and the patient usually
responds more slowly to the entire process (anesthesia and surgery).
• Complications most often seen after extraction of an isolated residual maxillary erupted molar
are fracture of the tuberosity or sinus floor. *Warning: beware of the lone molar.

During extraction of a maxillary 3rd molar, if you realize the tuberosity has also been extracted, the proper
treatment is to smooth sharp edges of the remaining bone and suture the remaining soft tissue. A
fracture of the maxillary tuberosity most commonly results from extraction of an erupted maxillary 3rd
molar (or 2nd molar if it is the last tooth in the arch). If the tuberosity is fractured but intact, it should
be manually repositioned and stabilized with sutures.

CAVERNOUS SINUS THROMBOSIS (CST) - usually caused by a late complication of an infection

(Staphylococcus Aureus) of the central face or paranasal sinuses. CST is an unusual occurrence that is
rarely the result of an infected tooth. It is usually afulminant process with high rates of morbidity and mortality.

• CST incidence has decreased greatly with the advent of effective antibiotics. Most cases are due to
an acute infection in an otherwise healthy individual. However, most patients with chronic sinusitis
or diabetes mellitus may be at a slightly higher risk.

• Infections of the face can cause a septic thrombosis of the cavernous sinus. Furunculosis and
infected hair follicles in the nose are frequent causes. Extractions of maxillary anterior teeth in the
presence of an acute infection and especially curettage of the socket under such circumstances can
cause CST. The infected thrombus ascends in the veins against the usual venous flow. It usually
occurs in the OPHTHALMIC VEIN because of the absence of valves in the angular, facial, &
ophthalmic veins.

• CST is not usually caused by a bacteremia, trauma, or ear infections.

LUDWIG'S ANGINA - most commonly encountered neck space infection that involves sublingual,
submandibular, &submental spaces.

SUBMANDIBULAR SPACE - a potential space of the neck bound by the oral mucosa and tongue
anteriorly and medially, superficial layer of deep cervical fascia laterally, and hyoid bone inferiorly. It
comprises two spaces (sublingual & submaxillary spaces), divided by the mylohyoid muscle.

• Submandibular space usually drains infections from mandibular premolars &molars since their
apices lie BELOW the mylohyoid muscle attachment.

• While extracting a mandibular 3rd molar, if you notice the distal root tip is missing, it is most likely
to be found in the SUBMANDIBULAR SPACE. To prevent this, avoid all apical pressures when removing
roots or root tips of all mandibular molars. If a mandibular molar root tip is displaced inferiorly, it
may be in the mandibular canal, or through the lingual cortical plate.

96
SUBLINGUAL SPACE - superior part of the submandibular space that contains the sublingual gland NOTES
&loose C.T. surrounding the tongue.

SUBMENTAL SPACE - medial part of the submaxillary space that contains submental lymph nodes
that drain the median parts of the lower lip, tip of tongue, and mouth floor. It usually drains infections
from mandibular incisors and canines because their apices lie ABOVE the mylohyoid muscle attachment.

MOST COMMON SITE for a supernumerary tooth is the MAXillARY INCISOR AREA. When it occurs here,
it is called a MESIODENS (these teeth are usually small, peg-shaped, and do not resemble the teeth
normal to the site). Treatment of mesiodens is by surgical removal.

The main reason to use water irrigation when cutting bone is because heat generated by the drill
affects bone vitality (you do not want to burn the bone). Irrigating the surgical wound during and after
the procedure is critical. Copious amounts of coolant spray are crucial in minimizing osseous necrosis
caused by heat generated from the bur. Irrigation also cleans the crypt and areas beneath the flap of bony
debris, tooth fragments, and blood.

Class" lever classification is used during tooth extractions. Teeth are extracted by luxation forces
perpendicular to the long axis of the tooth (not by pulling along the long axis). The fulcrum is as close
to the tooth apex as possible. *Rotational forces can be used on single rooted teeth.
• The extraction forcep beak is designed so most of the pressure exerted during extraction is transmitted
to the tooth root.

• Luxation-the loosening of the tooth in the socket by progressive severing of the POL fibers using
patience and controlled force, NOT brute strength . The force is applied as far down on the root as
possible. You should also support the jaw with your other hand , with a thumb and finger on either
side of the tooth being extracted.

#15 Scalpal is UNIVERSALLY used for oral surgical procedures. 3 incisions are used in oral surgery:
• Linear incision-a straight line incision used for Apicoectomies.
• Releasing incision-used to add a vertical leg to a horizontal creation incision for extractions,
augmentations. The correct position for ending a vertical releasing incision is at the TOOTH LINE
ANGLE (not over the tooth's buccal surface). If the incision ends over a buccal surface, the edges are
difficult to approximate, which can cause periodontal problems.
• Semi-lunar incision-a curved incision used mostly for Apicoectomies.

FLAP - a section of soft tissue that is outlined by a surgical incision, carries its own blood supply, allows
surgical access to underlying tissues, can be replaced in the original position, and maintained with
sutures and is expected to heal.
• Flap design should ensure adequate blood supply (flap base is always larger than the flap apex).
• Flap reflection should adequately expose the operative field .
• Flap design should permit atraumatic closure of the wound.

Sutures:
• Interrupted Suture Pattern/Method-offers strength and flexibility because each suture is
independent to one another. This is advantageous because if one suture is lost or loosens, the integrity
of the remaining sutures is not compromised. The major disadvantage of this pattern of suturing is
the extra time required for placement.
• Continuous Suture Pattern/Method-provides ease and speed of placement, distributes tension over
the entire suture line, and a more watertight closure than the interrupted pattern or method.
• Sutures should never be over tightened or closed under tension, should be 2-3mm apart, placed from
mobile tissue into fixed tissue, and from thin into thick tissue.
• Suture size is based on strength and diameter. This system uses "0" as the baseline average size
suture. As suture diameter decreases, "Os" are added or numbers followed by a "0" (i.e. 000 and 3-0
are the same size). As suture diameter increases above "0", numbers are assigned to the suture material.
• Because suture material is foreign to the body, the smallest diameter suture sufficient to keep the
wound closed properly should be used. Most OMS procedures require 3-0 or 4-0 sutures. 9-0 suture
size has the least strength and smallest diameter.

97
 The most severe tissue reaction occurs with PLAIN CATGUT SUTURE material. Resorbable sutures evoke
an intense inflammatory reaction (thus, plain and chromic gut are not used to suture the surface of a skin
wound).

Properties of "Resorbable" Suture Materials

Name TIssue Reactivity Knot Security Handling
Plain Catgut Severe Poor Fair
Chronic Catgut Moderate Good Good
Polyglactin 910 Minimal Fair Good
Polyglycolic Acid Minimal Fair Good

*Plain Gut - from sheep intestine, susceptible to rapid digestion by proteolytic enzymes.
Retains strength for 5-7 days.
*Chromic Gut-"chromitized" to produce more resistance to proteolytic enzymes.
Retains strength for 9-14 days.
*Polyglycolic Acid-does not enzymatically break down, undergoes slow hydrolysis,
less stiff than gut sutures (easier to tie), and more expensive.

Properties of "Non-Resorbable" Sutures

Name TIssue Reactivity Knot Security Handling
Silk Severe Good Excellent
Braided Polyester Moderate (if coating sheds) Poor Good
Stainless Steel Wire None Excellent Poor
Polypropylene Minimal Good Fair
Polyethylene Minimal Poor Fair

*Silk-is braided (multifilamentous), black, and inexpensive. Used for intraoral suturing.
*Nylon-is strong, not used orally, but is the suture material of choice for facial lacerations.
*Polypropylene-has the least tendency to induce inflammation.
*Non-resorbable sutures should be removed within 5-7 days.

Impacted maxillary 3rd molars are occasionally displaced into the maxillary sinus (antrum), from which
they are removed via a Caldwell-Luc approach. If a large root fragment or the entire tooth is displaced
into the maxillary sinus (antrum), it should be removed using a Caldwell-Luc approach (a surgical
procedure where an opening is made into the maxillary sinus via an incision into the canine fossa
above the level of the premolar roots. The tooth or root is then removed. *An oral surgeon to whom the
patient should be referred should perform this procedure.

• Strong apical pressure with a small straight elevator may displace root tips of maxillary premolars
& molars into the MAXILLARY SINUS. If the root tip is small (2-3mm), non-infected, and cannot be
removed through the small opening in the socket apex, no additional surgical procedure is performed
through the socket, and the root tip is left in the sinus. If the root tip is left in the sinus, measures
should be taken similar to those taken when leaving any root tip in place. The patient must be
informed of the decision and given proper follow-up instructions.
• Maxillary 3rd molars can also be displaced into the infratemporal space during elevation of the tooth,
the elevator may force the tooth posteriorly through the periosteum into the infratemporal fossa. If
access and light are good, the tooth may be retrieved with a hemostat. If the tooth is not retrieved after
a short amount of time, the area should be closed, and the patient informed that the tooth was displaced
and will be removed by an oral surgeon who will use a special technique to remove it.

98
DlSTOANGULAR IMPACTION - the maxillary 3rd molar impaction most likely displaced into the
antrum (maxillary sinus) and infratemporal space if correct extraction techniques are not used.
Mandibular 3rd molars with a distoangular impaction are the most difficult impaction to remove.

MESIOANGULAR IMPACTION - the most common and LEAST difficult impaction to remove,
comprising 43% of all impacted teeth.

• For impacted mandibular 3rd molars, mesioangular impactions are the least difficult to remove,
followed by horizontal and vertical impactions, then the most difficult to remove which is the
distoangular impaction.

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• For impacted maxillary 3rd molars, mesioangular impactions are the most difficult to remove, ;::0
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while vertical and distoangular impactions are the easiest to remove. r-
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Once sufficient amounts of bone are removed from around the impacted tooth, the tooth is usually
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sectioned to allow portions of the tooth to be removed separately with elevators through the opening
provided by bone removal. Bone is rarely, if ever, removed on the lingual aspect of the mandible because
of the likelihood of damaging the lingual nerve.
• Reasons to Section Teeth: allows for minimal bone removal, minimal force to remove the tooth, and
shortens the entire surgical procedure. Tooth sectioning is performed with a bur or chisel, but the
bur is used by most surgeons.

Dead space in a wound usually fills with BLOOD which creates a hematoma with a high infection
potential. Dead space in a wound is any area that remains DEVOID OF TISSUE after closing the wound.
Dead space is created by removing tissues in the depths of a wound or by not reapproximating tissue
planes during closure.

Dead space is eliminated by closing the wound in layers to minimize the postoperative void, applying
pressure dressings, using drains to remove any bleeding that accumulates, and placing packing into
the void until bleeding stops.

While attempting to remove a grossly decayed mandibular molar, the crown fractures. The recommended
next step to facilitate removal of the tooth is to separate the roots with a chisel, elevator, or most easily
with a bur. Teeth with two or more roots often need to be sectioned into single entities prior to successful
removal. A popular sectioning method is to make a bur cut between the roots, then inserting an elevator
in the slot and turning it 90° to cause a break.
• Roots can be removed by using a closed technique. The surgeon should begin a surgical removal if
the closed technique is not immediately successful.
• Teeth are resistant to crush, but are not resistant to shear. Thus, place the forcep beaks opposite
to each other at the same level on the tooth. Forcep beaks are applied in a line parallel with the
long axis of the tooth.
• When luxating a tooth with forceps, the movements should be firm and deliberate, primarily to the
facial with secondary movements to the lingual.
• Maxillary 1st premolar is the least likely to be removed by rotational forces due to its root structure
(molars are obviously NOT removed using rotation).

PALATAL is the primary direction of luxation for extracting maxillary primary/deciduous molars, while
the BUCCAL is the primary direction for adult maxillary molars. This is because primary molars are more
palatally positioned, and the palatal root is strong and less prone to fracture.
• In general , removing primary teeth is not difficult. It is facilitated by the elasticity of young bone and
resorption of root structure. Do NOT use a "cowhorn" forcep to extract mandibular primary molars
because the sharp beaks of these forceps can damage unerupted permanent premolar teeth.
• If the preoperative radiograph shows that the permanent premolar is tightly wedged between the
bell-shaped roots of the primary tooth, the best treatment is to section primary molar crown and
remove the two portions separately. This helps to not disturb the permanent tooth.
• After extracting mandibular teeth on a child after a mandibular block was given, always advise
the child not to bite his/her lip while he/she is numb. Also inform the parents to watch the child to
prevent this.

99
 When extracting maxillary teeth, the patient's maxilla is AT THE SAME HEIGHT as the dentist's
shoulders. Stand in front of and to the side of the patient for maximum visibility and leverage.

For mandibular extractions, the patient is positioned so the occlusal plane of the mandibular arch is
PARALLEl to the FLOOR when the mouth is opened, and the chair should be as low as possible. Stand
directly to the side or behind the patient.

Fingers on the left hand (for a right-handed dentist) serve to:

• Retract soft tissue, provide the operator with sensory stimuli to detect expansion of the alveolar plate
and root movement under the plate.
• Help guide the forceps into place on the tooth , protect teeth in the opposite jaw from accidental
C> contact with the back of the forceps, and support the mandible while performing mandibular
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GENIAL TUBERCLES - located on the lingual surface of the mandible midway between the superior
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& inferior borders. There are 4 (two are situated on each side and adjacent to the symphysis). While they
are usually relatively small, they may be fairly large and extend outward from the surface as spinous
processes. Geninal tubercles are the area of muscle attachment for the SUPRAHYOID MUSCLES.

In preparing the edentulous mandible for dentures, each may be safely excised by the OMS (labial and
lingual frenums, mylohyoid ridge, and exostosis). Genial tubercles are never excised, because it they
were removed, the tongue would be flaccid .
• When removing the mylohyoid ridge, be careful to protect the lingual nerve.
• When removing a mandibular exostosis (mandibular torus), an envelope flap design (has no vertical
components) should be used.

MAXILLARY TORUS (TORUS PALATINUS) - most frequently located on the MIDLINE of the hard
palate. They usually appear before age 30, and affect females more often than males. Maxillary tori
present few problems when the maxillary dentition is present and only occasionally interferes with speech
or become ulcerated from frequent trauma to the palate.

• Indications for Removel: a large, lobulated torus with a thin mucoperiosteal cover extending
posteriorly to the vibrating line of the palate that prevents seating of a denture and formation of a
posterior seal at the fovea palatine. Chronic irritation, interference with speech, rapid growth, and
patients with a cancer-phobia are also indications.

• Removal Technique: it should not be excised en masse to prevent entry into the nose (the palatine
bone will come out with the torus) . Subdivide the tori into segments with a bur and remove the
segments with an osteotome. Any protuberances are smoothed out with a bone file . The flap is then
loosely sutured and place a palatal splint to prevent hematoma formation and to support the flap .

Normal Post-Extraction Procedure:

1. All loose bone spicules and portions of the tooth, restoration, or calculus are removed from the
socket and from the buccal and lingual gutters and tongue.
2. Socket must be compressed by the fingers to reestablish the normal width present before the
buccal plate was surgically expanded. *The natural recontouring of the residual ridge occurs
primarily by resorption of the labial-buccal cortical bone.
3. Sutures are usually not placed unless the papillae have been excised. When there is severe
bleeding from the gingiva, or if the gingival cuff is torn or lose, only then would you place a
suture over a single extraction socket.
4. Socket is covered with a gauze sponge folded and moistened slightly at its center with cold water.
5. Patient is instructed to bite down on the pressure dressing for 30-60 minutes.
6. Printed instruction sheet is given to the patient. *The most common cause of post-extraction
bleeding is failure of the patient to follow post-extraction instructions.
7. Prescription for pain is given if the need is anticipated.

If bleeding persists for some time after an extraction, instruct the patient to bite on a tea bag. Tannic
acid in the tea bag helps promote hemostasis.

100
DRY SOCKET (POST-EXTRACTION ALVEOLlTlS OR LOCALIZED ALVEOLAR OSTEITIS) - most
common complication after surgical removal of a mandibular molar resulting from a pathologic process
combining the loss of a healing blood clot with a localized inflammation. Most common after extracting
MANDIBULAR MOLARS.

• A patient with DRY SOCKET develops a severe, dull throbbing pain 2-4 days AFTER a tooth
extraction. The pain is often excruciating, may radiate to the ear, and is not relieved by oral
analgesics. There may be an associated foul odor and taste, and the extraction site is filled with
necrotic tissue, which is delayed wound healing.

• Smoking, spitting, or drinking through a straw creates negative pressure in the oral cavity, thus
encouraging this condition. *Careful technique and minimal trauma reduce the chance of dry socket.

• Treatment: gently flush out debris with saline solution and place a sedative dressing in the socket
(eugenol is the active component in most sedative dressings). Gauze provides an attachment for the
obtundent paste so it stays in the socket. Prescribe analgesics if needed.

PERICORONITIS - inflammation of the soft tissues associated with the crown of a PARTIALLY erupted
tooth seen most commonly in relation to the MANDIBULAR 3rd MOLAR. Maxillary 3rd molar is the most
frequent contributing factor to pericoronal infections found around mandibular 3rd molars, so always
examine the maxillary 3rd molar because it may be supererupted or malaligned.

• Signs &Symptoms: pain, bad taste, inflammation, pus expressible from beneath, and the pericoronal
tissues are aggravated by trauma from the opposing tooth. Pericoronitis is a criteria by the NIH
(National Institute of Health) for removing 3rd molars.

• Unless the cause is removed, pericoronitis may present as a recurrent condition requiring multiple
treatments. In severe episodes, an acute pericoronal abscess may develop which may remain localized
or spread to involve one or more of the adjacent deep surgical spaces, and may be associated with
systemic and local signs and symptoms.

• Treatment: irrigate the area (if possible, establish drainage). Place the patient on antibiotics and
instruct the patient to rinse with warm saline mouthwashes. As soon as acute symptoms are relieved,
definitive treatment may be instituted (extraction).

Incision for Drainage (1&0) in an area of acute infection is only performed after LOCALIZATION of the
INFECTION. Physiologically, it is at this time that nature has constructed a barrier around the abscess,
walling it off from the circulation and making it possible to palpate the presence of purlent material
within the abscess cavity ("fluctuance").

• After you incise and drain the fluctuant mass, it may be prudent to culture for antibiotic sensitivity.
This should always be done if after I&D, the swelling does not subside despite large doses of antibiotics.
• Prior to actual abscess formation, however, the infection can produce a cellulitis in the soft
tissues of the involved region. The palpable tissues take on a condition called induration (appearing
hard, dense, and brawny). Treatment during this period involves localizing the infection. Early
administration of antibiotics may be extremely important in a severe and life-threatening infection.
Localization of the infection may be aided by using warm compresses and warm mouth rinses at
frequent intervals.

5 Phases of Healing of an Extraction Site:

1. Hemorrhage and blood clot formation.
2. Clot organization by granulation tissue. *Glucocorticoids have the greatest effect
on granulation tissue by retarding healing.
3. Replacement of granulation tissue by C.T. and epithelialization of the site.
4. Replacement of C.T. by fibrillar bone.
5. Recontouring of the alveolar bone and bone maturation.

The same stages that occur in normal wound healing of soft tissue injuries (inflammation, fibroplasias,
& remodeling) also occur in repair of injured bone. However, osteoblasts and osteoclasts are also
involved to repair damaged bone tissue.
101
 N Stages of Wound Healing:
1. Inflammatory stage-consists of a vascular and cellular phase where neutrophils
and lymphocytes predominate. The macrophage is the most important inflammatory cell for
wound healing.
2. Proliferative Stage (Fibroblastic Stage)-this stage is mediated by fibroblasts which
form collagen and new blood vessels.
3. Maturation Stage (Remodeling Stage)-foreign material, necrotic tissue, ischemia, and tension.

3% H202 is the agent of choice to debride intraoral wounds.

Bone &Soft Tissue HEAL by Primary or Secondary intention:

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• Primary Intention (Primary Closure or First Intention): bone repair that involves both endosteal
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:too &periosteal proliferation. Primary intention occurs when bone is either incompletely fractured, or
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with minimal callus formation. Primary intention occurs when wound margins are nicely apposed .
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-< Healing is more rapid with a lower risk of infection, with less scar formation, and less tissue loss than
wounds that heal by secondary intention. Examples of primary intention (well-repaired and well-
reduced bone fractures).

• Secondary Intention (Secondary Closure or Second Intention): occurs when a wound is large and
exudative. This side fills in with granulation tissue. Healing is slower and produces more scar tissue.
Bone repair that involves mostly endosteal proliferation. If fractured bones remain more than 1mm
apart, this type of repair occurs. lots of fibrous tissue is formed and a callus is formed (which
eventually ossifies). Examples (extraction sockets, poorly reduced fractures, and large ulcers).

Factors that DElAY the healing process of an extraction site: patient with protein deficiency or on
glucocorticoid therapy, older patients, and local infections.

GRAFTS
IDEAL GRAFT is replaced by the host bone, withstands mechanical forces, produces no immunological
response or rejection, and actively assists osteogenic (bone-form ing) processes of the host. The greatest
osteogenic potential occurs with an autogenous cancellous graft and hemopoietic marrow.
• Bones, plates, biphasic pins, titanium mesh, and intraosseous wires are used to fixate bone grafts.
Sutures are not generally used.
• Costochondrial Rib Graft-may be used with the cartilaginous portion simulating the TMJ and condyle.
When used for ridge augmentation, extensive shrinkage is noted.

ALLOGENEIC GRAFTS (ALLOGRAFTS OR HOMOGRAFTS) - composed of tissue taken from a

donor of the SAME SPECIES who is not genetically related to the recipient (usually cadaver bone).

• The most commonly used allogenic bone is FREEZE-DRIED. These grafts consist of freeze-dried
bone and freeze-dried decalcified bone from another source (human cadaver bone).

• Allogenic grafts are treated to reduce the anti-genicity. However, these treatments destroy any
remaining osteogenic cells it the graft. These grafts offer a hard tissue matrix only (this graft is
eventually replaced by the host's bone) .

• Host MUST produce ALL of the essential elements in the graft bed for an allogeniec bone graft to
become resorbed and replaced .

• Allogeneic Advantages: does not require another site of preparation in the host, and a similar bone
or bone of similar shape to the bone being replaced can be obtained.

102
AUTOGENOUS GRAFTS (AUTOGRAFTS) - composed of tissues taken from the SAME INDIVIDUAl. N
Most often used in oral surgery. Autogenous grafts, while often present surgical &technical problems,
do not usually involve rejection or immunological complications.

• OPTIMAL bone grafting material should be of autogenous origin. Autogenous bone is from the same
person (from one part of the body to another). Autogenous grafts are usually used to restore large
areas of lost mandibular bones after oncological surgery or trauma. Of all facial bones resected
in oncological surgery, the mandible is the most frequently removed.

• Bone marrow for grafting defects in the mandible & maxilla is usually obtained from the ILIAC
CREST. Also used for ridge augmentation.

ISOGENIC GRAFTS (lSOGRAFTS OR SYNGENESIOPLASTIC GRAFTS) - composed of tissues

taken from an individual of the SAME SPECIES who is GENETICAllY RELATED to the recipient.

XENOGENIC IMPLANTS (XENOGRAFTS OR HETEROGRAFTS) - composed of tissue taken from

a donor of ANOTHER SPECIES (i.e. animal bone grafted to man). Rarely used in oral surgery.

Rejection of a graft is MOST common when Allografts or Xenografts of bone and cartilage are used in
ora I su rgery.

Alloplastic Grafts - inert, man-made synthetic materials. Alloplastic materials used for augmentation
genioplasty tend to MIGRATE from the position they were placed at the time of surgery. Two additional
problems often experienced when using alloplastic materials for genioplasty are:
1. Erosion of the chin prominence contiguous with the implant.
2. Unpleasant sensation in the implant region when exposed to cold temperatures.

Modern artificial joint replacement procedures use metal alloplastic grafts. For bone replacement, a man-
made material that mimics natural bone is used. Most often, this is a form of calcium phosphate (i.e.
tricalcium phosphate, calcium carbonate, or hydroxyapatite) that is used for augmentation of the mandible.
• Hydroxyapatite-a dense, biocompatible material produced synthetically or obtained from biologic
sources like coral. The granular or particle form is most commonly used for alveolar ridge augmentation.
When placed in a subperiosteal environment, HA bonds phYSically and chemically to bone.

Advantages of Restructuring an Atrophic Ridge with HA granules:

• It is a simple surgical technique suitable as an office procedure.
• No donor site is required to obtain autogenous bone graft material.
• HA is totally biocompatible and non-resorbable.

Disadvantages of Restructuring an Atrophic Ridge with HA granules:

• Migration of the hydroxyapatite granules.
• Poor ridge form (inadequate height).
• Abnormal color under the mucosa.
• Mental nerve neuropathy (excessive augmentation).

Instruments that Remove Bone:

• Rongeur Forceps are the most commonly used instrument to remove bone. A chisel & mallet, and
bone file can also be used . However, the technique most oral surgeons use to remove bone is the bur
&handpiece.
• Most high-speed turbine drills used in routine restorative dentistry are TOTAllY UNACCEPTABLE
for oral surgery. Air exhausted from these drills goes into the wound and may be forced deeper into
tissue planes and produces tissue emphysema, a potentially dangerous situation. An acute infected
tissue emphysema is usually caused by indiscreet use of:
1. Air-pressure syringes: in drying out a root canal with a compressed air syringe, septic
material can be forced through the apical foramen into the cancellous portion of the alveolar
process, and ultimately out through the nutrient foramina into adjacent soft tissues, resulting
in formation of a septic cellulitis &tissue emphysema.

103
 NOTES 2. Atomizing spray bottles activated by compressed air: a similar condition can be induced by
using a compressed-air spray bottle for irrigating wounds (especially in the retromolar region).
It is safer to use a hand-activated syringe when irrigating wounds or drying root canals since
to reduce the chance of producing a tissue emphysema.

FRENUM - a membranous fold of skin or mucous membrane that supports or restricts movement
of a part or organ like the small band of tissue that connects the underside of the tongue to the floor of
the mouth. When a frenum is mal positioned and interferes with the normal alignment of teeth, or results
in pulling away gingiva from the tooth surface causing recession, it is often removed via a FRENECTOMY.
3 Surgical Techniques are used for a Frenectomy:
1. Simple excision and Z-plasty: are effective when the mucosal and fibrous tissue band is
relatively narrow. These techniques relax the pull of the frenum.
2. V-Y plasty (localized vestibuloplasty}-often preferred when the frenal attachment has a wide
base. This technique is good for lengthening tissue and usually results in less scarring.

Local anesthetic infiltration is usually sufficient fro surgical treatment of frenal attachments. Care is
taken to avoid excessive infiltration directly in the frenum area because it may obscure view of the
anatomy during the excision.

GINGIVOPLASTY - a surgical procedure to reshape the gingiva to create a normal, functional form.

OPERCULECTOMY - removal of the operculum (flap of tissue over an unerupted or partially

erupted tooth).

GENIOPLASTY - a procedure that surgically alters the chin's position. The most common techniques
for genioplasty are osteotomy or augmentation using natural or alloplastic materials. The best way to
enlarge the prominence of the chin for best long-term results is to reposition the lower border anteriorly
by OSTEOTOMY (horizontal sliding osteotomy).

ALVEOLOPLASTY - a surgical procedure used to recontour the supporting bone structures in

preparation of a complete or partial denture. It is the surgical preparation of the alveolar ridges (i.e.
removing undercuts) to receive dentures or shaping and smoothing the socket margins after extractions
with subsequent suturing to ensure optimal healing.
• Objectives of bone recontouring should provide the best possible tissue contour for prosthesis support,
while maintaining as much bone and soft tissue as possible.

Closed reduction-closing the space between a fractured bone without cutting through soft tissue or
surrounding bone.

Systemic Contraindications to Elective Surgery:

• Blood dyscrasias (i.e. hemophilia, leukemia)
• Uncontrolled diabetes mellitus (controlled diabetes is NOT a contraindication to elective surgery) .
• Addison's Disease or any steroid deficiency
• Fever of unexplained origin
• Nephritis
• Any debilitating disease
• Cardiac disease (i.e. coronary artery disease, uncontrolled hypertension, and cardiac decompensation)
can complicate exodontia. Usually a post-infarction patient is not subjected to oral surgery within
6 months of his infarction. However, emergency procedures can be performed, if the patient's
physician has been consulted.

Patients with these systemic conditions can be treated, but you need to consult with their physician
before treatment. In most cases, these patients are best treated in the hospital by an oral surgeon.

104
AUTOGENOUS TOOTH TRANSPLANTATION - a tooth from the same individual is move to another NOTES
socket in the mouth. The MOST common indication for tooth transplantation is SEVER DECAY of a 1st
MOLAR (the st molar is atraumatically removed, and the 3rd molar is placed into the socket) .

• Transplant success is most predictable when the root apices to be transplanted are 1/3-112
formed with open apices and the bordering bony plates are intact. Adequate M-D width of the
host implant site, absence of acute periapical or periodontal inflammatory states, and the general
good oral health are also required for successful tooth transplantation .

• The most likely cause of transplantation failure is a chronic, progressive EXTERNAL ROOT
RESORPTION .

• Universal sequelae of an allogeneic tooth transplant is ANKYLOSIS & PROGRESSIVE ROOT

RESORPTION. Allogeneic tooth transplant is when a tooth from one patient is placed into the socket
of another patient.

• The change in continuity of the occlusal plane observed after ankylosis of a tooth is caused by the
continued eruption of the other non-akylosed teeth and growth of the alveolar process.

IMPLANTS
Any toothless area can be considered for dental implants. Factors that determine whether implants
are an option and the type of implants to use include: patient's requirements and expectations, amount
of additional work needed (i.e. bone grafting), dentist's skill level, and long-term prognosis.

Implant Indications:
• A pronounced gag reflex may be an indication for implant placement because the patient may not
be able to tolerate the placement of a removable prosthesis.
• Alveolar ridge resorption of r other anatomic considerations that do not allow adequate retention of
a conventional removable prostheses.
• Patient is physiologically unable to tolerate a removable prosthesis.
• Medical condition where a removable prostheses may create a risk (i.e. seizure disorder).
• Loss of posterior teeth, particularly unilaterally.

Contra indications to Implant Placement:

• Inadequate bone space.
• Existing bone that does not meet implant criteria.
• Diabetes, pituitary and adrenal insufficiency, and hypothyroidism which may cause considerable
healing problems.
• Inability to fight infections.
• Diseases like tuberculosis and sarcoidosis.
• History of uncontrolled bleeding.

Implants placed in the MAXILLARY ANTERIOR region have the HIGHEST FAILURE RATE. Implant mobility
is the most common sign of implant failure.

Bone-Implant Interface:
• Fibro-osseous integration: C.T. encapsulated implant within bone. Success rate is 50% over a 10-
year period. Not seen often with newer materials.
• Osseointegration: a direct structural and functional connection between living bone and surfaces of
a load-carrying implant without soft-tissue. Yields the most predictable long-term stability. Several
important factors are involved (materials, surface characteristics, bone, timing). Oseointegrated
implants are anchored directly into living bone. This determination is made by radiographic and
light microscopic analysis.
• Biointegration: implant interface achieved with bioactive materials like hydroxyapatite (HA) or
bioglass that bonds directly to bone. HA coated implants develop bone faster than non-coated
implants, but after 1 year there is little difference between coated and non-coated implants.

105
 2 Ways Implants can be Placed:
1. submerged-requires a second surgical procedure (two-stage) to uncover the fixture.
2. non-submerged-does not require a second surgical procedure (one-stage).

3 Main Groups of Implants:

1. Endosseous Implants-the most frequently used implants today that are surgically inserted
into the jawbone. They are further subdivided into root-form implants and blade-form implants.
• root-form implants: are cylindrical in shape, can be threaded or non-threaded (pressfit)
depending on the exterior surface. They come in various widths (3.2mm-7mm) and lengths
(lOmm-18mm), and are typically made of titanium. Treatment with root-form implants is
divided into 3 phases (surgical, healing, & prosthetic). *root-form endosseous implants
o
::c
are the most popular.
:I>
r- • blade-form implants (plate-form implants): are flatter in appearance, and are used where
en
c:
::c there is insufficient bone width, but adequate bone depth. Available in single and two-stage
=
,....., forms. Typically made of titanium .
::c
-< • 80% of all current implants are ENDOSSEOUS (into bone).
2. Subperiosteal Implants-frameworks specifically fabricated to fit on top of supporting areas in
the mandible or maxilla under the mucoperiosteum. They are placed below the periosteum,
but above the bone.
3. Transosseous Implants-similar to endosseous implants because they are surgically inserted
into the jawbone. However, these actually penetrate the entire jaw so they emerge opposite to
the entry site, usually at the bottom of the chin. *Their primary indication is in the very atrophic
mandible where root form implants may further compromise the strength of the jaw.

Other types of implants: Transosteal: through the bone. Intramuscosal: within mucosa .

For an implant to be successful, you need adequate transfer of force and biocompatibility.
Success also requires:
• Histologically: 35-90% bone contact, C.T. adhesion above the bone, and an intact, non-inflamed JE.
• Clinically: no significant or progressive bone loss, no persistent infection, no discomfort during
chewing, no increased mobility when the prosthesis is removed, and the implant must be
prosthetically useful.

LESION BIOPSY
Types of Biopsies:
1. Incisional Biopsy-removes only part of the lesion. Most often used for oral lesions. A (-)
incisional biopsy report of a highly suspicious oral lesion suggest another biopsy specimen
is necessary in view of the clinical impressions. The key is a highly suspicious oral lesion.
2. Excisional Biopsy-removes the entire lesion. Most often used for oral lesions.
3. Needle Biopsy-aspiration biopsy.
4. Exfoliative Cytology-pap smear.

Method of tissue removal varies depending on the type of biopsy:

1. In a needle (percutaneous) biopsy, the tissue sample is simply obtained by using a syringe. A
needle is passed into the tissue to be biopsied, and the cells are removed through the needle.
2. In an open biopsy, an incision is made in skin, the organ is exposed, and a tissue sample
is taken.
3. Aclosed biopsy involves a much smaller incision than an open biopsy. The small incision is
made to allow insertion of a visualization device that can guide the physician to the appropriate
area to take the sample.

10% Formalin-the fixative of choice used for a routine biopsy specimen. After removal, the tissue is
immediately placed in 10% formalin solution (4% formaldehyde) that is at least 20x the volume of the
surgical specimen. The tissue must be totally immersed in the solution, and care is taken to ensure the
tissue has not become lodged on the container wall above the level of the formalin.

106
Biopsy Indications:
• A lesion that persists for more than two weeks with no apparent etiologic basis.
NOTES
• Persistent hyperkeratotic changes in surface tissues.
• Bone lesions not specifically identified by clinical and radiographic findings.
• A lesion with malignant characteristics.
• An inflammatory lesion that does not respond to local treatment after 14 days (i.e. removing
a local irritant).
• Apersistent swelling (visible or palpable) below relatively normal tissue.

Biopsy Techniques &Surgical Principles:

• Anesthesia: block local anesthetic techniques are used when possible. If not, infiltration may be
used, but the solution should be injected at least 1cm away from the lesion.
• Tissue stabilization: use fingers or clamps.
• Hemostasis: gauze compresses (avoid high speed suction).
• Incision: sharp scalpel
• Extent of Tissue: obtain some normal tissue adjacent to the lesion is possible.
• Handling of Tissue: use a traction suture through the specimen, not tissue forceps to avoid
specimen trauma.
• Specimen Care: after removal, the tissue should be immediately placed in 10% formalin solution that
is at least 20x the volume of the surgical specimen. *No other solution is acceptable.

Mandibular left 2nd molar of a 14-year old boy is unerupted. Radiographs show a small dentigerous cyst
surrounding the crown . The treatment of choice is to uncover the crown and keep it exposed.
• Dentigerous Cysts (Primordial or Follicular Cysts)-cysts associated with the crowns of unerupted
teeth, probably the result of degenerative changes in the reduced enamel epithelium .
• Eruption Cysts-cysts that form when a tooth is erupting and interfere with normal eruption of teeth,
and are more commonly found in the child or young adult, and may be associated with any tooth. If
treatment is indicated, a simple incision or "deroofing" is all that is needed.

Whether a bone cyst or other cysts are completely enucleated or treated by marsupialization depends on
the SIZE &LOCATION to vital structures.
1. Enucleation-process by which the TOTAL REMOVAL of a cystic lesion is achieved. Enucleation
is the treatment of choice whenever possible for congenital cysts, mucoceles, and most
odontogenic cysts.
2. Marsupialization, Decompression, &Partsch Operation all create a "surgical window" in the
wall of the cyst. The cyst is uncovered or "deroofed" and the cystic lining is made continuous
with the oral cavity or surrounding structures. The cyst sac is opened and emptied.

Marsupialization is the treatment of choice for ranulas (for a recurrent ranula, treatment also involves
excision of the sublingual gland). Also the treatment of choice when a cyst is large and close to vital
structures.

Wait 14 days before obtaining a biopsy of an oral ulcer, since almost all oral ulcers caused by trauma
heal within 14 days. Thus, any ulcer present for 2 weeks or more should be biopsied. A biopsy is also
indicated in these situations:
• Pigmented lesions (black/brown).
• When tissue is associated with paresthesia. This is often an ominous sign.
• If a lesion suddenly enlarges.

Always aspirate a central bone lesion to rule out a vascular lesion. If a lesion seems compressible,
pulsatible, blue, or a bruit is heard using a stethoscope, beware of a vascular lesion and biopsy only
under a controlled hospital setting.

107
 N DISORDERS &CONDITIONS
DYSPNEA - the unpleasant sensation of difficulty breathing.

APNEA - transient cessation or absence of breathing.

HYPERCAPNEA - excess C02 in arterial blood .

HYPOCAPNEA - below normal C02 in arterial blood.

HYPERAPNEA - abnormally deep and rapid breathing.

RESPIRATORY ARREST - permanent cessation of breathing (unless corrected).

HYPERVENTILATION - increased pulmonary ventilation in excess of metabolic requirements.

Hyperventilation results in loss of C02 from the blood (hypocapnea), thus causing a decrease in BP and
sometimes fainting.

HYPOVENTILATION - underventilation in relation to metabolic requirements. Hypoventilation results

in an increased level of C02 in the blood (hypercapnea) .

DEHYDRATION -loss of water and important blood salts like potassium (K+) & sodium (Na+). Vital
organs (i.e. kidneys, brain, and heart cannot function without a certain minimum of water and salt). Causes
include decreased intake (lack of water) and/or increased output (vomiting, diarrhea, blood loss, drainage
from burns, diabetes mellitus, diuretic use, or a lack of ADH (anti-diuretic hormone) owing to diabetes
insipidus (kidneys are unresponsive to AOH, or AOH is not being produced by the posterior pituitary).

• Initially, a patient suffering from dehydration will clinically demonstrate only dryness of the skin and
mucous membranes. However, a dehydration progresses, the turgor (fullness) of the skin is lost. If
dehydration persists, oliguria (..vurine output) occurs to compensate for the fluid loss. More severe
degrees of fluid loss are accompanied by a shift of water from the intracellular space to the
extracellular space (a process that causes severe cell dysfunction, especially in the brain). Systemic
BP falls with continuous dehydration, and declining perfusion eventually leads to death .

• Fluids in several forms should be continually urged on the patient. In severely dehydrated individuals,
they must get to the hospital immediately. IV fluids quickly reverse dehydration, and is often life-
saving in young children and infants.

• Symptoms of Dehydration: ..vBP, weight loss, l'HR, CO, body temperature, and sunken eyeballs.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) - a group of disorders characterized

by airflow obstructin during respiration . COPO is a chronic airway obstruction resulting from
emphysema, chronic bronchitis, asthma, or any combination of these diseases. In most cases, bronchitis
and emphysema occur together. *Secondary pulmonary hypertension is most often caused by COPD.
1. Bronchial Asthma-disorder marked by DYSPNEA & WHEEZING expiration caused by episodic
narrowing of the airways.
2. Emphysema-often coexists with chronic bronchitis. Labored breathing and increased
susceptibility to infection.
3. Bronchiectasis-copious purulent sputum, hemoptysis, and recurrent pulmonary infection.
4. Chronic Bronchitis-a condition of excessive bronchial mucus and a productive cough that
produces sputum (hypersecretion of mucus) for 3 months or more in at least 2 consecutive
years without any other disease that could account for this symptom. A productive cough,
often without wheezing, is the universal factor of chronic bronchitis.

108
 • Chronic bronchitis is a very common, debilitating respiratory disease, characterized by
increased production of mucous by the glands of the trachea & bronchi. It has a strong
association with CIGARRETIE SMOKING.
• Common results of Chronic Bronchitis: cor pulmonale (enlargement of the heart's right
ventricle), airway narrowing and obstruction, &squamous metaplasia of the bronchial tree.
Patient's with chronic bronchitis may be predisposed to lung cancer (bronchogenic carcinoma).
• Patients with chronic bronchitis (or any COPD) can have difficulty during oral surgery. Many of
these patients depend on maintaining an upright posture to breathe adequately. They often
experience difficulty breathing if placed in an almost supine position or if placed on high-
flow nasal oxygen.

ATELECTASIS - the collapse of part or all of a lung by blockage of the air passages (bronchus or c:::>
:::c
bronchioles), or by very shallow breathing. Atelectasis is the MOST COMMON anesthetic complication >
r-
en
occurring within the first 24hrs after surgery under general anesthesia. Symptoms include: diminished c:
:::c
breath sounds, fever, increasing dyspnea. Prolonged atelectasis can lead to PNEUMONIA. ..,
."

PNEUMOTHORAX - the presence of air in the pleural cavity. It can occur as a post-operative
complication of aspiration of liquid vomitus into the trachea and bronchi. Onset of pneumothorax is
accompanied by a sudden, sharp chest pain, followed by difficult, rapid breathing, cessation of normal
chest movements on the affected side, tachycardia, weak pulse, hypotension, diaphoresis, and elevated
temperature, pallor, dizziness, and anxiety.

• Pneumonitis (inflammation of the lung) &Atelectasis are the two most common causes of fever
in a patient who has had general anesthesia.

• Nausea is the most common pos-operative complication of outpatient general anesthesia .

ASTHMA - a syndrome consisting of dyspnea, cough, and wheezing caused by bronchospasm, which
results from a hyperirritability of the tracheobronchial tree. Two types of asthma exist (allergic asthma)
the most common , and idiosyncratic asthma.

• Avoid using aspirin, NSAlDs, barbiturates, narcotics, and erythromycin (if the patient is taking
Theophylline).

• Nitrous oxide is SAFE to administer in asthmatics, and is especially indicated for patients whose
asthma is triggered by anxiety. If the patient is taking steroids, consult their physician for the possible
need for corticosteroid augmentation.

• Inhalation of a selective beta2-agonist (Terbutaline, Albuterol) is the preferred treatment for an

acute asthmatic attack.

• Status Asthmaticus-the most severe clinical form of asthma, usually requiring hospitalization that
does not respond adequately to ordinary therapeutic measures. If not managed properly, chronic
partial airway obstruction may lead to death from respiratory acidosis (produced by hypoxemia &
hypercapnea) .

Management of an Acute Asthmatic Episode during oral surgery:

• Terminate all dental treatment and position the patient in an erect or semi-erect position.
• Patient should administer their own bronchodilator using an inhaler. In most severe asthma attacks
or when the patient's bronchodilator is ineffective, EPI (O.3ml of a 1:1,000 dilution) can be injected
1M or SC.
• Administer oxygen and monitor vital signs.

109
 HEMOPHILIA - a hereditary BLEEDING DISORDER that mostly affects MALES, where it takes a long time
for blood to clot and abnormal bleeding occurs. Atrue hemophiliac has prolonged partial thromboplastin
time (pm, but normal prothrombin time (PT) and bleeding time (BY).

• Hemophilia A&Bare inherited as a SEX-LINKED RECESSIVE trait where males are affected and
females are carriers. Most people afflicted with hemophilia have type A, and it presents under age
25yrs. Signs, symptoms, and clinical manifestations are excessive bleeding from minor cuts, epitaxis,
hematomas, and hemarthroses.

• Hemophilia A: represents most people with hemoph ilia. The classic type caused by a deficiency of
coagulation Factor VIII (anti-hemophilic factor).
CI
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• Hemophilia B (Christmas Disease): caused by a deficiency of Factor IX (plasma thromboplastin
c::
:::c com ponent) .
,...,
."

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• Hemophilia C(Rosenthal's Syndrome): is not sex-linked, and there is less severe bleeding due to
a deficiency of Factor XI (plasma thromboplastin antecedent).

VON WlllEBRAND'S DISEASE - inherited as an AUTOSOMAL DOMINANT BLEEDING DISORDER that

occurs equally in males and females. Due to a deficiency in the von-Willebrand factor (a large
glycoprotein with binding sites for Factor VIII, and facilitates platelet adhesion to collagen (important
for platelet plug formation).

THROMBOCYTOPENIA - the most common cause of hemorrhagic disorders (bleeding disorders).

It is a blood disease characterized by abnormally low number of platelets in the bloodstream. Normal
platelet count is between 150K-450K cells per microliter of blood. When platelet numbers falls below
150K cells per microliter of blood, the person is "throm bocytopenic" .
• Thrombocytopenia is common in people with Idiopathic thrombocytopenic purpura (lTP) where an
autoimmune disease causes very low platelet counts. Abnormal reductions in the number of
platelets are caused when abnormalities occur in any of 3 processes:
1. --vplatelet production by bone marrow.
2. 1'trapping of platelets by the spleen .
3. faster than normal destruction of platelets.

Thrombocytopenia Clinical Features:

• Spontaneous appearance of purpuric or hemorrhagic lesions of the skin which may vary in size from
tiny, red pinpoint petechiae, to purplish ecchymoses and even massive hematomas. Patients also
exhibit a tendency to bruise.
• Nosebleeds, GI bleeding, and urinary tract bleeding.
• Severe and often profuse gingival hemorrhage and petechiae on the oral mucosa.

2 concerns when doing surgery on Thrombocytopenia patients: post-operative hemorrhage caused

by a decrease in blood platelets, and patients with the chronic form may be on steroids and have adrenal
insufficiency. They may be unable to handle the stress of extractions.

Drugs that can potentiate Bleeding after extraction : aspirin, anti-coagulants, broad-spectrum
antibiotics, alcohol, and anticancer drugs. Antianxiety drugs do NOT potentiate bleeding after extraction .
• If a patient is taking any of these 5 drugs, be prepared to take special measures to control the
bleeding. Patients with specific systemic diseases also have prolonged bleeding time (i .e. non-
alcoholic liver disease, hepatitis, cirrhosis, and hypertension).
• Excessive bleeding causes formation of hematomas which increase the chance of infection.

• 5 Ways to Obtain Wound Hemostasis:

1. Assisting natural hemostatic mechanisms: usually by placing a cotton sponge with pressure
on the bleeding vessels or using a hemostat directly on the vessel.
2. Heat on the cut vessels (thermal coagulation).
3. Suture ligation of the vessel.
4. Placing a pressure dressing over the wound (most bleeding from oral surgery can be
controlled this way) .
5. Vasoconstrictive substances like EPI in local anesthetics.
110
Tests to Measure Clotting Mechanisms: the most important consideration to rule out hemorrhagic
disorders is history.
N
1. Normal Prothrombin Time (PT): < 11 sec (+ 2 sec). PT is the best test to determine if oral
surgery can be safely performed on a patient taking COUMADIN (or any oral anti-coagulant).
To be a good candidate for surgery, PT time should be within 5-7 seconds of the control sample.
2. Partial Thromboplastin Time (PIT): detects coagulation defects of the intrinsic system. The
basic test for hemophilia . Normal value is 25-36 seconds.
3. Bleeding Time (Ivy Method): normal value is < 9 minutes.
4. Platelet Counts: normal value 150,000-450,000 per mm3 of blood. Minimal platelet count for
oral surgery is 50,000.

Tests routinely performed in the pre-operative workup for a patient being admitted to the hospital o
::a
for surgery: :D-
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en
1. Complete blood count (CBC) that includes an evaluation of the hemoglobin and c:::
::a
hematocrit indices. ,..,
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2. Total WBC count with a differential count. -<
3. Assessment of circulating platelets
4. Urinalysis (a gross and microscopic urinalysis).
5. Patients scheduled for general anesthesia should have a chest x-ray (patients> 40yrs should
also have an E.K.G.)

Factors to Consider when deciding to hospitalize a patient for an Elective Procedure:

• Medical problems comprom ising treatment (diabetes, hemophilia).
• Difficulty and extent of surgery.
• Consideration of the individual patient (emotionally disturbed, handicapped, etc.).
• Hospitalization costs (time and money) .

Management of a Therapeutically Anticoagulated Patient:

• Surgery is deferred until the platelet-inhibiting drugs have been stopped for 5 days.
• Always consult with the patient's physician to determine the safety of stopping the anti-coagulant
for several days. Medical consultation is always indicated before surgery if the patient is taking anti-
coagulant or anti-platelet therapy.
• Take measures during surgery to help promote clot formation and retention .
• Restart the drug therapy the DAY AFTER surgery if no bleeding is present.

Anti-Coagulants (Blood Thinners): Dicumarol, Heparin, Antithrombin III, Enoxaparin, &Warfarin.

• Aspirin & NSAIDs inhibit platelet aggregation. Thus, if given to a patient already taking an
anticoagulant, the effects can be life-threatening.
• A patient on anticoagulant therapy (Warfarin, Heparin, Aspirin, or an NSAID) will most likely have a
prolonged prothrombin time (PT) and bleeding time (BT). For elective extractions, th is patient
should stop taking the anticoagulant for 5 days prior to extractions. Always consult with the patient's
physician before recommending this.
• When oral surgery is performed on patients taking anti-coagulants, these steps may help prevent
hemorrhage:
• Hemostatic agent is placed within the socket.
• Soft diet, intra-oral pressure packs, and avoid mouth rinses
• Multiple sutures are placed in the surgical area
• ice packs are applied extraorally.

ECCHYMOSIS - area of hemorrhage into the skin &subcutaneous tissue> 1cm in diameter often
caused by injury, but clotting and bleeding disorders can predispose an ecchymosis formation. Grossly,
an ecchymosis presents as a bluish lesion in its earliest stages of onset. As RBCs in the lesion undergo
progressive degeneration, & hemoglobin is converted through bilirubin hemosiderin, the lesion
progressively changes color from blue green purple brownish discoloration .

POST-OPERATIVE ECCHYMOSIS - a result of trauma to underlying blood vessels when blood

escapes from the vascular tree and accumulates in the tissues. It is common after extractions in
elderly patients due to the fragility of the vessel walls. All patients should be warned it can occur after
extractions. Sometimes the patient will complain of a diffuse, non-painful, yellowish discoloration of the
skin. Moist heat often speeds the resolution of postoperative ecchymosis.
111
 OSTEORADIONECROSIS (URN) - the most SERIOUS potential complication after extractions from
areas previously irradiated. ORN is a condition of non-vital bone in a site of radiation injury, that can
be spontaneous, but most often results from tissue injury. The absence of reserve reparative capacity is
a result of the prior radiation injury.

OSTEOMYELITIS - a bone infection characterized by progressive inflammatory destruction after

formation of new bone. It is most often caused by STAPHYLOCOCCUS AU REUS (but can be caused by
Streptococcus pyogenes, Pneumococcus species, Pseudomonas aeruginosa, and Escherichia coli).
Reduced blood supply predisposes bone to osteomyelitis.

• Osteomyelitis may be chronic or acute. It commonly results from a combination of local trauma
(usually trivial, but causing a hematoma) and an acute infection originating elsewhere in the body.
In children, long bones are usually affected, while in adults, the vertebrae and pelvis are most
commonly affected.

• Pus is produced in bone, which may cause a bone abscess which deprives the bone of its blood
supply.

• Chronic Osteomyelitis-results when bone tissue dies due to the lost blood supply.

• Acute Osteomyelitis-occurs more frequently in the MANDIBLE than the maxilla because the blood
supply in the maxilla is much richer and comes from many different arteries, while the mandible
draws its main blood supply from the inferior alveolar artery. Also, the dense overlying cortical bone
of the mandible prevents penetration of periosteal blood vessels, thus the mandibular cancellous bone
is more likely to become ischemic and thus infected.

First step when initiating CPR is establish unresponsiveness by shaking the patient and shouting "are
you OK", then use the "ABCs":
1. Airway: open the airway with the head tilt-chin lift. This is the easiest technique in most
medical emergencies.
2. Breathing: look, listen, and feel.
3. Circulation: check the carotid pulse.

Cardiopulmonary Resuscitation (CPR):

• A = Airway:
• Place the victim flat on his/her back on a hard tissue.
• Shake victim at the shoulders and shout "are you ok?"
• If no response, call EMS (911) then, do a head-tilt/chin lift (open the victim's airway by tilting
their head back with one hand while lifting up their chin with your other hand).
• B = Breathing:
• Position your cheek close to the victim's nose and mouth, look toward the victim's chest and
look, listen, and feel for breathing (5-10 seconds).
• If patient is not breathing, pinch the victim's nose closed and give 2 full breaths into the
victim's mouth .
• If breaths will not go in, reposition the patient's head and try again to give breaths. If it is
still blocked, perform abdominal thrusts (Heimlich Maneuver).
• C= Circulation:
• Check for a carotid pulse by feeling for 5-10 seconds on the side of the victim's neck. If
there is a pulse, but the victim is not breathing, give rescue breathing at a rate of 1 breath
every 5 seconds, or 12 breaths per minute. If there is no pulse, begin chest compressions
as follows:
• Place heal of one hand on the lower part of the victim's sternum. With your other hand
directly on top of the first hand, depress the sternum 1.5-2.0 inches.
• Perform 15 compressions for every 2 breaths (rate: 80-100 per minute). Check for pulse
return every minute and continue uninterrupted until advanced life support (ALS) is available.

If CPR efforts are effective, the pupils will constrict. If too much pressure is incorrectly applied directly
over the xyphoid process, the liver may be injured. The result of interruptions in chest compressions
while performing CPR is a reduction of blood flow and drop in BP to zero.

112
Only discontinue CPR under these conditions:
• Another trained person takes over the CPR for you .
• EMS personnel arrive and take over care of the victim .
• You are exhausted and cannot continue or the scene becomes unsafe.

Adults Children Infants

Rescue Breathing Rate 1 breath every 1 breath every 1 breath every
(victim has a pulse 5 seconds 4 seconds 3 seconds
but is not breathing) (12 breaths per minute) (15 breaths per minute) (20 per minute) 0
::c
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c:
No pulse Follow the ribs into the Follow the ribs into the One finger width below ::c
(locate compression notch with one finger notch with one finger the nipple line ,..,
",

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landmark) on the sternum on the stern um

Compressions 2 hands stacked (heal Heal of 1 hand 2 or 3 fingers on the

performed with of one on the sternum) on sternum sternum

Rate of com pression 80-100 80-100 At least 100

per minute

Com pression depth 1.5-2.0 inch 1-1.5 inch .5-1.0 inch

Ratio of compressions:
breaths
1 rescuer 15:2 15:2 5:1
2 rescuers 15:2 15:2 5:1

Most COMMON ERROR in recording BP is applying the blood pressure cuff TOO LOOSELY. This gives
falsely elevated readings. Using the wrong cuff size can result in erroneous readings.
• A normal adult BP cuff placed on an obese patient's arm produces falsely elevated readings . This
same cuff applied to a very thin arm of a child will produce falsely low readings.
• The compression cuff's width should be -20% greater than the extremity diameter on which the BP
is being recorded . If you need to take additional readings, wait at least 15 seconds before re-inflating
the BP cuff.

CONGESTIVE HEART FAILURE (CHF) - heart failure resulting from progressive diseases that
weakens the heart directly or cause an increased demand on the heart. CHF occurs most commonly in
association with atherosclerotic coronary heart disease, valvular deformities, and hypertensive
cardiopathy. *Usually the left ventricle fails first, follow soon after by right-sided failure.
• Common CHF Signs:
• Exertional dyspnea
• Paroxysmal nocturnal dyspnea (patient wakes up gasping for air). Earliest &most common sign.
• Peripheral edema (swollen ankles).
• Cyanosis, Orthopnea (sitting or standing to breathe comfortably), and high venous pressure.

• Treatment &Dental Management: prolonged rest, administer oxygen.

• Digitalis causes patient to be prone to nausea and vomiting.
• Patients taking diuretics/vasodilators are prone to orthostatic hypotension, also
avoid excessive EPI.
• Dicumarol patients may have bleeding problems.
• Nitroglycerin is given sublingually only to manage patients having chest discomfort or possible
MI. It is not used for asthma attacks.

113
 Calcium levels are regulated by PARATHYROID HORMONE (increased hormone causes bone resorption)
which then increase calcium levels. Calcium is also regulated to some extent by the kidney tubules and
GI mucosa (lowering pH causes increased calcium absorption). Low serum calcium levels result in
hyperirritability of nerves and muscles.

Serum calcium (Ca2+) is increased in these conditions:

• Hyperparathyroidism
• Chronic Glomerulonephritis
• Hypervitam inosis D
• Malignant diseases of the skeleton (i.e. multiple myeloma)

c
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*Serum calcium is decreased in Diabetes Mellitus.
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c::
::c Phosphorus concentration is also regulated by PARATHYROID HORMONE. Increased hormone causes the
..,
co
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kidneys to increase the rate of phosphate excretion, wh ich causes a decrease in plasma phosphate
-< concentration.

In good health, the ratio of calcium to phosphorus in the blood is 10:4. If a glandular imbalance exists
(especially with the parathyroid glands), then this ratio is maintained at a different level, causing long-
term health deterioration. A high ratio of phosphorus to calcium sensitizes the body and increases
inflammatory tendencies.

BLOOD GLUCOSE concentration is regulated by INSULIN (-.j.;blood glucose) and GLUCAGON (l'blood
glucose). Glucose normally does not appear in urine, although it is freely filtered because it is reabsorbed
in the proximal convoluted tubule of the kidney.
• Serum glucose is increased in Diabetes Mellitus, adrenal tumors, l'growth hormone, and
liver dysfunction.

Normal serum concentration of glucose is 70-120mgldl.

Normal Laboratory Values Blood Chemistry

Arterial Blood Gases:
Osmolality = 280-300 mOsm/L
HC03 = 21-28 mEq/L
pC02 = 35-45 mmHg Phosphatase: Acid = 0.2-1.8
pH = 7.35-7.44 international units
p02 = 83-108 mmHg Alkaline = 21 -91 international units

Calcium = 9-11mg/dl Phosphorus = 3-4.5 mg/dl, 1-1.5 mEq/L

C02 = 21-30m Eq/L Potassium = 3.5-5.0 mEq/L
Chloride = 98-106 mEq/L Protein = 5.5-8.0 g/dl
Cholesterol: Total= 180-240 mg/dl Sodium = 132-142 mEq/L
Esters = 100-180 md/dl
Creatinine = 1-2 mg/dl Urea nitrogen = 10-20 mg/dl
Glucose = 70-120 mg/dl Urine: pH = 6.0 (4.7 -8.0)
Specific gravity = 1.005-1.025

Adrenal cortex secretes 20mg of hydrocortisone daily. During stress, the cortex can increase its
hydrocortisone output to 200mg da ily.

Patients taking steroids or people with disease of the adrenals have a decreased ability to produce more
glucocorticoids (hydrocortisone) during stress (i.e. extractions) . This is because glucocorticoid secretion
is stimulated by ACTH which is produced in the anterior pituitary in response to stress by increasing
ACTH output, thus glucocorticoid production increases. A relative lack of glucocorticoids also increases
ACTH output. An overabundance of circulating systemic steroids inhibits ACTH production. Patients on
large steroid doses repress ACTH production, causing atrophy of the adrenal cortex.
114
 A S2-year old women requests extraction of a painful mandibular 2nd molar. She tells you she has not N
rested for two days and nights because of the pain . Her medical history is unremarkable, except that she
takes 20mg of Prednisone daily for Erythema Multiforme. To treat this patient, you would give steroid
supplementation and remove the tooth with local anesthesia and sedation.
• The fear here is that the patient may not have sufficient adrenal cortex secretion (adrenal
insufficiency) to withstand the stress of an extraction without taking additional steroids (this hold
true for any patient treated for any disease with steroid therapy).

• Erythema Multiforme-hypersensitivity syndrome characterized by polymorphous eruption and mucous

membranes. Macules, papules, nodules, vesicles, or bullae and target ("bulls-eye-shaped") lesions
are seen. A severe form of this condition is "Stevens-Johnson Syndrome" . These patients may be
receiving moderate doses of systemic corticosteroids, thus may be unable to withstand the stress of an
extraction. Consultation with their physician is absolutely necessary before treating these patients.

CUSHING'S SYNDROME (HYPERCORTISOllSM) - a relatively rare hormonal disorder caused by

prolonged exposure of the body's tissues to high levels of CORTISOL HORMONE. Most commonly affects
adult's ages 20-S0yrs. 10-IS out of every 1 million people are affected each year. Most common cause
of Cushing's Syndrome is pituitary adenomas.
• Cushing's Syndrome Symptoms:
• Upper body obesity, rounded face, increased fat around the neck, thinning arms and legs.
• Children tend to be obese with slowed growth rates.
• Skin becomes thin and fragile, and bruises easily and heals poorly.
• Purplish pink stretch marks may appear on the abdomen, thighs, buttocks, arms, and breasts.
• Bones are weakened, and routine activities like bending, lifting, or rising a chair may cause
backaches, rib and spinal column fractures.
• Most people have severe fatigue, weak muscles, high BP and high blood glucose levels.
I
~. • Irritability, anxiety, and depression are common.
• Women usually have excess hair growth on their face, neck, chest, abdomen, and thighs.
Their menstrual periods may become irregular or stop.
• Men have decreased fertility with diminished or absent desire for sex.
• ACushing Syndrome patient's cardiovascular status MUST be evaluated and treated
if necessary prior to surgery.

A person who has been on SUPPRESSIVE DOSES OF STEROIDS will take up to 1 year to regain full
adrenal cortical function. Guidelines to help determine if a patient's adrenal function is suppressed (if
any doubt exists, consult with the patient's physician):
• People on small doses (Smg of Prednisone/day) will have suppression if they have been on the regimen
for a month.
• People taking an equivalence of 100mg Cortisol per day (20-30mg of Prednisone/day) will have
abnormal cortical function in a week.
• Short-term therapy (1-3 days) of even high dose steroids does NOT alter adrenal cortical function.
• Aperson on suppressive steroid doses will take as much as 1year to regain full adrenal cortical function.
• Stress or fatigue can cause an adrenal crisis in a patient with suppressed adrenal function .

An abnormality in one or more of the pH control mechanisms can cause two types of major disturbances
in the body's acid-base balance. Depending on the condition cause, acidosis or alkalosis can be
respiratory or metabolic:
1. Metabolic Alkalosis-a condition where the blood is alkaline because it has too much base or
too little acid (high level of bicarbonate), occasionally causing an increase in blood pH. The
major effect on the body is over-excitability of the nervous system, which may cause tetany
(tonic spasm) .
• Major Causes: diuretics (thiazides, furosemide, ethacrynic acid) ingestion of alkaline drugs,
vomiting gastric acid contents, or overactive adrenal gland as in Cushing's Syndrome or
use of corticosterioids).
• Respiratory Alkalosis-a condition in which the blood is alkaline because rapid or deep
breathing results in a low blood C02 level. Major Causes: hyperventilation from anxiety, pain,
liver cirrhosis, low levels of oxygen in the blood (high altitudes), &aspirin overdose. *Much
LESS COMMON than respiratory acidosis.
• Treatment: ingestion of AMMONIUM CHLORIDE.

115
 N 2. Metabolic Acidosis-a condition in which the blood has too much acid or too little base, often
causing a decrease in blood pH (more acidic blood). When blood pH falls below normal (7.3), the
CNS becomes so depressed the person first experiences disorientation, then is comatosed . *The
normal blood bicarbonate-carbonic acid ratio is 20:1. A 10:1 ratio indicates uncompensated
acidosis. Severe acidosis always occurs during CPR. Metabolic acidosis is excessive blood
acidity characterized by an inappropriate level of bicarbonate in the blood. Major Causes:
chronic renal failure, diabetic ketoacidosis, lactic acidosis, poisons, and diarrhea.
• Respiratory Acidosis-excessive blood acidity caused by a buildup of C02 in the blood due to
poor lung function or slow breathing (decreased respiratory rate). Major Causes:
hypoventilation, emphysema, chronic bronchitis, severe pneumonia, pulmonary edema ,
and asthma.
• Treatment: ingestion of SODIUM BICARBONATE.

DIABETES - the most common pancreatic endocrine disorder and metabolic disease involving mostly
carbohydrates (glucose) &lipids owing primarily to a relative or complete lack of insulin secretion by
beta cells of the pancreas. Diabetes is caused by an absolute deficiency of insulin (Type I) or resistance
of insulin's action in the peripheral tissues (Type II). Classic triad of symptoms is polydipsia, polyuria,
&polyphagia.

Type 1 vs. Type 2 Diabetes Mellitus

Characteristic
Level of insulin secretion
Typical age of onset
% of Diabetics
Basic Defect
Associated with obesity
Speed of development of
symptoms
Development of Ketosis
Treatment
Type 10M Type 2 OM
None or little insulin is produced May be normal or exceed normal
Diagnosed in Childhood Adulthood
10-20% (less common) 80-90%
Destruction of B cells Reduced sensitivity of insulin's
target cells
No Usually
Rap id Slow
Com mon if untreated Rare
daily insulin injections and dietary Dietary control and weight
management to sustain life reduction; occasionally oral
hypoglycemic drugs

Symptoms of Diabetes Mellitus: glycosuria, polyuria, polydipsia, hyperglycemia , weakness, weight loss,
ketoacidosis, and vascular abnormalities.
• People with well-controlled diabetes are no more susceptible to infections than patients
without diabetes. However, they have more difficulty containing infections due to altered
leukocyte function.
• Patients who take insulin daily and check their urine regularly for sugar &ketones (controlled
diabetics), can usually be treated in the normal manner without additional drugs or diet
alterations. If any doubt exists as to the patient's medical status, consult with their physician and
do not assume anything!
• Treatment of choice for hypoglycemia in an UNCONSCIOUS diabetic is IV injection of 50% dextrose
in water.
• Treatment of choice for hypoglycemia in a CONSCIOUS diabetic is administration of an oral
carbohydrate (orange juice, cola beverages, candy bars)

116
NUMBER ONE cause of KIDNEY DISEASE, responsible for 40% of all kidney failures is DIABETES. High BP
is the 2nd cause (25%). Another form of kidney disease is Glomerulonephritis (a general term for many
types of kidney inflammations) . Genetic diseases, autoimmune diseases, birth defects, and other problems
can also cause kidney disease.

END-STAGE RENAL DISEASE (ESRD) - a condition in which there is a permanent and almost
complete loss of kidney function. The kidney functions at < 10% of its normal capacity. In ESRD, toxins
slowly build up in the body. Normal kidneys remove these toxins (i.e. urea and creatinine) from the body
through urine.
• Patients with ESRD are often on steroid therapy, are more susceptible to post-operative
infections, and have an increased tendency to bleed.
• When oral surgery procedures are performed on these patients, meticulous attention to good surgical c
::c
technique is necessary to reduce the risks of excessive bleeding and infection. >
r-
en
c:

When treating patients with Renal Insufficiency and patients on Hemodialysis:

....
::c
,...,
::c
-<
• Avoid using drugs metabolized or excreted by the kidneys.
• Do not use NSAIDs, as they are nephrotoxic.
• Perform oral surgery the day after dia lysis.
• Consult the patient's physician for possible prophylactic antibiotics.

RHEUMATIC FEVER (RHO) - an acute inflammatory disease with systemic manifestations and
particular involvement of the heart valves, which follows an upper respiratory infection with a Group A
beta-hemolytic streptococcus. Although rheumatic fever may follow a streptococcal infection, it is NOT
an infection, but an inflammatory reaction to an infection.

• Rheumatic fever is most common in children ages 5-15yrs. The onset is sudden and often occurs
1-5 sym ptom free weeks after recovery from a sore throat or from scarlet fever. Mild cases may last
3-4 weeks, while severe cases may last 2-3 months. Treatment: Penicillin &Rest.

• Clinical diagnosis or rheumatic fever is made when two major (or one major and one minor) criteria
(the "Jones Criteria") are met. Major Jones criteria: carditis, arthritis, chorea, erythema marginatum,
& subcutaneous nodules. Minor criteria include: fever, arthralgias, history of rheumatic fever, EKG
changes, and lab tests.

• Heart inflammation (carditis) disappears gradually usually within 5 months. However, it may permanently
damage the heart valves, resulting in rheumatic heart disease. The mitral valve (valve between left
atrium & ventricle) is most commonly damaged and may become leaky (mitral valve regurgitation),
abnormally narrow (mitral valve stenosis), or both. The pulmonary valve is RARELY involved.

• A history of rheumatic fever should lead the dentist to an in-depth dialogue history seeking the
presence of rheumatic heart disease. If RHD is present, antibiotic coverage is indicated to minimize
the risk of subacute bacterial endocarditis (SBE).

117
 General Considerations when Checking Vital Signs:
• The patient should not have had alcohol, tobacco, caffeine, or performed vigorous exercise within
30min of the exam.
• Ideally the patient should be sitting with their feet on the floor and their back supported . The
examination room should be quiet and the patient comfortable.
• History of hypertension, slow or rapid pulse, and current medications should always be obtained .
• Abnormalities of vital signs are often clues to diseases, and an alteration of vitals can be used to
evaluate a patient's prognosis. In complicated cases do not hesitate to contact a patient's physician
or previous dentist for a consultation.

Routine Vital Signs:

Q
:::c
1. BP (normal 120/80)
>
r- 2. Pulse Rate (normal 72)
en
c:
:::c 3. Temperature can be measured several ways:
,..,
'"
:::c
• Oral with a glass, paper, or electronic thermometer (normal 98.6°F or 37°C).
-<
• Axillary (under arm) with a glass, or electronic thermometer (normal 97.6°F or 36.3°C).
LEAST accurate.
• Rectal or "core" with a glass or electronic thermometer (normal 99.6°F or 37.7°C).
MOST accurate.
• Aural (ear) with an electronic thermometer (normal 99.6°F or 37.7°C).

5 Major Areas Discussed when taking Patient Medical History:

1. Chief complaint
2. History of present illness
3. Specific drug allergies
4. Review of systems (heart, liver, kidney, brain)
5. Nature of systems

118
 cHfiFTER fi

119
 NOTES Central Nervous System (CNS) Neurotransmitters: Catecholamines pass the blood-brain
barrier very poorly.
1. Acetylcholine-a neurotransmitter substance whose CNS effects are generated by the interaction
with a mixture of nicotinic and muscarinic receptors. Secreted by cholinergic fibers. After a
threshold stimulus, the liberation of acetylcholine alters the cell membrane's permeability.
2. Epinephrine-a direct-acting catecholamine &adrenergic agonist. CNS neurons containing EPI
have been identified, but their physiological properties are unknown.
3. Norepinephrine-a direct-acting catecholamine that works through aI, a2, & b adrenergic
receptors in the CNS.
4. Isoproterenol-a direct-acting catecholamine.
5. Dopamine (lntropin)-a catecholamine (immediate precursor of NE) that acts through at
least two subtype receptors, Dl (activtates adenylyl cyclase) and D2 (inhibits adenylyl cyclase).
6. Dobutamine
7. Serotonin (5-hydroxytryptamine)-works through at least 14 subreceptors "tryptominergic"
type neurons.
8. GABA (gamma-aminobutyric acid)-the major INHIBITORY neurotransmitter in the eNS.
9. Opioid peptides: beta-endorphin, enkephalins, &dynorphin.
10. Glutamate &Aspartate-CNS amino acids that elicit POWERFUL EXCITATORY effects on
neurons within every region of the CNS.

CATECHOLAMINES - anyone of a group of sympathomimetic compounds composed of a catechol

molecule and the alipathic portion of an amine. Some catecholamines are produced naturally by the body
(endogenous), and function as key neurological chemicals (i.e. EPI, NE, DA).

Sympathomimetics

Drug Clinical Application Comments

Catecholamines
EPI (direct acting) Anaphylaxis, glaucoma, asthma, and causes Stimulates the myocardium
vasoconstriction to prolong anesthesia .
NE (direct acting) Causes vasoconstriction in hypotension. Stimulates the myocardium
Isoproterenol Asthma
(direct acting)
Dopamine Shock and heart failure Immediate precursor of NE
Dobutamine Shock and heart failure
Non-Catecholamines
Am pheta mine, Treat narcolepsy, obesity, ADHD
Phenmetrazine
Ephedrine Urinary incontinence and causes
vasoconstriction in hypotension
Phenylephrine Causes mydriasis, vasoconstriction,
decongestion
Albuterol, Metaproterenol, Asthma & Premature Labor
Terbutaline
Oxymetazoline & Causes nasal decongestion (long-acting)
Xylometazoline

CNS STIMULANTS - a heterogenous group of compounds that produce various degrees of stimulation.
Historically, CNS stimulants were widely used therapeutically, but today they have limited clinical use.
Their use to treat respiratory depression caused by an overdose of CNS depressants is not safe or
recommended.

120
• Analeptic-a CNS stimulant with the ability to overcome drug-induced respiratory depression and
hypnosis. Analeptics and respiratory stimulants include: Pentylenetetrazol (Metrazol), Nikethamide
(Coramine), Doxapram (Dopram), Picrotoxin, & Strychnine. Analeptics have limited use, but a few
are occasionally indicated to stimulate respiration when a patient has pulmonary disease or to hasten
recovery from a genera I anesthetic.

• Xanthines-stimulants like caffeine, theophylline, and theobromine used to improve mental alertness,
reduce the urge to sleep, and elevate mood. Caffeine is the only approved OTC stimulant.
Theophylline & Theobromine are weaker CNS stimulants than caffeine. Theophylline is the only
xanthine important in asthma treatment, by stimulating medulla respiratory centers to cause
bronchial dilation.

• Sympathomimetic Amines-potent CNS stimulants like amphetamines and related agents (i .e.
Methylphenidate & Phenmetrazine). Sympathomimetic amines are used to treat narcolepsy, obesity,
and ADHD.

CAFFEINISM - a term for people dependent upon caffeine (CNS stimulant) (i.e. suffer side effects
from having too much caffeine, take larger amounts, and need to keep drinking caffeine to function
properly). It is thought to occur if you intake> 600-750mg of caffeine per day (more than 10 cups of
coffee). Drinking> 1OOOmg per day is well into the toxic range. Caffeine stimulates the CNS unequally,
with the CORTEX being the most excited, and the spinal cord being the least excited. Symptoms of
Chronic Caffeine Consumption: feelings of anxiety/nervousness, sleep disruption, irritability, diuresis,
stomach complaints, palpations, and arrhythmias.

Caffeine Content of Commonly Used Agents

Agent Caffeine Content (mg) Agent Caffeine Content (mg)
Beverages OTC Drugs (1 dose)
(1 cup or glass)

Brewed Coffee 100-150mg Anacin 32mg

Instant Coffee 50-100mg Excedrin 65mg
Decaffeinated Coffee 2-35mg Nodoz 100mg
Tea 40-110mg Vivarin 200mg
Cola Drinks 35-60mg

ADRENERGICS (SYMPATHETICS)
Autonomic Nervous System (ANS): an efferent motor system that functions independent of consciousness
(unconscious); controls automatic visceral functions required for life. Drugs block or mimic ANS transmitters
to clinically modify autonomic function (cardiac & smooth muscle, vascular endothelium, exocrine glands
and presynaptic nerve terminals). Other therapeutic drugs can produce autonomic side effects.
1. Sympathetic Nervous System Function: During rest, there is some sympathetic tone, but
parasympathetic tone dominates. SNS adjusts body function in response to stress (trauma,
fear, hypoglycemia, cold, exercise) "fight or flight" response is the activation of the sympathetic
nervous system during emergencies. All sympathetic effector organs and tissues are activated
due to its anatomic wiring and release of EPI from the adrenal medulla: HR, CO, & BP, blood
flows from skin and internal organs into skeletal muscle. Energy stores are mobilized, and
pupils and bronchioles dilate.
• AFEAR REACTION activates the ANS sympathetic division to cause HYPERTENSION. Activating
the sympathetic portion of the ANS causes alpha1 adrenergic receptor activation which causes
arteriolar vasoconstriction with an associated elevation of BP, leading to hypertension.
• Sym pathetic activation of the eye causes MYDRIASIS (dilation).
• Sympathetic activation of the heart causes tachycardia.
• Sympathetic activation of salivary glands causes a thick, ropey-type salivary flow
(decreased salivation). 121
 2. Parasympathetic Nervous System Function: required for life to maintain essential DIGESTION
& EXCRETION body functions.Parasympathetic actions oppose the sympathetic nervous system
and dominate during "rest & digest". Operates in discrete units based on specific body needs
(specific parasympathetic effectors are activated as needed). Does not discharge as a complete
system as it would produce massive, undesirable symptoms (organophosphate poisoning).
• Cranial nerves with parasympathetic activity: III, VII, IX, X.
• Miosis (pupillary constriction), bradycardia, and increased salivation are physiological
effects from activation of the parasympathetic nervous system of the ANS.

4 Types of Drug-Receptor Binding: implicit in the interaction of a drug with its receptor is the CHEMICAL
BONDING of that drug to one or more specific sites on the receptor molecule.
1. Ionic Bonds-result from the electrostatic attraction between ions of opposite charge.
2. Hydrogen Bonds-a special type of interaction between polar (water) molecules.
3. Van der Waals forces-collectively describe the weak interactions that develop when two
atoms are placed in close proximity.
4. Hydrophobic interactions-occur between the drug, its receptor, and the aqueous environment
-c that can playa major role in stabilizing drug-receptor binding.
:c
:D-
::a
:s:
:D- COVALENT BONDS - arise from the sharing of electrons by a pair of atoms, and are required for the
C">
o
r- structural integrity of molecules. Covalent bonds are generally NOT involved in drug-receptor
...,
o
interactions. Ex: Nitrogen Bonding.
-<

Implicit in the interaction of a drug with its physiologic receptor is that the drug does not create effects,
but rather modulates intrinsic physiological cell functions. Drugs can bind to 4 major families of
physiological receptors to produce effects:
1. Receptors as Enzymes (cell surface protein kinases)-kinases exert their regulatory effects by
phosphorylating proteins within the cell which alters the cell's biochemical activities. By binding
to kinases, drugs can also alter biochemical activities resulting in a drug effect.
2. Ion Channels-drugs can bind to ion channels in cell membranes to cause channel opening
or closing. This alters the cell's membrane potential to result in a drug effect.
3. G-protein Coupled Receptors-when drugs bind to G-protein receptors, second messengers
like cyclic AMP are produced to cause an effect within the cell, resulting in a drug effect.
4. Receptors in the Cell Nucleus-receptors for steroid hormones are soluble DNA-transcription
factors within the nucleus that regulate the transcription of specific genes. Modifying
transcription of these genes produces a drug effect.

Alpha (a) Receptors: are mainly EXCITATORY in nature (responsible for most excitatory effects like
vasoconstriction and contraction of the uterus and spleen. Alpha adrenergic receptors are located on vascular
smooth muscle, pre-synaptic nerve terminals, blood platelets, fat cells, and CNS neurons. Exception:
some alpha receptors mediate relaxation of GI smooth muscle. 2 types of alpha (a) receptors:
1. post-junctional a1 adrenergic receptors: found in radial smooth muscle of the iris, arteries,
arterioles, and veins, and in the GI tract. The most common alpha receptor. Causes
CONTRACTION & VASOCONSTRICTION. NE & EPI combine with a1 receptors. Found in arterioles
in skin, mucosa, viscera, and kidney (resistance vessels).
2. pre-junctional a2 adrenergic receptors: inhibits the release of norepinephrine (NE). less
common alpha receptor. NE & EPI combine with a2 receptors. Found on presynaptic nerve
endings to inhibit NE release. Found on post-synaptic endings in the CNS to decrease
sympathetic tone.

Beta (b) Receptors: MAINLY responsible for INHIBITORY effects like vasodilation & relaxation of
respiratory smooth muscle. Exception: some beta receptors mediate excitatory increases in the heart's
force & rate of contraction.

122
2 types of Beta (b) receptors:
1. post-junctional b1 adrenergic receptors: found in HEART myocardium cells (heart mainly
contains b1 receptors), intestinal tract smooth muscle, and adipose (fat) tissue. These are the
less common beta receptors). NE & EPI bind to b1 to 1'HR, CO, BP, and the force of contraction.
2. post-junctional b2 adrenergic receptors: the most common beta receptor found in
BRONCHIOLAR & VASCULAR smooth muscle. These are found in arterioles and arteries in skeletal
muscle to cause vasodilation and in bronchial and uterine smooth muscle to cause relaxation.
Only EPI combines with 2 receptors to vasodilate bronchioles (treats asthma), skeletal muscle,
uterus (relaxation), 1'blood glucose (gluconeogenesis, glycogenelysis). NE usually combines
weakly or not at all to b2 receptors.

PHARMACOLOGIC AGONIST - a drug that binds to physiologic receptors to result in specific cellular
effects producing a predictable pharmacological response. Drugs that bind to physiologic receptors and
mimic the regulatory effects of endogenous signaling compounds produce a pharmacologic effect due to the
binding to the receptor. Adrug that elicits a full response through this process is a pharmacologic agonist.
• Partial Agonist-a drug that acts on the physiologic receptor, but elicits an effect that is only partly
as effective as an agonist drug.

Pharmacological Antagonist-a drug that binds to the physiologic receptor, but does not trigger
an effect. When an antagonist drug is present, the agonist drug cannot reach the receptor site to
produce an effect.
1. Competitive Antagonism-occurs when a response can be achieved by increasing the agonist
dose in the presence of an antagonist.
2. Non-Competitive Antagonism-occurs when a response cannot be achieved with increasing
doses of agonist in the presence of an antagonist.

SYMPATHOMIMETIC AGENTS (ADRENERGIC AGONISTS): both directly & indirectly mimic effects of
STIMULATION of organs and structures of the sympathetic nervous system. These agents bring about
tissue responses resembling those produced by stimulation of the sympathetic nervous system .
Adrenergic receptors: a1, a2, b1, & b2. Adrenergic agonists therapeutic uses:
• Control superficial hemorrhage-a 1 adrenergic agonist causes vasoconstriction with EPI (Adrenalin).
• Allergic shock (anaphylaxis)-a1 adrenergic agonist causes vasoconstriction with EPI (Adrenalin), and
b2 adrenergic agonists causes relaxation of bronchial smooth muscle (airway dilation). Adrenergic
agonists are used to reverse an anaphylactic reaction. EPI is the prototypical adrenergic agonist.
• EPI stimulates both beta-adrenergic receptors and alpha-adrenergic receptors in the
sympathetic division of the autonomic nervous system (ANS) .
• Anaphylaxis is characterized by rapid, extreme reduction in BP and bronchospasms. When
injected, EPI rapidly reverses hypotension by cuasing vasoconstriction via the a1 receptor
stimulation (EPI dilates bronchial tubes via b2 receptor stimulation, and increases cardiac
output via b1 receptor stimulation on the cardiac muscle).
• Nasal decongestant-a1 adrenergic agonist causes vasoconstrictor with Phenylephrine (Neo-
Synephrine).
• Bronchial relaxation/dilation & airway dilation (Asthma)-b2 adrenergic agonist
• Asthma-a respiratory disorder characterized by recurring episodes of paroxysmal dyspnea,
wheezing on expiration , coughing, and viscous mucoid bronchial secretions. Asthma episodes
may be precipitated by inhalation of allergens or pollutants, infection, vigorous exercise,
or emotional stress.
• Bronchodilators (b2 adrenergic agonists that treat an acute asthma attack): EPI, Albuterol
(Proventil), Salmeterol (Serevent), & Metaproterenol (Alupent). These drugs stimulate beta
receptors in the airway to cause bronchodilation, thus are used to help reverse an acute
asthmatic attack. They are taken via aerosol , inhalers, and nebulizer.
• Aminophylline-a THEOPHYLLINE compound administered orally as bronchodilators in
reversible airway obstruction due to asthma or capo (chronic obstructive pulmonary disease).
Theophylline compounds RELAX bronchial smooth muscle to improve airway function. A CNS
stimulant that treats asthma.
• Cardiac stimulation-b1 adrenergic agonist like Isoproterenol.
• Epinephrine (Adrenalin), Phenylephrine (Neo-Synephrine), Albuterol (Proventil; Ventolin), &
Isoproternol are all adrenergic agonists bind to adrenergic receptors.

123
 2 Types of Adrenergic Agonists (Sympathomimetic Agents):
1. Direct-Acting Agonist: those drugs that interact with a or b receptors. Direct-acting adrenergic
agonists can be receptor selective or receptor non-selective:
• Phenylephrine (Neo-Synephrine): a1 selective agonist. Anasal decongestant, and mydriatic
in ophthalmic preparations to treat chronic orthostatic hypotension, and in combination
with local anesthetics to prevent anesthetic diffusion away from the injection site. 100x less
potent than EPI,
• Clonidine (Catapres): a2 selective agonist. Used primarily as an anti-hypertensive agent.
• Dobutamine: b1 selective agonist.
• Terbutaline: b2 selective agonist administered orally, subcutaneously, or by inhalation.
Primarily used in long-term treatment of obstructive airway diseases or emergency treatment
of bronchospasm. Given parenterally in emergency treatment of status asthmaticus and to
delay premature delivery.
• Albuterol: b2 selective agonist. Administered orally or by inhalation. Primarily used in long-
term treatment of obstructive airway diseases, emergency treatment of bronchospasm,
or to delay premature delivery.

• Epinephrine (Adrenaline): a vasoconstrictor and a1,2 &b1,2 direct acting agonist

(stimulates 4 receptors).
• Physiologic actions produced by EPI:
• Constricts arteriolar blood vessels (vasoconstriction) via binding to a1 receptors. Alpha
receptor stimulation causes a vasopressor response (1'BP).
• Relaxes bronchial smooth muscle (bronchodilation) by binding to b2 receptors. Beta-receptor
stimulation causes airway dilation and increased cardiac output. In this way, EPI counteracts
the vascular effects of histamine-related anaphylaxis.
• Decreases blood volume in nasal tissues.
• Causes a hypertensive response.
• Produces physiologic actions that are opposite (antagonize) the effects of HISTAMINE.

EPI (Vasoconstictor) Therapeutic Indications:

• Alleviates symptoms of an acute asthma attack via its bronchodilator properties. EPI treats
bronchospasm associated with hypotension (i.e. anaphylaxis) . EPI is the agent of choice to
treat/reverse anaphylactic reactions (given sublingually or subcutaneously) because it has
desirable vasopressor activity, bronchodilator properties, and has a rapid onset of action. EPI has
stimulatory effects on a & b adrenergic receptors. EPI treats hypersensitivity reactions.
• The major reason that EPI vasoconstrictor is added to local anesthetics is to prolong the
activity/duration of the local anesthetic (anesthesia) by decreasing the rate of diffusion and
absorption from the injection site.
• EPI also reduces systemic toxicity by reducing the rate of vascular absorption into the systemic
circulation, &provides hemostasis by reducing/controlling local bleeding at the injection site. EPI
also enhances the onset of action, decreases bleeding, and allergic reactions.
• EPI is used to restore cardiac activity in cardiac arrest relieves congestion of the nose, sinuses,
and throat.
• Treats glaucoma by reducing internal eye pressure.
• Controls superficial hemorrhage/bleeding.
• EPI is administered IV, sublingually, subcutaneously, or intramuscularly. It has a very rapid onset
of action when given via these routes.
• If NE or EPI stimulate or combine with eye a-receptors, they cause MYDRIASIS (pupil dilation).
• EPI is ineffective in treating hypotension because of its alpha receptor stimulatory actions on the
vasculature which could cause an even further elevation of BP. EPI does not reduce anxiety, but
increases anxiety because it has CNS stimulatory effects.

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• EPI is a sympathomimetic agent used in dentistry as the vasoconstrictor for anesthetic solutions to
prolong the duration of local anesthesia, and is the vasoconstrictor component used in gingival
retraction cords.
• Contra indications: patients with ANGINA conditions because EPl's cardiostimulatory effects
aggravate this condition.
• Common EPI side effects: headaches, agitation (anxiety), and tachycardia. EPI is used with caution in
patients with high BP and hyperthyroidism. These patients may have an increased sensitivity to EPI.

NOREPINEPHRINE (NE): a1,2 & b1 agonist.

ISOPROTERENOl: b1,2 agonist (a synthetic catecholamine) and the MOST POTENT BRONCHODILATOR.

2. Indirect-Acting Agonists (Sympathomimetics): drugs that cause release of stored NE at post-

ganglionic nerve endings to produce their effects (Tyramine, Amphetamine, Methamphetamine,
Hydroxyamphetamine, Methoxamine, & Ephadrine). Sympathomimetics are pharmaceutical
agents that bring about tissue responses resembling those produced by stimulation of
the sympathetic nervous system (SNS).
• Sympathhomimetics, sympathomimetic amines, and adrenergic agents are all
synonymous terms.
• In medicine, sympathomimetics (DA, EPI, NE, isoproterenol, and phenylephrine) are used
as pressor agents to maintain BP in vascular shock. They are used as bronchodilators for
asthma attacks and for allergic states like anaphylactic shock.
• Amphetamines-sympathomimetic amines (indirect-acting agonists) that stimulate CNS
(central nervous system) & PNS (peripheral nervous system), increase systolic & diastolic
blood pressures, and act as weak bronchodilators and respiratory stimulants. Amphetamines
have a high abuse potential resulting in tolerance, psychological dependence, and severe
social disability. Abuse causes extreme violence and paranoid psychotic behavior. They pass
readily into the CNS and cause a rapid release of NE in the brain.

• Amphetamine Therapeutic Uses:

• Attention Deficit Hyperactivity Disorder (ADHD; Hyperkinesis)-ADHD Drugs:
• Methylphenidate (Ritalin) -a mild CNS stimulant that increases attention span, reduces
hyperactivity, and improves behavior in children with ADHD.
• Focalin (Dexmethylphenidate)-a new form of methylphenidate.
• Concerta (Extended-Release Methylphenidate)-a long-acting form of Ritalin.
• Adderal (Mixed Amphetamine Salts)-acts the same as Ritalin to treat ADHD. Adderal is a
mixture of Dextroamphetamine and Amphetamine (Adderall). Adderall XR is sometimes used
instead of Methylphenidate (Ritalin).
• Strattera (Atemoxetine)-first non-stimulant approved for treating ADHD in children &adults.
• Metadate CR (Controlled-Delivery Methylphenidate)-another long-term acting ADHD drug.
• Dextroamphetamine (Dexedrine)

NARCOLEPSY -Dextroamphetamine (Dexedrine) is used to prevent daytime sleepiness.

WEIGHT LOSS-Phentermine (Lonamin) is structurally similar to Dextroamphetamine.

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 NOTES ANTI-ADRENERGICS (BETA & ALPHA BLOCKERS)
SYMPATHOLYTIC AGENTS (ANTI-ADRENERGIC) - drugs that acts in a way opposite to the
sympathetic nervous system. 4 types that all treat hypertension:
1. Beta-Adrenergic Receptor Blockers (b Blockers): with all "selective" beta-blockers, selectivity
for the bI is lost at high doses. As the dose is increased, they also block b2 receptors, thus having
effects on bronchial smooth muscle. The most common adverse side effects of beta blockers
are WEAKNESS &DROWSINESS. Beta blockers treat hypertension, angina, cardiac arrhythmias,
MI, glaucoma, and prophylaxis of migraine.
• Propranolol (lnderal), Timolol, &Nadolol (longest-acting)-lipid soluble drugs that blocks
both bI & b2 receptors (thus are "non-selective" beta-blockers). Widely used to treat
hypertension (~BP by ~CO). Non-selective beta blockers are absolutely contraindicated in
patients with asthma or other chronic obstructive airway disease as they cause fatal
bronchospasm. Selective bI blockers are contraindicated in the patients. Also, contraindicated
in patients with insulin-dependent diabetes as they block hypoglycemia recovery.
""C
Propranolol exerts its major anti-anginal effect by BLOCKING beta-adrenergic
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r- • Acebutolol (Sectral)-a bl cardioselective antagonist that treats hypertension and controls
o
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-< ventricular arrhythmias. It has low lipid solubility which reduces is likelihood of producing
adverse CNS effects, and has mild intrinsic sympathomimetic activity (partial agonist activity
at b2 receptors) similar to Pindolol.
• Metoprolol (Lopressor)-competitive b1 cardioselective antagonist that blocks bI receptors
to treat hypertension, acute angina pectoris, and may be helpful after a heart attack (very
sim ilar to Atenolol).
• Atenolol (Tenormin)-competitive b1 cardioselective antagonist that blocks bI receptors to
treat hypertension, chronic angina pectoris, or after a heart attack (MI recovery). Has a long
plasma 1h life (long duration of action). Due to its low lipid solubility, it is excreted by the
kidneys, minimally metabolized, and has a low potential for causing CNS side effects
compared to lipid-soluble beta-blockers like Propranolol.
• Metoprolol &Atenolol are longer-acting and more predictable than Propranolol in
producing therapeutic plasma levels. Since they are bI selective, they are safer to use
in patients with asthma or bronchitis.

2. Alpha-Adrenergic Receptor Blockers (a Blockers)-pharmacological agents that can cause

tachycardia, lower BP, vasodilation, and orthostatic hypotension (postural hypotension)-a
fainting spell that occurs due to a rapid fall in BP when moving from the supine to the upright
position when getting out of the dental chair. The symptoms are similar to simple fainting, but
the condition is related to positioning. Any alpha antagonist can cause EPI reversal. The major
pharmacological effect of alpha-antagonists (blockers) is to ~BP, eliciting reflex tachycardia.
Alpha blockers are medications that act by competitively inhibiting catecholamine actions at
the alpha receptor site to CAUSE BLOOD VESSELS TO RELAX (DILATE) and are used to reduce
high BP and treat an enlarged prostate. While HYPOTENSION is the major adverse effect
of alpha blockers, they cause relatively few adverse effects.

Orthostatic Hypotension (Postural Hypotension)-abnormally low BP occurring when an individual

assumes the standing posture. After vasovagal syncope, orthostatic hypotension is the 2nd most likely
cause of transient unconsciousness in the dental office.
• Factors that can cause orthostatic hypotension: administration and ingestion of drugs, prolonged
recumbency and convalescence, inadequate postural reflex, pregnancy, various defects in the legs,
Addison's Disease, physical exhaustion, starvation, and chronic orthostatic hypotension (Shy-
Drager Syndrome). The incidence of orthostatic hypotension increases with age. NSAIDs are not
known to produce orthostatic hypotension as an adverse effect.

126
• Drugs that can cause orthostatic hypotension:
1. Antihypertensives: (Guanethidine/lsmelin).
2. Phenothiazines: (ChlorpromazinefThorazine & Thioridazine/Mellaril).
3. Tricyclic Antidepressants: (Doxepin/Sinequan, Amitriptyline/Elavil, & ImipraminefTofranil).
4. Narcotics: (Meperidine/Demerol & Morphine).
5. Antiparkinson Drugs: (Levodopa/Larodopa/Dopar & Carbidopa + Levodopa (Sinemet).

2 types of Alpha Blockers (a1 & a2).

1. Selective Alpha Antagonists: block a1 receptors to treat cardiac conditions (hypertension) &
Benign Prostatic Hyperplasia (BPH).
• Doxazosin (Cardura)-selective to block a1 receptors to treat hypertension. The preferred
agent for hypertension due to its longer duration of action.
• Prazosin (Minipress)-selectivly blocks al receptors and RARELY used to treat hypertension
due to unwanted adverse effects.
• Terazosin (Hytrin)-selective to block a1 receptors to manage mild-to-moderate hypertension,
and treat benign prostate hyperplasia (BPH).
2. Non-Selective Alpha antagonists: blocks al & a2 receptors and usually DO NOT TREAT CARDIAC
CONDITIONS as blocking both alpha receptors can cause tachycardia (rapid heart beat) &
palpitations (pounding heart beat). Used in pre-surgical management of Pheochromocytoma
& Raynaud's Phenomenon.
• Tolazoline (Priscoline)-a NON-selective alpha 1 and alpha 2 blocker(has a moderate a2
adrenergic blocking activity). A parenteral anti-hypertensive agent whose actions are caused
by a direct peripheral vasodilation (Tolazoline is not a centrally acting anti-hypertensive).
Treats persistent pulmonary hypertension of the NEWBORN.
• Phentolamine hydrochloride (Regitine) & Phenoxybenzamine hydrochloride (Dibenzyline)-
a non-selective blocker of both a1 & a2 receptors. Their major clinical use is in pre-surgical
management of Pheochromocytoma (an adrenal medulla tumor that releases excessive EPI
& NE causing hypertension, tachycardia, & arrhythmias).

EPINEPHRINE REVERSAl- a predicatable result of using EPI with a patient who has received an
a-blocker. One of the best known effects of the alpha-receptor blocking agents (anti-adrenergic) is their
ability to reverse the "pressor" action of adrenaline (EPI). In the absence of blocking agents, EPI & NE
both cause BP to increase. After the alpha-receptors have been blocked by an alpha blocker, the pressor
effect of NE is reduced or abolished while EPI causes a fall in BP. This is because EPI stimulates a & b
receptors in the cardiovascular system, but NE only stimulates alpha receptors (NE lacks b2 effects).
After blocking the a receptors, only beta-receptors can be stimulated.

"PRESSOR" RESPONSE - produces an increase in BP and is mediated by a-receptors. A"depressor"

response produces a decrease in BP, and is mediated by b2 receptors.

3. Centrally-Acting Anti-hypertensive Agents-a2 selective agonists that inhibit adrenergic nerve

transmission through actions within the CNS. They reduce BP by reducing cardiac output,
vascular resistance (or both).
• Clonidine (Catapres)-an a2 selective agonists used in combination with a thiazide diuretic
& hydralazine that works by controlling nerve impulses along certain nerve pathways to relax
blood vessels so blood flows through them easier to help lower BP (reduces HR, CO, and total
peripheral resistance).
• Guanfacine (Tenex) & Guanabenz (Wystensin)-stimulate a2 adrenergic receptors to inhibit
sympathetic nervous system outflow, reducing peripheral vascular resistance, and are used
either alone, or with a thiazide diuretic.
• Methyldopa (Aldomet)-most effective when combined with a diuretic to produce a FALSE
transmitter (alpha-methylnorepinephrine) that replaces NE in the vesicular storage sites
and is released by the nerve impulse. Most beneficial for treating hypertension in patients
with RENAL DAMAGE.
• Methyldopa Adverse Effects: cardiovascular (orthostatic hypotension, bradycardia), CNS
(sedation & fever), GI (colitis), and possible hepatitis and cirrhosis.
4. Neuronal Depleting Agents-deplete catecholamine (NE, EPI, & serotonin) stores from adrenergic
terminals and in the brain. Reserpine (blocks uptake of NE, EPI, and serotonin into storage
vesicles) . & Guanethidine (blocks release of NE).

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 Alpha and Beta adrenergic blocking agents act by COMPETITIVE INHIBITION of postjunctional adrenergic
receptors.

Organ & Tissue Responses to Adrenergic Agonists {Sympathetics}

Organffissue Receptor Response to Adrenergic Agonists
Heart bi 1'conduction velocity, contraction force &rate, and CO
Arterioles al Constricts cerebral arterioles
b2 Dilates skeletal muscle arterioles
Eye al Contracts sphincter/radial muscle causing Mydriasis
b (dilation of pupil) Relaxes ciliary muscle to
accommodate for far vision &increases intraocular
pressure (increases aqueous humor secretion) .
Lung b2 Relaxes tracheal and bronchial muscles (treats asthma)
Liver b2 stimulates gluconeogenesis &glycogenolysis
Kidney bi Stimulates renin release
Intestine a2, b2 Decreases peristalsis (digestion)-relaxes walls to
al decrease motility &tone, Contracts smooth muscle
sphincters
GI secretions NO SYMPATHETIC EFFECT
Urinary Bladder al Contracts trigone &sphincter muscles
bi Relaxes detrusor muscle to release pressure (urinate)
Uterus a Excites uterine contractions (contracts uterus)
b2 Inhibits uterine contractions (relaxes uterus)
Penis &Seminal Ejaculation
a
Vesicles

Organ & Tissue Parasympathetic Responses

OrganlTissue Receptor Response to Adrenergic Agonists
Heart M2 --vHR (- chronotropic effect) & ventricular filling
Arterioles M3 Relaxes vessel endothelium that lines all blood vessels
Eye M3 Contracts circular muscle of pupil to constrict (Miosis)
Contracts ciliary muscle to accommodate for near vision
Increases aqueous humor outflow into Canal of
Schlemm to decrease intraocular pressure.
Lung M3 Contracts bronchioles (causes bronchoconstriction)
Liver PARASYMPATHETICS DO NOT EFFECT
Kidney PARASYMPATHETICS DO NOT EFFECT
Intestine M3 Relaxes smooth muscle sphincters
GI secretions Increase GI secretions
Urinary Bladder M3 Contracts bladder wall to increase pressure
Uterus PARASYMPATHETICS DO NOT EFFECT
Penis &Seminal M Erection
Vesicles

Autonomic nervous system (ANS) has CHOLINERGIC FIBERS that secrete Acetylcholine, and ADRENERGIC
FIBERS that secrete Norepinephrine, EPI, or Dopamine (catecholamines).
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CHOLINERGIC FIBERS (NEURONS) - release/secrete ACh. Cholinergic is a nerve ending that
releases acetylcholine (ACh) as the primary neurotransmitter. It is also a synapse in which ACh is the
primary neurotransmitter.
1. Preganglionic sympathetic & Preganglionic parasympathetic fibers
2. Postganglionic parasympathetic fibers. The action of ACh at postganglionic parasympathetic
sites is called a "muscarinic response"

Postganglionic sympathetic fibers are NOT cholinergic fibers, but ADRENERGIC fibers. Adrenergic
blocking agents block the effect of impulses transmitted by adrenergic postganglionic sympathetic fibers
via competitive inhibition. Postganglionic sympathetic neurons (fibers) that innervate sweat glands
secrete acetylcholine.

ACETYLCHOLINE RECEPTORS - cholinergic receptors that are subdivided as either:

1. Muscarinic receptors-are located mainly in autonomic effector cells (heart, vascular
endothelium, smooth muscle, presynaptic nerve terminals, and exocrine glands) in the CNS.
Muscarinic receptors respond to muscarine and ACh. The action of ACh at postganglionic
parasympathetic sites is called a "muscarinic response".
2. Nicotinic receptors-are located in ganglia, skeletal muscle end plates, and CNS. Nicotinic
receptors respond to nicotine and ACh, but not to muscarine. A "nicotinic response" describes
the stimulating action of ACh on the ganglia and its action at the neuromuscular junction of
skeletal muscle. There are 2 major nicotinic receptors:
1. Nicotinic receptors at neuromuscular junctions of the somatic nervous system (SNS).
Neuromuscular blockers act here.
2. Nicotinic receptors at autonomic ganglia in both sympathetic & parasympathetic systems.
Ganglionic blockers act here.

Drugs that chemically resemble ACh bind to muscarinic and nicotinic receptors and imitate the effects
of parasympathetic postganglionic activity. Acetylcholine is the chemical mediator at all autonomic
ganglia and parasympathetic postganglionic synapses, and transmitter substance at the
neuromuscular junction in skeletal muscle and sweat glands. Local anesthetics prevent or reduce the
liberation of ACh at the NMJ. ACh causes an alteration in cell membrane permeability to produce the
following cholinergic actions:
• Cholinergic Drug Actions: slowing of the heart (bradycardia), pupil constriction (miosis), stimulation
of smooth muscles of the bronchi, GI tract, gallbladder, bilde duct, bladder, and ureters (urination).
Stimulation of sweat, salivary, tear, and bronchial glands.

• Cholinergic drugs are very useful to induce salivation and stimulate Acetylcholine (ACh) cholinergic
receptors to cause salivation, miosis (papillary constriction), excessive sweating, flushing, increased
GI motility (peristalsis), and bradycardia.

• Cholinergic drugs increase secretions, a cholinesterase inhibitor also increases secretions because
it reduces acetylcholine metabolism.

• An overdose of a cholinergic drug causes: sweating, urination, bradycardia, copious serous saliva,
but does NOT cause mydriasis (pupil dilation), since this is an adrengeric response.

• All "M" receptors are CHOLINERGIC that bind to Acetylcholine (ACh) and are antagonized by Atropine.

• There are 3 classes of CHOLINERGIC AGONISTS (Choline Esters, Cholinergic Alklaloids, &
Cholinesterase Inhibitors). These drugs stimulate muscarinic sites by mimicking the actions of
Acetylcholine. However, if any of the cholinergic agents are administered before Aceytlcholine,
the action of ACh is enhanced and prolonged. These drugs are referred to as muscarinics,
cholinergics, cholinomimetics, or parasympathomimetics:

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 Indirect-Acting Cholinergic Agonists (Cholinesterase Inhibitors): their action increases the effects
of Acetylcholine within the autonomic nervous system (ANS) and at neuromuscular junctions. By
inhibiting cholinesterase, acetylcholine produced in the body is NOT broken down into by-products, but
is allowed to accumulate into substantial levels to stimulate the cholinergic portions of the ANS and to
stimulate skeletal muscle contractions at neuromuscular junctions. Thus, the actions of cholinesterase
inhibitors causes a CHOLINERGIC EFFECT (indirect cholinergic effect) since these drugs indirectly cause
a cholinergic response by allowing acetylcholine to build up in the body. The stimulation of skeletal muscle
by EXCESS acetylcholine eventually causes muscle paralysis. Cholinesterase inhibitors inhibit
acetylcholinesterase as both muscarinic and nicotinic sites.
1. Edrophonium-an indirect-acting cholinergic agonist (cholinomimetic). Drug of choice to
"diagnose" myasthenia gravis because of its rapid onset of action and reversibility. However,
it does not treat myasthenia gravis due to its very short duration of action. It is also useful in
differentiating between a myasthenic crisis and cholinergic crisis. It is a rapid, short-duration,
parental cholinesterase inhibitor.
2. Neostigmine & Pyridostigmine: prescribed to treat myasthenia gravis and can reverse the
blockade caused by non-depolarizing neuromuscular blocking drugs during general anesthesia .
3. Malathion & Parathion-insecticides.
4. Physostigmine

PRALIDOXIME (PROTO PAM) - a cholinesterase reactivator used as an antidote to reverse muscle

paralysis due to organophosphate anticholinesterase pesticide poisoning. It also reverses the effects
of an overdose of anti-cholinesterase agents used in the treatment of myasthenia gravis (i.e. Neostigmine,
Pyridostigmine, and Ambenomium). Pralidoxime treats poisoning with an organophosphate
cholinesterase inhibitor.

• Organophosphate Poisoning Symptoms: excessive salivation, bronchoconstriction, diarrhea, and

skeletal muscle fasciculations (twitching).

• Organophosphates-esters of phosphoric acid and an organic alcohol that inhibits the

cholinesterase enzyme.
1. Isoflurophate &Echothiophate-treats glaucoma.
2. Malathion-a widely used insecticide.
3. Parathion-an insecticide.
4. Tabun-one of the most potent and toxic nerve gases.
5. Metrifonate-an anthelmintic agent that destroys intestinal worms.

Direct-Acting Cholinergic Drugs: drugs that produce a cholinergic effect via direct stimulation of the
cholinergic receptors. Esters and Alkaloids are used to stimulate smooth muscle activity and are direct-
acting cholinomimetic agents wose effects resemble Acetylcholine. Two groups of drugs directly stimulate
cholinergic receptors to cause a "direct cholinergic effect":
1. Choline Esters: the most noticeable effects of choline esters are decreased BP due to
generalized vasodilation, flushing of the skin, slowing of HR, and increased tone and activity of
the GI and urinary tracts. Topical application of these drugs to the eye causes miosis and
decreases intraocular pressure .
• Methacholine (Provocholine}-not used much anymore.
• Carbachol (Isopto-Carbachol}-used in ophthalmology to produce miosis.
• Acetylcholine Chloride-used in ophthalmology to produce miosis.
• Bethanecol (Urecholine}-used for post-operative abdominal distension and urinary retention.

2. Cholinergic Alkaloids:
• Pilocarpine (Pilocar or Salagen}-the most useful alkaloid used as a MIOTIC and to treat
open-angle glaucoma and xerostomia.
• Muscarine, Nicotine, & Lobeline.

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XEROSTOMIA - caused by medications (i.e. antihypertensives &antidepressants), cancer therapy NOTES
(chemotherapeutic drugs & radiation treatment), Sjogren's Sydrome, head & neck trauma causing nerve
damage, and conditions like bone marrow transplants, endocrine disorders, stress, anxiety,
depression, and nutritional deficiencies.

• While xerostomia is not a disease, it can be a symptom of certain diseases, and can cause health
problems by affecting nutrition and psychological health. Xerostomia can contribute to and increase
the chances of having tooth decay and mouth infections.

• Temporary relief of xerostomia can come from saliva substitutes, sugarless hard candies, glycerine-
based cough drops and lemon flavored glycerine mouthwash. Additionally, medications can be added ,
changed, or dosages altered to provide increased salivary flow.

In dentistry, cholinergics drug treat dry mouth (Xerostomia) by inducing salivation. Cholinergic drugs
used are:
1. Pilocarpine (Salagen)-a cholinergic agonist and alkaloid indicated to treat xerostomia caused
by salivary gland hypofunction caused by radiotherapy for head and neck cancer by stimulating
salivary flow. Common side effects: excess sweating, nausea , heartburn, and diarrhea due to the
drug's cholinergic nature.
2. Cevimeline (Evoxac)-a cholinergic agonist indicated to treat xerostomia in patients with
Sjogren's Syndrome. Common side effects: increased sweating, nausea, heartburn , diarrhea
due to the drug's cholinergic nature. Specific for the M3 receptor on the salivary glands.

Saliva Functions:
1. washes away food debris and plaque from teeth to prevent decay.
2. limits bacterial growth that cause decay and other mouth infections.
3. bathes the teeth and supplies minerals that allow remineralization of early cavities.
4. lubricates foods so they can be swallowed easier.
5. provides enzymes that aid in digestion.
6. helps us "enjoy" food by aiding in the "tasting" process.
7. moistens skin inside the mouth to make chewing and speaking easier.

Cholinergic Crisis Symptoms: bradycardia (decreased HR), lacrimation, extreme salivation , vasodilation ,
and muscle weakness. Because a cholinergic crisis can causes muscle weakness like that of a myasthenic
crisis, distinguishing the two conditions is difficult. Administering a short-acting cholinomimetic like
edrophonium improves a myasthenic crisis, but worsens a cholinergic crisis.

Typical cholinergic effects caused by stimulation of acetylcholine receptors (cholinergic receptors)

are salivation, miosis, excessive sweating, flushing, increased GI motility and bradycardia.

MECAMYLAMINE (lNVERSINE) - a nicotinic ganglion-blocking drug.

ANTI-CHOLINERGIC (ANTI-MUSCARINIC) DRUGS: produce the opposite effects of cholinergic agents

like dry mouth (xerostomia), mydriasis (papillary dilation), anti-spasmodic actions, decreased GI motility,
reduction in gastric and salivary secretions, tachycardia, and dry skin .
• Anti-cholinergic drugs are contraindicated in GLAUCOMA PATIENTS. Adrenergic, Cholinergic, and
Adrenergic blocking drugs are not contraindicated with glaucoma patients.

• Anti-cholinergic Actions:
• Inhibits secretions of all nasal glands, mouth (dry mouth/xerostomia), pharynx, and
respiratory tract.
• An inhibitory effect on GI motility, thus can cause constipation and urinary retention .
• Increases HR (tachycardia) and body temperature, and dilates the pupils (mydriasis).
• Anti-cholinergic agents cause xerostom ia by blocking postganglionic cholinergic fibers.
• Anticholinergic drugs block receptor sites for acetylcholine and decrease salivary flow and
respiratory secretions during surgery.

131
 NOTES • Anti-cholinergic drugs do not have their own intrinsic activity, but simply occupy the receptor site and
prevent acetylcholine from occupying the same receptor.

• Accepted Therapeutic Indications: Parkinson Disease, motion sickness, post -operative bladder
syndrome, and traveler's diarrhea .

• Anti-cholinergic Contraindications: glaucoma, card iovascular problems, GI or GU tract obstruction ,

and asthma.

• Anticholinergic/Anitmuscarinic Drugs:
• Glycopyrrolate (Robinul)-treats traveler's diarrhea and post-operative bladder syndrome.
• Methantheline
• Propantheline Bromide (Pro-Banthine)-treats traveler's diarrhea and is an anti-secretory.
• Benzotropine Mesylate (Cogentin)-treats Parkinsonism (an anti-parkinsonism).
• Trihexyphenidyl HCL (Artane)-treast Parkinsonism (an anti-parkinsonism).
• Atropine Sulfate-produces mydriasis and cycloplegia.
-c • Scopolamine-prevents or reduces motion (sea) sickness.
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NICOTINIC RECEPTOR ANTAGONIST (NICOTINIC BLOCKERS) - are divided into ganglionic-
In
-< blocking drugs and neuromuscular blocking drugs:
1. Ganglionic Blockers-among the most potent agents available, but are SELDOM USED due to
the annoying and sometimes disabling parasympathetic blockade which causes pronounced
xerostomia, constipation, blurred vision, and postural hypotension. Ganglionic blockers have
very limited clinical use.
• Mecamylamine (lnversine) &Trimethaphan (Arfonad)-treat severe or malignant
hypertension, and during an emergency hypertensive crisis. These ganglionic blockers cause
a rapid and reversible FALL IN BP that enables them to immediately reverse an emergency
hypertensive crisis. Also used to create a "bloodless surgical field".
• Hexamethonium &Tetraethylammonium-are no longer available in the U.S. for clinical use.

2. Neuromuscular Blockers-important for producing complete skeletal muscle relaxation and

faciltating ENDOTRACHEAL INTUBATION as an adjunct to surgical anesthesia . Neurmuscular
blocking drugs interact with nicotinic receptors at the skeletal neuromuscular junction. Major
danger of these drugs is they can lead to excessive paralysis (patient cannot breath and
subsequent death). 2 classes of neuromuscular blockers.
1. Non-Depolarizing (Competitive) NMJ Blockers-competitively bind and compete with ACh at
cholinergic nicotinic receptors to prevent acetylcholine from stimulating motor nerves, to cause
muscle paralysis. Tubocurare (Curare)-the prototype non-depolarizing NMJ blocker.
• Other NMJ blockers: Gallamine (Flaxedil), Mivacurium (Mivacron), Vecuronium (Norcuron),
Doxacurium (Nuromax), Pancuronium (Pavulonl, Atracurium (Tracriuml, Cisatracuronium
(Nimbex), and Rocuronium (Zemuron).
• Neostigmine or Pyridostigmine-are cholinesterase inhibitors used to reverse the NMJ
blockade (paralysis) caused by NMJ blockers.
2. Depolarizing NMJ Blockers (Non-Competitive)-Succinylcholine (Anectine)-the prototype
depolarizing NMJ blocking agent, and only depolarizing NMJ blocker used in the U.S.
Succinylcholine acts as a nicotinic agonist and depolarizes (desensitizes) the neuromuscular
end-plate. It binds to the ACh receptor and stimulates depolarization causing initial excitation ,
followed by a block of neurotransmission and muscle paralysis. Succinylcholine is used with
caution in patients with low levels of pseudocholinesterase (enzyme that breaks down
succinylcholine) which can result in respiratory failure . Succinylcholine can also cause
muscarinic responses like bradycardia and increased glandular secretions.
• Administration of succinylcholine to a patient deficient in serum cholinesterase would
most likely result in prolonged apnea.

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SKELETAL MUSCLE SPASMOLYTIC DRUGS (SKELETAL MUSCLE RELAXANTS) - agents that
relieve muscle spasms without paralysis by acting in the eNS or in skeletal muscle, but not at the
neuromuscular end plate. Skeletal muscle relaxant drugs are used in certain chronic CNS diseases
(i.e. multiple sclerosis, cerebral palsy, and cerebrovascular accidents/strokes) associated with painful
muscle spasms. By reducing the muscle spasms, pain is reduced and patient mobility is improved.
1. Baclofen (lioresal)-a derivative of GABA to treat chronic muscle spasm. Its site of action in
reducing muscle spasms is the spinal cord to treat multiple sclerosis and other spinal cord
diseases. (Note: Diazepam (Valium) & Tizanidine (Zanaflex) also act in the spinal cord and are
effective muscle relaxants).
2. Carisoprodol (Soma)-used to treat chronic muscle spasms and pain associated with acute TMJ
pain. Its exact mechanism of action is not clear, but many effects have been attributed to its
central depressive action.
3. Cyclobenzaprine (Flexeril)-used to treat acute muscle spasm through a central action, possibly
at the brain stem level. Used to relive acute, painful musculoskeletal conditions. It is not effective
for muscle spasm secondary to cerebral or spinal cord disease.
4. Methocarbamol (Robaxin)-a centrally acting muscle relaxant used to relive acute, painful
musculoskeletal conditions and to manage tetanus.
5. Quinine-widely used to effectively relieve nocturnal leg cramps.

BIOAVAILABILITY - measures the rate &amount of therapeutically active drug that reaches the
systemic circulation. A drug's bioavailability is affected by the dissolution of a drug in the GI tract and
destruction of a drug by the liver.
• IV injection route provides complete 100% bioavailability.
• Bioavailability = amount of drug absorbed/amount of drug administered .

DRUG ADMINISTRATION ROUTES: drug's onset of action is PRIMARILY determined by the RATE
of ABSORPTION. The major effect of a drug is a factor (is determined by) how much of the drug is
FREE IN PLASMA.

Enteral Administration (via the intestine or GI tract):

1. Oral Route (P.OJ-takes -30m in for the onset of a drug's effect after swallowed. The oral route
allows the use of many different dosage forms like tablets, capsules, and liquids.
• Oral route is an example of an ENTERAL ROUTE of administration. It is the most common
route where the drug is swallowed. It is the most convenient for safe drug administration. It is
safe, painless, and economical. The oral route is the safest and easiest route for drug
administration, but it is also the most unpredictable and least effective route available.
• Oral route is most known for its significant hepatic "FIRST PASS" metabolism. The oral
administration of a drug is the one most accepted by patients. It is convenient because drugs
can be given via tablets or capsules that contain an exact dose, making it easy for the patient
to take the drug without assistance.
• After oral administration, drugs are generally absorbed best from the DUODENUM which
has a large surface area due the presence of villi and microvilli.
• Drugs taken by mouth have to be absorbed (usually from the small intestine) before they can
be transported to their site of action. Absorption may be slow, unpredictable and irregular due
to the presence of variable amounts of food in different stages of digestion and to the varying
degrees of acidity and alkalinity of the digestive juices. Moreover, blood from the intestinal
tract passes first to the liver (some drugs are metabolized in the liver, while others may be
stored there to be released only slowly). These considerations make it clear that oral
administration is usually NOT USED IN MEDICAL EMERGENCIES or other occasions when
a rapid effect is needed.
• Oral Route Disadvantage: drugs must be absorbed (usually from the small intestine) before
they can be transported to their site of action. Blood from the intestinal tract passes first to
the liver (some drugs are metabolized in the liver "first-pass effect", while others may be
stored there to be released slowly). This consideration makes it clear that oral administration
is not suitable in emergencies or other occasions when a rapid effect is needed. Emotional
stress decreases the rate of absorption of a drug when given orally.
• Other Enteral Routes:
• Rectal Route-a drug in solution/enema or suppository form is inserted into the rectum.
• Buccal or Sublingual Route-a tablet is placed under the tongue or in the cheek.

133
 NOTES Parenteral Administration (not by way of the intestine or GI tract):
2. Intramuscular Injection (lM)-the onset of action of drugs injected into muscle occurs rapidly
(-5min) because of high blood flow through the muscles. 1M injection is an injection made into
a large muscle. Absorption from an 1M injection is often faster and yields a higher bioavailability
than oral administration .
• Advantages:.results in uniform absorption and can be used for solutions too irritant for
subcutaneous injection. The speed of absorption of drugs given 1M depend on the vehicle in
which they are dissolved (absorption is rapid from aqueous solutions and slow from oily
solutions). Other factors affecting absorption are vasoconstriction and congestive heart failure
(slow absorption) .
• 1M injections Sites: buttocks, deltoid muscle, and anterior thigh (usually the site for young
children). The bicep muscle is NOT an acceptable site for an 1M injection. Proper needle depth
in muscle is 1 inch into big adult muscle and 1A inch in children. NEVER go deeper than 2/3
of the needle length.

3. Subcutaneous Injection-the onset of drugs injected under the skin takes -15 minutes. Injected
.." beneath the skin . Absorption may be less rapid .
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4. Intra-arterial Injection-injected into a specific artery. Use caution because it burns.
c:::>
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-< 5. Intravenous Injection-the drug administration route that produces the MOST RAPID ONSET of
pharmacological effect by injecting directly into the bloodstream. When a drug is given IV, it is
placed directly into the systemic circulation and delivered rapidly to all tissues and the drug
receptor sites. For all other drug administration routes (except intra-arterial injection), the drug
must be systemically absorbed prior to distribution to the drug's receptor sites. Thus, the onset
of pharmacological effects is slower.
• When a drug is given by IV injection there is complete 100% bioavailability (the entire dose
is placed into systemic circulation). With other administration routes, the drug can be lost
before reaching the systemic circulation (i.e. with "first pass" effects a portion of an orally
administered drug is eliminated through degradation by liver enzymes before the drug
reaches its receptor sites) .
• A major advantage of IV drug administration is it allows for TITRATION of the drug. Other
advantages: rapid onset, drugs that cause irritation when administered subcutaneously can
be given IV without irritation. In case of an emergency, there is an open line through which
emergency drugs can be injected .
• A major disadvantage of IV injection is due to its rapid onset of action , overdose may have
effects so immediate, that it can be impossible to reverse the overdose effects.

6. Inhalation-gases like nitrous oxide are rapidly absorbed through the lungs and gain access to the
general circulation within 5 minutes. Inhalation (using nitrous oxide) is the MOST frequently
utilized route of administration to sedate pediatric patients. The drug is given as an aerosol
into the respiratory tract.

7. Topical Administration-includes ointments & creams applied to the skin and mucous
membranes. The drug is placed on the skin to produce a LOCAL DRUG EFFECT. Not intended
for systemic drug administration .

8. Patch Delivery-skin patches release drug into the bloodstream over 12-24hrs. Not intended for
rapid drug administration . Transdermal route allows the drug to be placed on the skin to
produce a SYSTEMIC EFFECT.

Initial distribution of a drug into the tissues is mainly determined by the RATE OF BLOOD FLOW TO THE
TISSUE, while a drug's affinity for the tissue determ ines if the drug will concentrate at that site. *Gastric
emptying time and degree of plasma protein binding (albumin) also effect drug distribution, but are
less important that the RATE of blood flow to the tissues.

134
MOST DRUGS travel through the bloodstream by binding to ALBUMIN protein which is abundant is
plasma which enables the drug to be carried to all tissue and organs. Adrug bound to plasma albumin
always has some portion of the drug that does not bind. This portion is free to leave the blood compartment
to be taken up by tissues where the drug will elicit its pharmacological effect. The remaining "bound"
portion of the drug then continuously releases more free drug to be taken up by tissues. Eventually, all
of the drug in the blood compartment will be absorbed by this process.

Interactions between two or more drugs can occur if they compete for binding on the plasma albumin. If
drug "A" is bound to albumin before the patient takes drug "8", and drug "8" has a greater binding
affinity to albumin than drug "A", then when drug "8" is binds, it will displace drug "A" from albumin,
resulting in large amounts of unbound drug "A". This may cause adverse reactions due to the sudden large
amounts gaining access to the tissues and organs.

Physiochemical properties of drugs that influence their passage across biologic membranes are lipid
solubility, degree of ionization, molecular size, and molecular shape. The mechanism of drug transfer
across biological membranes is by:
1. Passive Transfer-is essential to various processes of metabolism.
• Simple Diffusion: a process where lipid-soluble substances move across the lipoprotein
membrane. Most drugs penetrate biomembranes by simple diffusion through membrane
phospholipids. The amount of drug dissolving in the membrane at any time is directly
proportional to the concentration gradient and its degree of lipid solubility (Note: only
non-ionized drugs are soluble in lipid).
• Filtration: water-soluble molecules small enough to pass through membrane channels may
be carried through the pores by the bulk flow of water. Drugs of molecular weights of 60,000
or less can "filter" through capillary membranes.
• Osmosis: movement of a pure solvent like water through a semi-permeable membrane from
a solution that has a lower solute concentration, to a solution with a higher concentration.
The membrane is impermeable to the solute, but is permeable to the solvent.

2. Specialized Transport:
• Active Transport: involves lipid-insoluble substances (i.e. glucose) which are "shuttled"
across plasma membranes by forming complexes with specific membrane constituents or
"carrier molecules" that are are within the cell to provide energy for transporting drugs to
regions of high concentration .

Facilitated Diffusion: term given to carrier-based transfer when the driving force is simply the concentration
difference of the drug across the membrane. Most drugs are absorbed by facilitated diffusion.

Factors Influencing Hepatic Drug Metabolism:

1. Microsomal enzyme inhibition: many drugs and environmental agents can inhibit many of the
CYP isoforms of the P450 microsomal drug metabolizing system . Thus, many drugs usually
metabolized by the particular CYP inhibited, will not be effectively metabolized and will achieve
higher than expected blood levels.
2. Microsomal enzyme induction: agents that induce higher levels of the microsomal drug
metabolizing enzymes may cause a more rapid metabolism of other drugs, thus resulting in
lower than expected blood levels of a drug.
3. Plasma protein binding: drugs highly bound to plasma proteins will not enter the liver to be
metabolized . This causes a longer plasma half-life of the drug.
4. Genetic factors: there is individual variance through genetic factors that contribute to different
rates of drug metabolism in the hepatic microsomal enzyme system.
5. Pathology: hepatic impairment and liver disease usually wil impair the microsomal drug
metabolizing system . This causes elevated levels of unmetabolized drug.

135
 Factors that Control Urinary Elimation of Drugs:
1. Glomerular Filtration: all drugs are filtered through the glomerulus to enter the renal tubules.
The amount of drug varies based on the degree of plasma protein binding, and bound drugs
are not subjected to filtration .
2. Tubular Reabsorption: once the drugs enter the renal tubules, they may be reabsorbed back into
the bloodstream through the rena l tubular cells. Reabsorption favors the highly lipid soluble
agents; the converse is that highly polar compounds are not effectively reabsorbed and are
effectively excreted from the renal tubules.
3. Active Transport: rate of renal elimination also depends on if active transport into or out of
the tubular fluid occurs.

Other Excretory Drug Pathways:

• GI tract excretes some drugs through feces . This is not as common as urinary excretion.
• Most drugs can be detected in saliva after administration, but the salivary glands are not considered
a route of drug excretion since the drug is re-swallowed along with saliva.
• Lungs excrete volatile compounds that were inhaled into the respiratory system. Nitrous oxide and
volatile general anesthetics are excreted by the lungs.
• Some drugs are excreted through sweat glands, but this route accounts for only a small percentage
of drug excretion.

The most important enzyme systems for the biotransformation of drug molecules are found in the
LIVER. Hepatic metabolism of drugs occurs in Phase I reactions catalyzed by a microsomal mixed-function
oxidase system (P450 system) and in Phase II reactions is known as conjugation reactions.
1. Phase I Reactions: occur in the liver microsomal enzyme system (mixed -function oxidase system
or P450 system). In this system , drug metabolism occurs in 3 basic patterns. First, the active
parent drug can be converted into the inactive metabolite. Second, an active parent drug may
be converted into a second active compound that is subsequently converted into an inactive
compound. Third, an inactive parent drug may be transformed into an active compound .
• The most common reaction in drug metabolism is an oxidation reaction in which oxygen in
the form of a hydroxyl group is attached to the drug molecule.
• There are at least 5 distinct groups of microsomal drug metabolizing enzymes. These enzyme
"families" are identified as a cytochrome (CYP prefix) followed by their numerical digestion
(i.e. lA2). Thus, the enzyme CYP lA2 is a distinct drug metabolizing enzyme that converts
a variety of drugs into the oxidized product.

2. Phase II Reactions: conjugation reactions involve coupling the drug with an acid present in cells
(usually glucuronic acid). When coupled to glucuronic acid , the process is known as glucuronide
conjugation with the resulting metabolite referred to as the "glucuronide". Conjugations occur in
the liver, kidney, and to a lesser extent in other tissues.
• Conjugation of drugs results in polar, water-soluble compounds that are rapidly excreted
in urine. Thus, the parent drug is effectively rendered inactive and transported out of the
body by th is process.

Controlled Substance Act of 1970-uses 4 criteria for including a drug into one of five DEA drug schedules:
• Potential for abuse (most important criteria).
• Medical usefulness.
• Degree to which the drug produce a physiological and/or physical dependence.

DEA Drug Schedule: prescriber must have a Drug Enforcement Agency authorization number (OEA#) to
prescribe scheduled drugs.
1. Schedule I: not legitimate for medical use. Among the substances classified by the DEA are
Mescaline, LSD, Heroin, & Marijuana. Special licensing procedures must be followed to use these
and other Schedule I substances. These drugs cannot be prescribed, and are made available
only for specific approved research projects.
2. Schedule II: considered to have a strong potential for ABUSE or ADDICTION, but have
legitimate medical use. Substances classified by the DEA like Amphetamines, Morphine,
Cocaine, Pentobarbital, Oxycodone, Methadone, and straight Codeine. Must have a written
prescription signed by a health professional (laws vary by state).These drugs can be prescribed,
but cannot be refilled. Anew prescription must be written for refills. Prescriptions cannot be
called into the pharmacy over the phone.
136
 3. Schedule III: have less potential for abuse or addiction than Schedule I or II drugs. These include
various analgesic combination compounds containing codeine (i.e. Acetaminophen with codeine
NOTES
= Tylenol 3) and various analgesic combination compounds containing hydrocodone (i.e.
hydrocodone and acetaminophen = Vicodin; Lorcet) . Must have a written prescription signed
by a health professional (laws vary by state). These drugs may be called into the pharmacy.
The prescriber can authorize refills without writing a new prescription.
4. Schedule IV: a category of drugs with less abuse or addiction potential then Schedules I-III.
These substances include Diazepam (Valium), Lorazepam (Ativan), Triazolam (Halcion),
Alprazolam (Xanax), and chloral hydrate.
5. Schedule V: a category of drugs that have only a small potential for abuse and addiction.
These substances include many commonly prescribed medications that contain only a
small amount of Codeine.

FDA determines which drugs are to be sold by prescription only. The prescription must have the address
of the patient and dentist, and the dentist's DEA number/license.

Sample Prescription:

Dr. John Doe, DDS License #

10 Any Street Federal Drug Registry #
Huntington Beach, CA 90210
555-655-1212

Patient's Name: _ _ _ _ _ _ _ __ Age: _ _

Patient's Address: _ __ __ _ __ Date:

Rx: Amoxicillin 500mg tablets

Disp. Four (4) tabs.
Sig: Take 4 tabs (2000mg) 1 hour prior to dental appointment

Signature _ _ _ _ __
Substitution permisSible _ _
Substitution not permissible _ _
Number of refills

• Superscription: patient's name, address, age, date.

• Inscription: drug name and strength (i.e. 500mg tablets).
• Subscription: directions to the pharmacist (dosage form and amount to be dispensed).
• Transcription (signa): directions to the patient (sig).
• Signature: signature of person prescribing the medication MUST appear.

Always document prescriptions given to a patient in the patient's chart, along with the date they were
written and any specific instructions for patient use.

Common Abbreviations Used For Writing Prescriptions:

q.i.d. Four times a day

q.4.h. Every 4 hours
q.12.h. Every 12 hours
b.i.d. Twice a day
t.i.d. Three times a day
Stat. Immediately
p.r.n. As needed
p.c. After meals
a.c. Before meals
h.s. At bedtime

137
 ANESTHETICS
Local Anesthetics: adverse side effects of local anesthetics either cause TOXICITY or ALLERGY.
1. Toxicities: caused by too much anesthetic in the bloodstream, affecting the CNS
and cardiovascular system.
• CNS toxicity effects: restlessness, stimulation, tremors, convulsive seizures followed by
CNS depression, slowed respiration, and even coma.
• Cardiovascular effects: bradycardia and reduced cardiac output.

2. Allergies:
• hypersensitivities and allergic reactions to local anesthetics, especially from amides are
rare. These reactions are manifested as dermatologic reactions and edema at the
injection site.
• Asthmatic wheezing syndromes have occurred in response to local anesthetic injections.
• Allergic reactions are more prevalent with ester local anesthetics (nasolabial swelling,
itching, and oral mucosal swelling), not amide local anesthetics.

BISULFITES - the component of a local anesthetic solution that causes an ALLERGY. Patients may
exhibit hypersensitivity to sulfites contained in some anesthetics. Sodium meta bisulfite prevents the
oxidation (deterioration) of the EPI vasoconstrictor in commercial preparations containing EPI. Most
patients who react to bisulfites have a history of asthma, and the airway is hyperactive to the sulfites.
Allergic reaction usually results in an asthmatic syndrome of wheezing and bronchial constriction.
Bisulfites are present in only those commercial preparations containing EPI (vasoconstrictor).
Preparations without EPllike Mepivacaine 3% (Carbocaine) do not contain bisulfites. Hypersensitivity
or allergic reactions to local anesthetics (especially amides) are much more rare than allergic reactions
to bisu Ifites.

Local anesthetics REVERSIBLY BLOCK nerve impulse conduction and produce the reversible loss of
sensation at their administration site. They are incorporated within the nerve membrane or bind to
specific Na+ ion channels, restricting sodium permeability in response to partial depolarization. Local
anesthetics do not produce loss of consciousness
• Mechanism of Action: on the nerve axon, local anesthetics DECREASE Na+ UPTAKE through the
axon's sodium channels. When a local anesthetic is injected near the nerve, the solution interferes
with the uptake of sodium from outside inside the nerve by blocking the specific sodium channels,
thus blocking Na+ uptake. This decreases the nerve's excitability below a critical level, and nerve
impulses fail to propagate along the axon. Since axons carry pain sensations, these sensations will
not be carried, and a blockage of pain results. Local anesthetics have NO EFFECT ON POTASSIUM
(K+) at the nerve axon.

• Local Anesthetic Mechanism: decrease pain sensation by blocking propagation of nerve impulses
("nerve block"). At therapeutic doses, locals block voltage-gated sodium (Na+) channels to inhibit
generation and conduction of action potentials.

• Local anesthetics help reduce saliva flow during operative procedures by reducing sensitivity and
anxiety during tooth preparation.

Local anesthetics DEPRESS small, unmyelinated nerve fibers that conduct pain & temperature
sensations FIRST, and depress large, myelinated fibers LAST. Small nerves have a greater surface-
volume ratio which accounts for the rapid onset of action. Clinically, the order of loss of function caused
by local anesthetics is:
• PAIN (first) temperature touch proprioception skeletal muscle tone (last)
• pain threshold-the lowest level of pain a patient will detect.

138
Factors Influencing Absorption &Effects:
• Site of injection- pH in area (acidic~absorption; alkalinel'absorption), extent of tissue vascularity
& perfusion, effects of local inflammation, or tissue damage (often a problem after injury).

• Inflammation-lowers pH of surrounding tissue, making it more difficult for local anesthetic to

permeate the membrane. An inflamed, acidic environment penetration of local anesthetic into
tissue. Thus, is more difficult to achieve nerve block and satisfactory anesthesia in inflamed
injured tissue.

Local anesthetics in theory are LESS effective in acutely inflamed tissue than in normal tissue because
inflamed tissue's pH decreases (becomes more acidic) which decreases the available free base. At
body pH (7.4), a local anesthetic when infiltrated , will chemically exist as a portion which is ionized (has
a proton attached which is merely a hydrogen H+ atom) and as a non-ionized portion (no proton attached).
The ionize portion has difficulty penetrating the nerve and will not be effective. The non-ionized portion
penetrates the nerve to cause anesthesia (this non-ionized portion is the "free base") . The more proportion
of anesthetic in the "free base" form, the more effective the anesthetic.

When tissue conditions are normal (pH = 7.4), -10-20% portion of an infiltrated local anesthetic is
in the free base form (non-ionized form), which is enough to penetrate the nerve to cause anesthesia.
When tissues are acidic (i.e. tissue infection), less free base portion exists and more ionized (H+) portion
exists. Thus, there is not enough free base form to penetrate the nerve to cause anesthesia, and the local
anesthetic when infiltrated into the tissue site is ineffective at the normal anesthetic doses.

Non-ionized (free base form) is the form that readily penetrates tissue membranes. Loca I anesthetic
free bases are fat-soluble (lipophilic) drugs that are converted into their water-soluble (hydrophilic)
hydrochloride salts to allow preparation of an injectable solution. In solution, an equilibrium is established
between the ionized & non-ionized forms of the local anesthetic. The amount of drug in the ionized form
depends on the pKa of the drug, and pH of the solution . At the usual solution pH of 6.0 or less, most
locals are almost completely in the ionized form. Local anesthesia is obtained only if sufficient free base
form is available. The lower the drug's pKa, and higher the pH of the solution or injected tissues, the
MORE free base available.

Once the local anesthetic is injected , the buffering capacity and tissue's pH (normally 7.4), shifts the
equilibrium in favor of the free-base form. At physiologic 7.4 pH, approximately 5-20% of the local
anesthetic is in the free-base form, which is enough to penetrate and produce anesthesia. If infection
or inflammation exists, the tissue's pH may be acidic which greatly reduces the concentration of the
free-base form, rendering the local ineffective.

Main Point: the potential action of all local anesthetics depends on the ability of the anesthetic SALT
to LIBERATE THE FREE-BASE.

If you inject Lidocaine (pKa = 7.8) into tissues with a 7.8 pH, the Lidocaine will exist in an equal mixture
of ionized & non-ionized forms which will be more than enough to produce anesthesia .

139
 NOTES Ester Local Anesthetics: are metabolized in PLASMA. All esters have an "ester" grouping them within
their chemical structure. An ester grouping is a bridge or link containing the -COOCH2- configuration.
Drugs with 1 letter "i" in the name.
• Ester local anesthetics are mainly available as TOPICAL anesthetics (Benzocaine, Tetracaine, &
Dibucaine) . Esters are also available as medical anesthetic preparations like Propoxycaine
(Ravocaine). Ester-type local anesthetics are no longer available as dental anesthetic injectable
preparations due to their relatively high allergy incidence.

• Esters are metabolized by the plasma enzyme "plasma cholinesterase" or "pseudocholinesterase"

which splits the ester linkage within the chemical structure rendering the anesthetic ineffective.

• Procaine {Novocaine)-one of the original ester-type local anesthetics. When Procaine was
metabolized by plasma cholinesterase, a highly allergic compound "Paraaminobenzoic Acid"
(PABA) was formed . Many patients developed an allergy to PABA. Hydrolysis of procaine occurs mainly
in the plasma.

• Cocaine-the only local anesthetic that increases the pressor activity of EPI &NE. However, cocaine
has no place in the routine practice of dentistry. Cocaine is a naturally occurring ESTER of benzoic
acid and was the first local anesthetic used in dentistry and medicine. Cocaine is potent and highly
toxic, and is the only local anesthetic that causes DEFINITE VASOCONSTRICTION. Cocaine is
commercially available in various forms, and is applied to mucous membranes of the oral,
laryngeal, and nasal cavities for use as a topical anesthetic. Cocaine causes euphoria , and abuse
can lead to a physical dependence. Although it is an excellent local anesthetic, the risk of abuse and
intense local vasoconstriction prevents cocaine from being more widely used clinically. Cocaine's
pharmacology is unique among local anesthetics because it inhibits catecholamine uptake (NE,
EPI, Dopamine, Serotonin) by adrenergic nerve terminals. This increases (potentiates) the action
of endogenously released and exogenously administered sympathomimetic amines like Dobutamine,
Dopamine, or EPI. Cocaine increases the risk of developing cardiac arrhythmias and hypertension
(cocaine increases the pressor activity of these sympathomimetic amines).

• ESTERS have a rapid onset &short duration of activity (except tetracaine which has a longer
duration). Esters hydrolyzed in blood by butylcholinesterase have short t1I2 . Allergic reactions &
precipitation of acute asthmatic attacks are concerns with ester-type generally used topically

AMIDE LOCAL ANESTHETICS - all are metabolized in the LIVER (except Articaine), and the
metabolites are then renally excreted. All amides have an "amide" grouping within their chemical
structure. An amide grouping is a bridge or link containing the -CONHCH2- configuration. Amides are
present in urine as the parent compound in a greater percentage due to their more complex process of
biotransformation . Amides are the only local anesthetics presently available as dental injectables
(Lidocaine (Xylocaine), Prilocaine (Citanest), Bupivacaine (Marcaine), &Mepivacaine (Carbocaine),
Etidocaine, &Articaine). All drugs with two letter "i" in the name. Amides are metabolized by the "hepatic
microsomal enzyme system", and the products formed to not have anesthetic actions and are excreted
from the body by the KIDNEY. Amides are used with caution, or not at all in patients with compromised
liver function. AMIDES-have a longer duration of action, and are metabolized by P450 enzymes in the liver
so toxicity is more likely if amides are given to individuals with liver dysfunction or if given with other
drugs that may alter hepatic metabolism. Amides less likely to produce allergic reactions.

• Articaine {Septocaine)-the only amide-type local anesthetic metabolized in the BLOODSTREAM. It

is chemically unique because it has an ester group attached to its molecule that can be acted upon
by plasma cholinesterase to render it ineffective. Thus, it is the only amide metabolized in the
bloodstream, and not the liver. Articaine is supplied as articaine HCL 4% solution with EPI1:100,OOO.
It is indicated for local, infiltrative, or conductive anesthesia in simple and complex dental and
periodontal procedures. The onset of anesthesia after administration is 1-6min after injection .
Complete anesthesia lasts -lhr. Articaine is contraindicated in patients with hypersensitivity to
local anesthetics of the amide type or to sodium bisulfite.

140
 .........

• Maximum dose of Articaine (Septocaine) recommended in one appointment is expressed

as mg/kg body weight (not as total mg). 7mg/kg is the maximum recommended dose of
NOTES
Articaine in children and adults. In a typical kg adult male, the 7mg/kg dose = 490mg. Thus,
the maximum recommended amount of Articaine that could be given to a 70kg adult in one
appointment is 490mg.

• The table below shows the number of dental cartridges containing Uml volume of solution to
provide the indicated amounts of Articaine Hydrochloride 4% and EPI 1:l00K. The carpule
fluid volume of 1. 7ml is unique for Articaine. and is not the standard carpule volume of
1.8ml as with other dental anesthetics.

Number of Cartriges (1.7ml) Articaine HCI (45) EPll: lOOK

1 68 0.017
2 136 0.034
3 204 0.051
4 272 0.068
5 340 0.085
6 408 0.102
7 476 0.119
8 544 0.136

• Prilocaine (Citanest}-a local anesthetic amide used for nerve block, epidurals, and regional
anesthesia. It has an intermediate duration of action and is longer acting than Lidocaine, produces
less vasodilation than equal amounts of Lidocaine. and is somewhat less potent than Lidocaine.
Prilocaine is available as a 4% solution with or without EPI, which prolongs the anesthetic effect.
While Prilocaine is 50% as toxic as Lidocaine, since methemoglobinemia is a possible reaction,
Prilocaine is not used for patient with hypoxic conditions or patients with Hepatic (liver) disease.
Prilocaine is metabolized into orthotoluidine (a product than can produce methemoglobinemia, a
condition characterized by increased levels of methemoglobin in the blood which is less effective then
hemoglobin in carrying oxygen in the blood.

• Bupivacaine (Marcaine)-has the longest duration of action of any dental local anesthetic
available. May be used with EPI. Appropriate for extended procedures although long duration of
effect increases risk of systemic absorption &toxicity. Radiotoxic in some patients and used
with caution if cardiovascular disease. elderly, or pediatric population. Often used in labor &
procedures where motor control is essential because exhibits strong preference for sensory fibers
& is long-acting.

• Lidocaine (Xylocaine): an ANTI-ARRHYTHMIC AGENT effective ONLY on the ventricle, often

administered intravenously to treat life-threatening ventricular arrhythmias. When given IV to treat
ventricular arrhythmias, it acts on the fibrillating ventricles to decrease cardiac excitability and
spares the atria. It can effectively reverse a life-threatening situation.
• Lidocaine and Mepivacaine are most likely to show cross-allergy.
• Lidocaine is a local anesthetic drug used topically in dentistry.

• Mepivacaine (Carbo cain e)-EQUAL TO LIDOCAINE in efficacy and used without EPI. Ineffective for
topical application. Levonordeferin can be used as a vasoconstrictor. Duration of anesthesia in soft
tissue is shorter than Lidocaine, thus less useful for procedures lasting> 25 minutes. TOXIC TO
NEONATES. so avoid for labor and infants. Not best for dental procedures more than 30 minutes
(short effects).

141
 Dental Amide Preparations &Average Duration by Route

Amide Local Infiltration Inferior Alveolar Block

Mepivacaine (Carboca ine 3%) 20 min 40 min
Prilocaine (Citanest Plain 4%) 20 min 2.5 hrs
Prilocaine 4% c l:200K EPI (Citanest Forte c EPI) 2.25 hrs 3.0 hrs
Lidocaine 2% c 1:100K EPI 60 min 90 min
Marcaine 0.5% c EPI (Bupivacaine c EPIl:200K) 60 min 5-7 hrs

Local Anesthesia in Children: WEIGHT determines the maximum dose of a local anesthetic that can be
administered in children. For Lidocaine (2%), a dosage of 4.4mg/kg is not exceeded (maximum adult dose
of 300mg) .

Maximum Recommended Doses of Lidocaine for Children

Drug Max Dose (mg/kg) Mg/Carpule
Lidocaine (2%) w/wo EPI 4.4mg/kg (300 mg max) 36mg = 1 Carpule
Patient Weight (kg/lb) Mg # of Carpules
10kg = 231bs 44mg 1.2
15kg = 34.51bs 66mg 1.B
20kg = 461bs BBmg 2.4
25kg =57.5Ibs 100mg 2.6

*1 kg = 2.31bs
*2% =(20mg/ml) x (1 .8mI)/1 carpule = 36mg/1 carpule
A dental local anesthetic carpule contains 1.Bml of a 2% Lidocaine solution with 1:100,000 EPI. Thus,
the carpule contains 36mg of Lidocaine and 0.018mg of EPI.
• Important: ImL of a 2% solution of Lidocaine with 1:100K EPI contains 20mg of Lidocaine
and O.OlOmg of EPI.
• Important: 1 dental capule contains 1.Bml solution . Thus, 1.Bml of 2% Lidocaine solution with
1:100K EPI contains 36mg of Lidocaine and O.OlBmg EPI.

Maximum recommended adult dose of Lidocaine is 300mg. To reach this max level, 15ml of 2%
Lidocaine is needed.
• Important: there are 20mg of Lidocaine in every 1ml of 2% Lidocaine.
• 300mg/20mg = 15ml.
• 20mg x 1.Bml (in every carpule) = 36mg per carpule.
• 300mg/36mg = 8.3 carpules (B carpules of 2% Lidocaine can be used).

Maximum Recommended Doses of Local Anesthetics

Drug Maxmg Max mL Concentration % # of Carpules
Lidocaine (Xylocaine) 300mg 15ml 2% 8.3
Mepivacaine (Carbocaine) 300mg 10ml 3% 5.6
Prilocaine (Citanest) 400mg 10ml 4% 5.6
Bupivicaine (Marcaine) 90mg 1Bml 0.5% 10

142
CHLORAL HYDRATE - only non-barbiturate sedative-hypnotic agent indicated in the practice of NOTES
dentistry. Traditionally used ORALLY in pre-operative management of the ANXIOUS PEDIATRIC DENTAL
PATIENT. It has an unpleasant odor and bitter, caustic taste that can be partially masked in a flavored syrup.

• Rapidly absorbed after oral administration with an onset of action of 15-30min.lts duration of action
is -4hrs.

• Chloral hydrate is a sedative and hypnotic widely used for pediatric sedation.

• For children, chloral hydrate is available as a 500mg/5ml solution. The usual child dose is 50mglkg up
to a max of 19. Children will often enter a period of excitement and irritability before sedation, as it
affects brain centers that control wakefulness and alertness. Chloral hydrate DOES NOT RELIEVE PAIN.

• Chloral hydrate is a prodrug that is metabolized to the active metabolite (Trichloroethanol) which
may displace Warfarin from its protein binding sites causing an increase in the
hypoprothrombinemic response to warfarin.

• Sedative effects and/or respiratory depression with Chloral hydrate may be additive with other CNS
depressants, so monitor for increased effects (includes ethanol, anti-depressants, narcotic
analgesics, and benzodiazepines.

NITROUS OXIDE (N20) - a slight sweet smelling, colorless, inert gas at room temperature and
pressure that cannot produce general anesthesia EXCEPT if administered at concentrations> 80%
(thus, it cannot be used as a single agent to produce general anesthesia). At these concentrations, the
lack of oxygen causes hypoxia. Inhalant anesthetics like halothane & isoflurane can produce general
anesthesia at concentrations of 3-5%, thus are very useful in anesthesia. Nitrous oxide is stored under
pressure in steel cylinders painted blue. Oxygen is stored in green tanks.

• Advantages of Nitrous Oxide Analgesia: rapid onset of action, elevates pain threshold, produces
euphoria, pleasant induction, titratable, rapid and complete recovery, virtually no adverse effects in
absence of hypoxia, therapeutic for many medically compromised patients, and is suitable for all ages.

• Nitrous oxide is used to produce SEDATION &MILD ANALGESIA. Nitrous oxide's main therapeutic
effect is relaxation/sedation (mild analgesia is a secondary effect). N20 is usually used in 30-50%
concentrations along with pure oxygen. It is a colorless, non-irritating gas at root temperature and
pressure, and is non-flammable and non-explosive. Nitrous oxide delivery machines are pre-equipped
with a failsafe mechanism that will not allow less than 20% oxygen to be delivered to the patient
(nitrous oxide MUST be coupled with AT LEAST 20% oxygen). Nitrous oxide does not have local
anesthetic (analgesic) properties. Thus, local anesthesia must be used in conjunction with nitrous
oxide any procedure where pain is anticipated.

• Onset of sedation occurs within 5 min and the recovery is just as rapid. The FIRST SYMPTOM of
nitrous oxide onset is TINGLING OF THE HANDS. It is excreted unchanged by the lungs. Most common
complaint from patients taking N20 is mild nausea. Always give the patient 100% oxygen after the
procedure to prevent diffusion hypoxia.

• N20 is quickly absorbed from the lungs and is physically dissolved in the blood. There is no
biotransformation, and the gas is rapidly excreted by the lungs when the concentration gradient is
reversed. It is recommended that the patient be maintained on oxygen for 5-10 minutes AFTER the
sedation period. Nitrous oxide has a rapid onset (5min) and rapid recovery (5min).

• Contra indications: patients with upper respiratory infections, emphysema, bronchitis, 1st trimester
of pregnancy (long-term exposure to low nitrous oxide doses can increase the incidence of spontaneous
abortions), and in patients where communication is difficult (i.e. autistic patients). Nitrous is never
used on patients with a contagious disease as it is difficult to sterilize the entire tubing.
Environmental contamination by nitrous oxide is kept to a minimum by employing a scavenger system .

• Important: Nitrous oxide is a SEDATIVE, NOT a general anesthetic because hypoxic levels are required
to produce anesthesia . It is used alone to produce sedation or in combination with inhalation agents
to supplement the anesthetic response.
143
 Dose Response of Nitrous Oxide (Always given with at least 20% oxygen)
10-20% (N20) 20-40% (N20) >50% (N20)
Tingling of hands, feet, Mild sleepiness, relaxation, some This is too much nitrous
body warmth analgesia, mind dissociation, causes nausea & sweating
heightened auditory perception

INHALED AMMONIA - drug of choice for acting against SYNCOPE. Inhaled ammonia irritates
trigeminal nerve sensory endings to cause a reflex stimulation of the medullary respiratory and
vasomotor centers. An aromatic ammonia vaporole is crushed between the fingers and held near the
patient's nose. Administration of oxygen aids in combating tissue anoxia.

• Syncope Symtoms: beads of sweat on the upper lip, weak thready pulse, cold clammy skin, pallor
and a dizzy feeling. Loss of normal vasomotor tonus produces pooling of blood peripherally so that
normal blood volume becomes insufficient. Placing the patient in a SUPINE POSITION & ELEVATING
THE FEET gives the patient a transfusion of whole blood by utilizing forces of gravity. The head should
not be more than 10° lower than the rest of the body. Types of Syncope:
• Vasovagal, Neurogenic, & Orthostatic (treat all with high-flowing 100% oxygen).
• Hyperventilation Syndrome-oxygen is not indicated.
• 100% oxygen is contraindicated in patients with Chronic Obstructive
Pulmonary Disease (COPD).

4 Stages of General Anesthesia that apply to INHALANTS (not IV general anesthesia):

1. Stage 1 (Amnesia/Analgesia)-patient experiences analgesia, eventually amnesia.
2. Stage 2 (ExcitementlDelerium)-patient experiences excitation, struggles, and is possibly
delirious. Begins with unconsciousness, ending with loss of eyelid reflex, purposeless movements,
hyper-reaction, dilated pupils, reflex vomiting, tachycardia, and hypertension .
3. Stage 3 (Surgical Anesthesia)-patient begins stage with regular breathing, loss of reflexes, loss
of pupil eyelash reflexes, complete loss of pain. Has 4 planes.
4. Stage 4 (Medullary Paralysis)-patient begins stage with loss of all spontaneous breathing and
severe depression of vasomotor and respiratory centers in the Medulla. Cessation of respiration,
ending in death without proper treatment.

General Anesthesia Agents:

1. Inhalation Agents/Anesthetics: volatile liquids (i.e. Desflurane, Sevoflurane, Halthane, Isoflurane,
& Enflurane) that decrease arterial pressure.
• Isoflurane-increases coronary blood flow and is the safer drug to use if the patient has
ischemic heart disease. Used for elderly.
• Halothane & Enflurane-decreases cardiac output so NOT used for patients with history of
cardiac arrhythmias. Halothane sensitizes the heart to catecholamines, increasing risk of
ventricular arrhythmias in susceptible patients (cardiac disease, patients on
sympathomimetic drugs or high levels of catecholamines) . Enflurane-has CNS irritant effect
at high doses, abnormal spike patterns, so avoid in patients with seizure disorders.
• Ether (diethyl ether), Halothane, Enflurane, Isoflurane, Sevoflurane, Methoxyflurane, &
Desflurane are inhalation anesthetics. Inhalation anesthetics are drugs that are vaporized
from the liquid form and inhaled to produce general anesthesia. These diverse drugs are
simple lipophilic molecules ranging from ethers (diethyl ether), halogenated hydrocarbons
(halothane), and halogenated ethers (isoflurane, enflurane, sevoflurane, methoxyflurane,
and desflurane).

2. Intravenous Agents: a primary advantage of IV sedation is the ability to TITRATE

individualized dosage.
1. Barbiturates: Thiopental/Pentothal, Methohexital/Brevital.
• Thiopental (Pentothal)-most commonly used ultrashort-acting barbiturate.
• Methohexital (Brevital)-used in outpatient procedures due to more rapid recovery. High lipid
solubility so enters brain very rapidly and is redistributed to other tissues, so very short-
acting unless prolonged procedure (can accumulate, especially if liver dysfunction).
Respiratory depression with decreased CO & arterial BP.
144
2. Benzodiazepines-IV preparations of longer-acting Lorazepam (Ativan) &Diazepam (Valium) NOTES
provide preoperative seation (benzodiazepines do not provide anesthesia) but are more
irritating. Provide anterograde amnesia to procedure.
• Midazolam (Versed)-short-acting (very short Y2 life) and more common for pre-anesthesia
as part of "balanced anesthesia" program because it only makes the patient groggy, and
does not induce loss of consciousness. Preffered to diazepam for IV injection because
it is more water soluble.
• Diazepam (Valium) &Lorazepam (Ativan)-anti-anxiety drugs. Contraindicated in patients
with Narrow Angle Glaucoma. Diazepam is used for muscle spasticity in patients with
cerebral palsy. IV diazepam is useful in status epilepticus.
• Flumazenil-benzodiazepine antagonist that accelerates post -operative recovery from
benzodiapine sedation.
• Chlordiazepoxide (Librium), Clonazepam (Rivotril), Flurazepam (Dalmane), Temazepam
(Restoril), Triazolam (Halcion)
• Alprazolam (Xanax)-has selective anxiolytic effects in patients who suffer from Agoraphobia.
• Benzodiazepines are frequently prescribed for symptomatic treatment of ANXIETY &
SLEEP DISORDERS. They produce their effects via specific receptors involving GABA.
Benzodiazepines are the most effective ORAL SEDATIVE DRUGS USED IN DENTISTRY.
• Benzodiazepines are NOT useful to manage obsessive-compulsive disorders.
• Benzodiazepines (especially Diazepam & Chlordiazepoxide) are often prescribed for pre-
operative sedation. These drugs are tranquilizers used to produce conscious sedation in
anxious patients. Diazepam is more potent than Chlordiazepoxide. These drugs do not produce
hangovers like barbiturates and other sedative drugs. *00 not used these drugs
during pregnancy.

3. Neuroroleptanalgesics-neuroleptic-opioid combinations that combine Fentanyl & Droperidol.

Opioids-all provide analgesia and anesthesia . IV morphine &Fentanyl.
• Fentanyl-highly potent opioid used as premedication or adjunct to inhalational agents.
Used with haloperidol derivative Droperidal & NO to provide balanced anesthesia
"Neuroleptanesthesia." Often used with gaseous anesthesia. Fentanyl decreases pulmonary
ventilation &halothane's induction rate. Adverse: impaired ventilation &respiratory
depression, increase intracranial pressure, and may precipitate acute attacks in asthmatics.
Opioid adverse effects are reversed &recovery hastened by administration of Naloxone
(Narcan) an opioid antagonist.
• Fentanyl is available as a transumucosal preparation (Actiq), a transdermal
patch formulation (Duragesic), and as an IV preparation (Sublimaze).

4. Others:
• Propofol (Diprivan)-IV anesthetic with rapid onset/recovery (more rapid than barbiturates)
and better tolerated than other IV agents (popular "day surgery"). Metabolized in liver via
conjugation with very short t1I2. A respiratory depressant like thiopental, but produces
significant in arterial BP &CO.
• Benefits: antiemetic agent unlikely to produce vomiting and nausea, used for
induction or anesthesia maintenance. Does not increase intracranial pressure
so used in concerned patients. Safer for pregnant women and less likely to
produce bronchospams.
• Concerns: contraindicated in children because has produced severe acidosis if
respiratory infection present. Use with caution if patient has hypotension. Serious
infections in some patients after use.
• Etimodate (Amidate)-major advantage over other IV drugs with minimal respiratory &
cardiovascular depressant effects. Rapid induction & recovery, but no analgesic effects.
Often used with opioids, does not produce hypotension or have significant HR effects.
Used if coronary artery disease or hypovolemia is present, and maintains cardiovascular
stability. Adverse: high incidence of vomiting, and serious adrenocorticosuppression.

145
 • Ketamine-drug of choice for "Dissociative Anesthesia". IV ketamine causes catatonia,
amnesia, &analgesia without loss of consciousness by acting as an antagonist at N-
methyl-D-Asparate (NMDA) receptor, blocking excitatory effects. Ketamine is highly
lipophilic and undergoes redistribution & hepatic metabolism. Ketamine is the ONLY
anesthetic that acts as cardiovascular stimulant. Significantly increases cerebral blood flow
& intracranial pressure, so avoid use of brain tumor or head injury. Adverse: abnormal
sensory perception, strange dreams, disorientation ("emergence phenomena"). Give
Diazepam to minimize. limited use, but sometimes used in children or patients in shock due
to its cardio-stimulatory properties. Does not produce bronchospasms so used in
asthmatics. Not good for adults, children tolerate it better.

ANTI-ANXIETY AGENTS
Benzodiazepines, Barbiturates, & Narcotic Analgesics ALL produce SEDATION and can cause
physiologic dependence.
• Flumazenil {Mazicon)-a benzodiazepine ANTAGONIST used to REVERSE residual effects of
benzodiazepines in the event of an overdose.

Tranquilizer-a drug that promotes tranquility by calming, soothing, Quieting, or pacifying without
sedation or depressant effects.
• Major tranquilizers: anti-psychotic agents.
• Minor tranquilizers: anti-anxiety agents (Benzodiazepines).

BENZODIAZEPINES (MINOR TRANOUILIZERS) - used as oral preparations to alleviate anxiety

(anti-anxiety), induce sleep (sedative-hypnotic), anti-convulsant, and skeletal muscle relaxant. Used for
IV conscious sedation during outpatient surgery. Benzodiazepines produce their calming effects by
DEPRESSING THE LIMBIC SYSTEM &RETICULAR FORMATION through potentiation of the central inhibitor
neurotransmitter (neurons) gamma-amino-butyric acid (GABA). Tolerance and physical dependence can
occur with prolonged high dosage, but they are much safer than barbiturates.
• Adverse Effects: CNS depression (fatigue, slurred speech, drowsiness, sleepiness/sedation, &
confusion, disorientation), GI disturbances (dry mouth, vomiting, nausea, diarrhea), other effects
are hypotension, ataxia, and muscle relaxation. Never take benzodiazepines with alcohol as
serious potentiation of the sedative effects of each can occur causing unexpected inebriation &
respiratory depression. However, with normal doses, benzodiazepines rarely effect the respiratory
system of healthy individuals.

• Benzodiazepines taken orally as Tranquilizers: Chlordiazepoxide (Librium), Lorazepam (Ativan),

Alprazolam (Xanax), & Diazepam (Valium) .

• Benzodiazepines presrcribed as HYPNOTICS for Insomnia: Flurazepam (Dalmane), Temazepam , &

Triazolam (Halcion).
• Triazolam {Halcion)-a pre-operative sedative in dentistry that is metabolized in the liver by
P450 isoform GYP 3A4 enzyme. Drugs that inhibit the actions of GYP 3A4 affect triazolam by
causing an increase in serum levels of triazolam . Triazolam interacts with drugs that inhibit
its metabolism via the GYP 3A4 enzyme. Drugs that inhibit the metabolic pathway may have
a profound effect on the clearance of triazolam . The resultant effects would be an increase in
serum concentrations with an associated unexpected increase in the actions of triazolam.
Thus, triazolam is avoided in patients receiving potent inhibitors of CYP 3A4.
• Antifungal agents (ltraconazole, Ketoconazole, Fluconazole, Miconazole, Voriconazole)
can significantly elevate triazolam serum levels causing toxicity with therapeutic doses.
These antifungals inhibit GYP 3A4 isoform responsible for hepatic metabolism of triazolam,
thus inhibiting the normal metabolism of triazolam. 00 not administer triazolam to
patients taking these antifungals.

• Midazolam (Versed)-comes in liquid form for pre-operative sedation in children, and as an

injectable for IV conscious sedation. An important adjunct in the practice of anesthesiology, used as
pre-operative sedatives and induction agents, and to maintain anesthesia .

146
DIAZEPAM (VALIUM) - prescribed to treat anxiety, nervous tension, muscle spasm, & NOTES
seizures/convulsions. Diazepam is preferred over a barbiturate as an anti-anxiety medication since it
has less addiction potential, and produces less profound CNS depression . Diazepam affects the limbic
system of the brain (controls emotion).

• Indications: agent of choice to reverse status epilepticus induced by a local anesthetic overdose.

• If given IV for status epilepticus, use a LARGE VEIN to decrease the risk of thrombophlebitis
(propylene glycol is the substance in the IV mixture that is the main cause of thrombophlebitis
after IV administration of Diazepam). An important adjunct in the practice of anesthesiology, used
as pre-operative sedatives and induction agents, and to maintain anesthesia .

• Contraindications: acute narrow-angle glaucoma & psychoses.

• Adverse Effects: most common side effects are drowsiness and fatigue. At a high therapeutic index,
produces some amnesia, can be locally irritating to tissue, and may produce local thrombophlebitis.
Serious adverse reactions are withdrawal symptoms caused by discontinuation of treatment. .."
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• Diazepam is the drug of choice to treat lidocaine-induced seizures. ".
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BUSPIRONE (BUSPAR) - a minor tranquilizer orally administered anxiolytic (anti-anxiety agent) ."
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whose mechanism works by DIMINISHING SEROTONERGIC ACTIVITY. Buspar is structurally and
pharmacologically distinct from all other anxiolytics (including benzodiazepines & barbiturates) and
distinct as it does not have anti-convulsant or muscle relaxant properties, does not impair
psychomotor function or cause sedation (lacks CNS depressant activity) or physical dependence.
Buspirone's special characteristics:

• Slow onset of action (may take up to two weeks).

• Different mechanism of action than barbiturates or benzodiazepines. Most likely acts as a partial
agonist on certain 5-hydroxytryptamine (serotonin) receptors, and diminishes serotonergic action.

• Fewer side effects and less sedation than benzodiazepines.

• Low abuse potential (benzodiazepines & barbiturates have abuse potential and may
cause dependence).

• Does not possess hypnotic or anti-convulsant properties (benzodiazepines & barbiturates do).

• Side effects: limited to restlessness, dizziness, headache, nausea, diarrhea, &paresthesias. Tardive
dyskinesia is possible with long-term Buspirone therapy.

ETHYl ALCOHOL (ETHANOL) - causes a well-marked DIURESIS by inhibiting the production of

ANTIDIURETIC HORMONE (ADH) or "vasopressin". ADH decreases urine production by increasing water
reabsorption by the renal tubules. Without ADH, there would be extreme water loss into the urine.

• Ethyl alcohol DILATES blood vessels in the skin , depresses the CNS, and in blood levels> 400mg%
usually causes coma and death. Alcohol euphoria results from removal of inhibitory activity of the cortex.

• Recent evidence shows that frequent ingestion of moderate amounts of alcohol in any form (beer,
wine, distilled spirits) reduces the risk of heart disease, especially in men .

• Ethanol is a sedative; a hypnotic drug and the most important alcohol of pharmacologic interest.
Ethanol abuse is responsible for many socioeconomic problems. Methanol and Ethylene Glycol are
other alcohols.

• Drugs that are synergistic with Ethanol: Diazepam, Meperidine, Pentobarbital, &Chlorpromazine.
When combined with alcohol, these drugs can cause fetal oversedation. *Synergism-the combined
action of two or more drugs that is GREATER than the sum of their individual actions or that achieved
with a single drug.
147
 DISULFIRAM (ANTABUSE) - used to manage ETHANOL ABUSE. Disulfiram is not a cure for alcoholism,
but deters ethanol consumption. It is an antioxidant that interferes with the hepatic oxidation of the
acetaldehyde metabolized from alcohol by inhibiting ALDEHYDE DEHYDROGENASE, a mitochondrial
liver enzyme.

• Even the ingestion of small amounts of ethanol results in high concentrations of acetaldehyde in the
body. The unpleasant reaction that occurs "Disulfiram-Ethanol Reaction WER)" consists of a
throbbing headache, dyspnea, throbbing in the neck, nausea, copious vomiting, thirst, tachycardia,
and hypotension.

• Metronidazole also inhibits aldehyde dehydrogenase.

BARBITURATES - are HYPNOTICS/SEDATIVES that depress neuronal activity by increasing membrane

ion conductance (mainly chloride), reducing glutamate-induced depolarizations, & potentiating
(prolonging) the inhibitory effects of GABA. The primary pharmacologic effect of barbiturates is to
DEPRESS NERVOUS TISSUE. They are metabolized in the liver, and possess serious drug dependence
potential (can produce dependence). They do not possess analgesic properties. Barbiturates all have
abuse and addiction potential, thus are controlled substances that require a DEA number. Barbiturates
depress neuronal activity in the midbrain reticular formation, facilitating and prolonging the inhibitory
effects of GABA and Glycine.

Barbiturates use is determined by their DURATION OF ACTION:

1. Ultra-short acting Barbiturates: used IV to induce general anesthesia. The brief duration of
general anesthetic action is due to the rapid rate of redistribution from the brain (CNS) to
peripheral tissues. Ultra-short barbs will only maintain anesthesia while in the brain. Due to
their high lipid solubility, they rapidly exit the brain to other tissues, causing the patient to
awake within a few minutes after administration. For extensive procedures, ultra-short barbs are
used to induce Stage III surgical anesthesia. For very brief procedures, they can be used alone.
Length of hypnotic action: 5-20 minutes. These are the MOST LIPID SOLUBLE (so shortest
duration of action).

• Thiopental (Pentothal), Thiamylal (Surital) & Methohexital (Brevital)-ultra-short barbs only

given by IV injection. Thiopental is the barbiturate that MOST readily penetrates the blood-
brain barrier. Contra indications: porphyria, liver dysfunction (since they are metabolized in
the liver), emphysema, & previous addiction to sedative hypnotic drugs.

2. Short-acting Barbiturates: used orally for their hypnotic, calming effect to treat INSOMNIA.
Given pre-operatively before a dental appointment to relieve anxiety. Length of hypnotic
action: 1-3 hours.
• Secobarbital (Seconal) & Pentobarbital (Nembutal).

3. Intermediate-acting Barbiturates: may also be prescribed to relieve anxiety before a dental

appointment, although their side effects last longer than short-acting barbs. Also used for daytime
sedation and to treat insomnia by suppressing REM sleep. Length of hypnotic action: 3-6 hours.
• Amobarbital (Amytal) & Butabarbital (Butisol).

4. Long-acting Barbiturates: treats mainly daytime sedation & epilepsy (anti-convulsant). Duration
of action is related to the lipid solubility, thus long-acting barbs are the LEAST LIPID SOLUBLE
(longest duration of action). Metabolized in the liver, these drugs produce serious drug
dependence, but do not possess significant analgesic properties. Length of hypnotic action:
6-10 hours.
• Phenobarbital (Luminal)-a barbiturate used as a sedative-hypnotic (eNS depressant).
Not used in oral surgery.

• Mephobarbital (Mebaral), & Primidone (Mysoline)

148
• Barbiturates may decrease the half-lives of those drugs metabolized by the liver by inducing
formation of the liver's microsomal enzymes that metabolize drugs, which leads to an increased
clearance of the affected drugs and a decrease in the drug's effectiveness. Barbiturates exhibit a
steeper dose-response relationship than benzodiazepines, and may precipitate acute porphyria in
susceptible patients.

• Cause of death from ACUTE barbiturate poisoning or overdose is RESPIRATORY FAILURE. Other
adverse reactions are eNS depression, euphoria, and habituation . The most important therapeutic
measure taken in the event of barbiturate poisoning is to ASSURE ADEQUATE RESPIRATION.

• Barbiturates are contraindicated in patients with respiratory disease or pregnant patients.

• Physical dependence usually develops if barbiturates are abused. The dependence has a strong
phychological and physical basis. Sudden withdrawal from high doses can be fatal.

CARDIOVASCULAR AGENTS
ANTI-ARRHYTHMICS AGENTS - are classified according to Vaughan-Williams Classification System
which places available anti-arrhythmic agents into 4 groups denoted by Roman numerals (I, II, III, IV).
This system is loosely based on the channel or receptor that is involved. Most drugs that treat cardiac
arrhythmias act primarily by INCREASING the refractory period of cardiac muscle.
1. Sodium Channel Blockers: are further classified based on their effects on "action
potential duration":

• Group IA: Quinidine, Procainamide, Amiodarone, &Disopyramide PROLONG action potential.

• Procainamide-a potent Group IA anti-arrhythmic agent used to treat severe
cardiac arrhythmias (atrial fibrillation, atrial flutter, paroxysmal atrial tachycardia,
and ventricular tachycardia). It is a derivative of the ester local anesthetic procaine
(novocaine). Its properties are similar to other Group IA agents which decrease
myocardial conduction velocity, excitability, and contractility by inhibiting Na+
influx through "fast" channels of the myocardial cell membrane, thus increasing
the recovery period after repolarization.
• Quinidine-primary used to treat supraventricular tachyarrhythmias, but is
contraindicated in some arrhythmias, especially those associated with heart block.

• Group IB: Lidocaine, Mexiletine, &Tocainide SHORTEN action potential.

• Group IC: Flecainide, Moricizine, & Propafenone do not effect action potential duration.

• Lidocaine (Xylocaine): a sodium-channel blocker ANTI-ARRHYTHMIC AGENT effective ONLY on

the ventricle, often administered intravenously to treat life-threatening ventricular
arrhythmias. When given IVto treat ventricular arrhythmias, it acts on the fibrillating
ventricles to decrease cardiac excitability and spares the atria. It can effectively reverse a
life-threatening situation .

• Quinidine-a sodium-channel blocker and PROTOTYPE anti-arrhythmic agent used mainly to

treat ATRIAL FIBRILLATION. It is not effective for treating life-threatening ventricular fibrillation.

• Disopyramide (Norpace)-a newer anti-arrhythmic agent (sodium-channel blocker) used to

convert atrial arrhythmias into normal sinus rhythm.

• Propafenone (Rythmol)-another newer sodium-channel blocker to treat ventricular

arrhythmias & supraventricular tachycardias.

149
 2. Beta-Adrengeric Blockers: Propranolol & Esmolol are prototype anti-arrhythmic beta-blockers.
Beta-blockers (Group II agents) as anti-arrhythmics are reserved for patients who only require
control of ventricular rate during atrial tachyarrhythmias, or who have mildly symptomatic
ventricular arrhythmias. Side effects: bradycardia & hypotension.

3. Potassium Channel Blockers: Amiodarone (Cordarone)-the prototype Group III agent that is
considered a Group III agent even though it also blocks Na+ channels (Group I action).
Amiodarone is unique because it is the most potent and "broad-sprectrum" anti-arrhythmic
compound available. It blocks Na+, Ca2+, K+ channels, and beta receptors. It has impressive
efficacy in suppressing supraventricular and ventricular arrhythmias.

4. Calcium Channel Blockers: Verapamil is the prototype Diltiazem & Nifedipine are also calcium
channel blockers useful as anti-anginal agents to treat chronic stable angina pectoris by
blocking calcium entry through the membranous calcium ion channels of cardiac and vascular
smooth muscle to cause two effects:
1. peripheral arterioles dilate (vasodilators), and total peripheral resistance (TPR) decreases,
reducing after-load and reducing myocardial oxygen requirements.
2. increases oxygen delivery to the myocardium.
• Verapamil-prototypical Group IV (calcium channel blocker) anti-arrhythmic agent that
inhibits intracellular entry of calcium through the slow channels of calcium-dependent
myocardium tissues that are concentrated in the heart's SA & AV nodes. Of the calcium
ion channel antagonists, only Verapamil and Diltiazem possess significant anti-arrhythmic
activity. Drug of choice to suppress paroxysmal supraventricular tachycardias stemming
from the AV node, characterized by rapid cardiac rate of 160-190 beats/minute. Useful to
treat angina, hypertension, and supraventricular tachyarrhythmias.
• Calcium Channel Blockers have been associated with causing GINGIVAL HYPERPLASIA.

ANTI-HYPERTENSIVE AGENTS - lower BP by reducing total peripheral resistance (TPR) &cardiac

output (CO) via various mechanisms. 4 anti-hypertensives classified by their mechanisms of action:
1. Diuretics-inhibit Na+ reabsorption in the renal tubular cells in the kidney to cause excess Na+
and urinary excretion, causing reduced blood volume.
2. Beta-Adrenergic Receptor Blockers (Beta Blockers)-reduce the volume of cardiac output into
the circulation, causing reduced peripheral pressure. There are 2 types of Beta Blockers:
• Cardioselective Beta Blockers-block beta 1 receptors in the heart muscle, such as Atenolol
(Tenormin) and Metoprolol (Lopressor & Toprol XU.
• Non-Cardioselective Beta Blockers-include Nadolol (Corgard) and Propranolol (Inderal).
3. Angiotensin-Coverting Enzyme Inhibitors (ACE Inhibitors)-include Lisinopril (Prinivil; Zestril),
and Enalapril (Vasotec). ACE inhibitors, "inhibit" the conversion of inactive Angiotensin
I Angiotensin II (a vasoconstrictor). This causes peripheral vasodilation and secondarily increases
urinary volume excretion. Both actions cause reduced BP.
4. Calcium Channel Blockers-include Amlodipine (Norvasc), Diltiazem (Cardizem), and Nifedipine
(Procardia). These drugs inhibit calcium from entering into vascular smooth muscle, to cause
vasodilation of the coronary and peripheral blood vessels, causing lower BP.

Miscellaneous Anti-Arrhythmic Drugs: Adenosine & Digoxin (Lanoxin/Digitalis):

DIGOXIN (LANOXIN) - the most versatile and widely used cardiac glycoside that causes a positive
inotropic effect (stronger heart beat) that directly increases the force of myocardial contractions (an
anti-arrhythmic drug) . This positive inotropic effect is independent of a normal sinus rhythm and
adrenergic stimulation.
• Cardiac glycosides-are often called "Digitalis" since several are derived from the digitalis (foxglove)
plant. Treat most supraventricular arrhythmias, cardiogenic shock, & congestive heart failure
(CHF) by helping the heart beat stronger (positive inotropic effect), slower (bradycardia), and
more efficiently.
• Cardiac glycosides INHIBIT the Na-K-ATPase membrane pump by inhibiting adenosine
triphosphate (ATP) enzymes (transport ATPase or Na-K-ATPase). Na-K-ATPase splits ATP in the
nerve and muscle cell to provide energy to transport Na+ across the cell membrane. Inhibition the
Na-K-APTase enzyme causes increased Ca2+ influx to augment the positive inotropic effect of
cardiac glycosides.

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• Adverse Effects: appetite loss and diarrhea. Contraindications: ventricular fibrillation &ventricular NOTES
tachycardia.

ANGINA PECTORIS - pain in the heart &chest that occurs during occlusion of the coronary arteries,
triggered by physical exertion, increased BP, &vasoconstriction. ANTI-ANGINAL DRUGS: Prevent or
Provide Relief of Angina Pectoris:
1. Nitroglycerin/Nitrostat (Nitrates)-a coronary artery vasodilator that relaxes blood vessels to
provide increased blood flow and oxygenation to heart muscle. If administered SUBLINGUALLY, it
is effective within 2-4min. The skin patch releases the drug over a 12-hour period to provide
sustained blood levels to prevent angina. It is the single most effective anti-anginal agent
available to manage acute angina episodes. It is fast-acting and relieves ACUTE ANGINAL
ATTACKS in the dental office. For angina, Nitroglycerin & Nifedipine are usually used
BEFORE Verapamil.
2. Amyl Nitrite (Nitrites)-a vasodilator and highly volatile substance only administered by
INHALATION. Used in the emergency treatment of CYANIDE pOisoning because it OXIDIZES
HEMOGLOBIN into methemoglobin which binds cyanide tightly to keep it in the peripheral
circulation and prevent it from accessing tissues. It is the most rapidly acting anti-anginal drug
that produces effects within 10 seconds, but its duration of action is only 3-5min. Due to its
extreme potency, there are uncomfortable side effects that invariably occur with its use (fainting
and pounding headache) . Amyl nitrite is rarely prescribed, and is NOT the drug of choice to
treat angina. It is abused to produce euphoria and as a sexual stimulant. Adverse Effects:
orthostatic hypotension &headache.
3. Dipyridamole (Persantine)-a non-nitrate vasodilator that treats angina (anti-anginal).
4. Verampamil (lsoptin), Nifedipine (Pro cardia) &Diltiazem (Cardizem)-calcium channel
blockers that prevent angina attacks by dilating coronary blood vessels to improve blood flow to
the heart muscle. Ca2+ channel blockers are "indirect vasodilators" given ORALLY to treat
mild-to-moderate hypertension.
5. Propranolol (lnderal), Nadolol (Corgard), &Atenolol (Tenormin)-beta adrenergic blockers
that prevents angina pectoris attacks by decreasing the heart's work load so that less oxygen
is required.

DIRECT VASODILATORS - exert anti-hypertensive effects (treat hypertension) by causing a direct

vasodilator action on the SMOOTH MUSCLE of arterioles, to produce a decrease in peripheral resistance
&BP. Compensatory responses may be marked such as salt retention and tachycardia. Adverse Effects:
GI upset, headache, dizziness, and tachycardia.
1. Hydralazine (Apresoline)-a direct vasodilator that treats hypertension.
2. Minoxidil (Loniten)-extremely efficacious direct vasodilator, thus is reserved for
SEVERE HYPERTENSION.
3. Diazoxide (Hyperstat)-parenteral vasodilator used in hypertensive emergencies.
4. Sodium Nitroprusside (Nipride)-parenteral vasodilator used in hypertensive emergencies.
5. Nitroglycerin (Nitrostat)-a direct vasodilator that treats angina pectoris and hypertension.

ACE Inhibitors & Angiotensin II Receptor Blockers: indirectly inhibit fluid volume increases when
interfering with Angiotensin II because Angiotensin II stimulates the release of ALDOSTERONE which
promotes Na+ and H20 retention.
• Angiotensin-Converting Enzyme (ACE) Inhibitors: interfere with the conversion of Angiotensin I (weak
vasoconstrictor) into Angiotensin II (highly effective vasoconstrictor that simulates the release of
Aldosterone) by inhibiting the ACE enzyme. ACE inhibitors drugs treat hypertension and congestive
heart failure (CHF). Adverse Effects: cough, hypotension, neutropenia, anorexia, and polyuria.
• Captopril (Capoten)-an angiotensin-converting enzyme inhibitor (ACE inhibitor).
• Benazepril (Lotensin), Enalapril (Vasotec), Fosinopril (Monopril), lisinopril (Zestril), Perindopril
(Aceon), Quinapril (Accupril), Ramipril (Altace)
• Angiotensin II Receptor Blockers-a new class of BP medications that INHIBIT Angiontensin II at
its receptor site to prevent ANG-2 from constricting blood vessels that raise BP. Losartan, Valsartan,
Candesartan, &Irbesartan.

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 RENIN - a proteolytic enzyme produced by and stored in the juxtaglomerular apparatus in the kidney
that surrounds each arteriole as it enters the glomerulus. Renin is released into the bloodstream where
it has an important role in ANGIOTENSIN FORMATION . Renin acts on the precursor substance
angiotensinogen which is manufactured by the liver and is present in the blood. Renin converts
Angiotensinogen Angiotensin I. Then Angiotensin I is converted into Angiotensin II by Angiotensin
Converting Enzyme (ACE) which is associated with the capillary walls in the lungs.
• Angiotensin II-a potent vasopressor that increases total peripheral resistance (TPR), and
stimulates aldosterone release to cause an increase in plasma volume, venous return, stroke
volume, and ultimately an INCREASE IN CARDIAC OUTPUT.

DIURETICS - antihypertensive agents used to treat congestive heart failure by relieving edema and
symptoms of dyspnea arising from pulmonary congestion. Diuretics also treat hypertension and manage
edema associated with hepatic or renal disease. There are 4 categories of widely used diuretics:
1. Potassium (K+)-Sparing Diuretics-cause Na+ & K+ concentrations at the end of the distal
convoluted tubules. Postassium sparing diuretics act in the collecting tubule to inhibit Na+
reabsorption, K+ secretion, & H+ secretion. HYPERKALEMIA is the most important toxic effect of
potassium-sparing diuretics. Potassium-sparing diuretics conserve K+ while cuasing diuresis.
Thus, no potassium is lost from the body as with other diuretics (i.e. Thiazides & Loops). 2 Types
of Potassium-Sparing Diuretics:
1. Aldosterone Antagonists in Collecting Tubules:
• Spironolactone (Aldactone)-a pharmacologic antagonist of aldosterone in the collecting
tubule. Treats primary aldosteronism & heart failure since hyperaldosteronism is common
in heart failure patients. Spironolactone competes with aldosterone receptor sites in the
renal tubules causing increased secretion of Na+, CI, and H20, while conserving K+.
2. Sodium Channel Blockers in Collecting Tubules:
• Amiloride (Midamor)-blocks Na2+ channels in luminal membrane of principal cells in
the late distal tubule &collecting duct which decreases K+ excretion. It inhibits Na+
transport through ion channels in the luminal membrane causing a decrease in
Na+K+ exchange.
• Triamterene (Dyrenium}-K+ sparing diuretic that promotes Na+ & H20 excretion, but
maintains K+.

2. Thiazides Diuretics-inhibit sodium reabsorption in the distal portion of the renal tubule within
the kidney causing increased excretion of Na+ & H20 (affects salt transport in the distal convulted
tubule). Thiazide diuretics are the most widely used diuretic drugs used to treat hypertension,
but may require supplemental administration of K+ (postassium). Inhibits Na+/CI- symport.
• Dyazide-brand name forthe combination ofTriamterene + Hydrochlorothiazide (HCTZ). Dyazide
combines the K+-sparing diuretics with HCTZ for greater efficacy than either drug individually.
• Metolazone-oral Quinazoline & sulfonamide diuretic to manage edema &hypertension; not
a true thiazide. Produces diuresis in patients with impaired renal function. More potent than
thiazides causing Na+ excretion in advanced renal failure unlike thiazides.
• Indapamide-an oral antihypertensive & diuretic and first of a new class of
antihypertensive/diuretics (indolines). Fat-soluble, non-thiazide diuretic with lO-22hr );2 life.
Used in advanced renal failure to stimulate additional diuresis in conjunction wi loop
diuretics.Metabolized & excreted by GI tract and kidneys, and is less likely to accumulate in
patients with renal failure, and may be useful in their treatment.
• Other thiazide diuretics: Chlorothiazide, Cyclothiazide, Polythiazide, Benzthiazide.
• Sulfonamide derivatives structurally related to carbonic anhydrase inhibitors.
• All are secreted by the organic acid secretory system in the kidney.
• Major Actions:
• Inhibits sodium chloride (NaCI) resorption from luminal side of epithelial cells by inhibiting
Na+/CI co-transporterlsymporter on the membrane.
• Inhibits NaCI transport in early segment of distal convoluted tubule.
• Increases concentration of Na+ & CI- in tubular fluid.

152
 • Thiazides Treat: NOTES
1. Hypertension (anti-hypertensive drugs) by decreasing systolic & diastolic BP.
2. Edema of CHF decreasing extracellular volume.
3. Renal Edema (nephrotic syndrome) if loop diuretics fa il.
4. Hypercalciuria (increase uric acid in urine-inhibit urinary Ca2+ excretion) . Treats patients
wi calcium oxalate stones in urinary tract (calcium nephrolithiasis).
5. Nephrogenic Diabetes Insipidus (lack of responsiveness to ADH)-thiazides produce
hyperosmolar urine due to volume contraction causing increased reabsorption at proximal
tubule. Thiazides treat this by substituting ADH.

• Thiazide Adverse Effects (CNS, hematological, sexual, GI, dermatological disorders) :

1. Hypokalemia (K+ deficiency) is the most common problem with thiazide diuretics & can
predispose patients on digitalis to ventricular arrhythmias. Treat with Spironolactone to
maintain K+ levels.
2. Hyperuricemia (increase serum uric acid) by decreasing acid excreted . Can cause gout
(uric acid deposits in joints).
3. Hypercalcemia (inhibits Ca2+ secretion causing increased Ca2+ in blood).

3. Loop (High-Ceiling) Diuretics-inhibit Na+K+2CI- symport or cotransport. Inhibit reabsorption

of Na+ and chloride in the ascending Loop of Henle to cause increased secretion of H20, Na+, &
CI. Furosemide (Lasix) is the prototype loop diuretic. Other loop diuretics: Bumetanide,
Torsemide, & Ethacrynic acid
• Mechanism of Action: increase Ca2+ content of urine, while thiazide diuretics decrease
Ca2+ concentration of urine.
• Cause decreased renal vascular resistance and increased renal blood flow.
• Acutely loop diuretics increase excretion of uric acid, where as chronic admin causes
reduced uric acid excretion, and increases renal blood flow.

• Therapeutic uses: acute pulmonary edema of CHF, loop diuretics are DRUG OF CHOICE.
Useful in emergencies due to their rapid onset of action. Treats hypercalcemia by stimulating
tubular Ca2+ secretion, and treat hypertension when other diuretics and antihypertensives do
not produce a satisfactory response .

• Adverse Effects: OTOTOXICITY as tinnitus, hearing impairment, deafness, vertigo, &sense

of ear fullness.
• Loop diuretics are toxic to the ear especially when used with aminoglycosides (antibiotics).
• ETHACRYNIC is the most ototoxic.
• Irreversible damage may result with continued treatment, and vestibular function is less
likely to be distributed, but it too may be affected by prolonged combined treatment.
• Hyperuricemia, acute hypovolemia (reduced blood volume), increase plasma LOL
cholesterol and triglycerides, and decrease HOL.
• Skin rashes, photosensitivity, paresthesias, K+ depletion, &bone marrow depression.

4. OSMOTIC DIURETICS-highly fi ltered by the glomerulus and exerts a solute-induced diuresis in the
proximal tubule. Osmotic diuretics are used to reduce excess edema associated with
neurosurgery or trauma to the CNS. Mannitol (Osmitrol), Glycerin (Glyrol), Isosorbide (lsmotic),
&Urea (Ureaphil). Must be given via injection.
• Mannitol-treats cerebral edema, increases delivery of Na2+ & water out of loop of Henle.
Mannitol is NOT absorbed orally so it MUST be given intravenously.
• Osmotic diuretics are not useful in treating conditions where Na+ retention occurs, but are used
to maintain urine flow after acute toxic ingestion of substances capable of producing acute
renal failure.
• Osmotic diuretics treat patients with increased intracranial pressure, or acute renal failure
due to shock, drug toxicities, and trauma.

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 NOTES CORTICOSTEROIDS (STEROIDS) - steroid hormones produced by the ADRENAL CORTEX that DO
NOT CURE any disease (they represent replacement only Addison's Disease).
• Corticosteroids treat asthma, arthritis (if patient has peptic ulcer disease, do not use
corticosteroids for arthritis), allergic reactions, Addisons, Lupus Erythematosus, Apthous
Stomatitis, and TMJ pain.

Corticosteroids consist of two major groups:

1. MINERALCORTICOIDS-regulate Na+ and K+ reabsorption (metabolism) in the kidney's
collecting tubules.
• Aldosterone-the MAJOR natural mineralcorticoid in humans, secreted by cells in zona
glomerulosa of the adrenal cortex. Aldosterone secretion is regulated by ACTH and the ren in-
angiotensin system , and is very important in regulating blood volume &blood pressure, and
promotes Na+ reabsorption into the blood from the glomerular filtrate . K+ is lost in urine
because of the electronegativity created by the reabsorption of Na+ in the kidney tubules.
Increased blood aldosterone levels result in high sodium and low potassium levels in
the plasma.
• Decreased Na+ concentration causes the juxtaglomerular cells of the kidneys to secrete
RENIN which converts angiotensinogen angiotensin I. Angiotensin I is converted into
Angtiotensin II which then stimulates the adrenal cortex to release aldosterone.
• Addison's Disease-caused by HYPOSECRETION of aldosterone & cortisol. For adrenal crisis,
treat with 2ml of cortisol (hydrocortisone). Corticosteroids represent replacement only in
Addison's Disease.
• ADH (vasopressin)-decreases urine production by increasing water reabsorption by the renal
tubules (it increases the permeability of the collecting ducts &distal tubules). Without ADH,
there would be extreme water loss into the urine. At high concentrations, ADH causes
arterioles to constrict (increases BP).
• Other Mineralocorticoids: Deoxycorticosterone & FI ud rocortisone.
• Pharmacological Effects of Mineralocorticoids: increase in Na+ retention, and decrease
K+ that can cause edema and hypertension. If excessive, it may lead to dehydration . If
insufficient, may lead to hypotension .

2. GLUCOCORTICOIDS-have important effects on carbohydrate, lipid , and protein metabolism,

catabolism, immune responses, and inflammation (used as anti-inflammatory agents). The
majority of anti-inflammatory and immunosuppressive actions of the glucocorticoids are the
result of their action on ARACHIDONIC ACID METABOLISM. They induce the synthesis of a
protein that inhibits phospholipase A2, which decreases production of prostaglandins
and leukotrienes.
• Cortisol (Hydrocortisone)-the MAJOR glucocorticoid that treats Addison's Disease.
• Synthetic Glucocorticoids: Prednisone (Deltasone) & Prednisolone (Prelone),
Methylprednisolone, Dexamethasone (Decardon) & Triamcinolone (Atolone).
• Beclomethasone, Budesonide, &Flunisolide: special glucocorticoids (INHALERS) developed
to treat chronic asthma and bronchial disease by readily penetrating the airway mucosa ,
but have very short half-lives after they enter the blood so system ic effects and toxicity are
greatly red uced .
• Fluticasone (Flonase or FloventJ-a corticosteroid administered by inhalation to treat
ASTHMA by decreasing inflammation in the airway of asthmatics. This reduced inflammation
enhances bronchodilating effects of the b2 adrenergic agonists.
• Other inhaled (aerosol) corticosteroids that treat asthma: Triamcinolone (Azmacort) ,
Beclomethasone (Beconase), & Budesonide (pulmicort).
• Inhaled steroids very often cause fungal infections of the mouth &throat. Localized
infections with Candida albicans occur frequently in the mouth and pharynx with repetitive
use of inhalant corticosteroids.
• Inhaled corticosteroids used for asthma, and nasal spray corticosteroids used for
seasonal allergies do not achieve significant blood levels to cause the adverse effects
caused by oral corticosteroids, so are used for their localized effects. Popular nasal spary
corticosteroid products are Triamcinolone (Nasocort), Fluticasone (Flonase), and Budesonide
(Rhinocort).

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Pharmacological Effects of Glucocorticoids: NOTES
• Decrease in glucose utilization and inhibits protein synthesis.
• Increases protein catabolism and gluconeogenesis (by breaking down endogenous proteins to amino
acids, that are then converted to glucose for storage in the liver or for use by the body.
• Impaired wound heal ing and decreased resistance to infection .
• Anti-inflammatory action, immunosuppression, and anti-allergenic action. These effects occur in
target cells after the interaction of the steroid with a specific glucocorticoid receptor.

CORTICOSTEROID CONTRAINDICATIONS - latent TB, viral (herpes), or fungal infections, AIDS,

and patients with peptic ulcer disease (specifically gastric ulcers), and congestive heart failure.
Corticosteroids may cause PEPTIC ULCERS.

CORTICOSTEROID TOXIC EFFECTS - growth inhibition, hyperglycemia, osteoporosis, psychosis,

and salt retention.

CORTICOSTEROID ADVERSE REACTIONS - Cushing's Syndrome (obesity and weakening of

muscles), hyperglycemia, osteoporosis, peptic ulcers, and increased risk of infection.

HMG-COA REDUCTASE INHIBITORS ("STATIN" DRUGS) - a class of drugs that LOWERS BLOOD
CHOLESTEROL levels by inhbiting a key enzyme in the cholesterol synthesis pathway in the liver. HMG-
CoA Reductase is an enzyme called "hydroxyl methylglutaryl coenzyme Areductase which is necessary
in the key step to synthesize cholesterol. When the "statin" drugs inhbit this enzyme, cholesterol is not
produced in the liver, which decreases blood cholesterol levels.

• "Statin" Drugs: Atorvastatin (Lipitor), Simvastatin (Zocor) , Fluvastatin (Lescol), Lovastatin

(Mevacor), & Pravastatin (Pravachol).

• Coronary Artery Disease (CAD)-a condition of narrowing of the heart's blood vessels, restricting
oxygen flow to the heart muscle. CAD has been correlated with the levels of blood cholesterol and
triglycerides. If not treated, CAD can lead to myocardial infarction (heart attack). "Statin" drugs
which lower blood cholesterol, are also effective in minimizing the treat of CAD.

• "Statin" drugs have the capability to increase the breakdown of skeletal muscle, thus releasing
muscle protein. If skeletal muscle protein overloads the kidneys, renal failure can result. The
erythromycin drugs (Macrolides) enhance the capabilities of the "statins" to cause this effect. It is
advised that patients medicated with a "statin" drug, do not take erythromycin (macrolide) products.

ANTI-DEPRESSANTS
5 Major Categories of Antidepressant Drugs:
1. Tricyclic Antidepressnts
2. Monoamine Oxidase Inhibitors
3. Selective Serotonin Reuptake Inhibitors
4. Serotonin & Norepinephrine Reuptake Inhibitors
5. Second Generation Miscellaneous

AMITRIPTYLINE (HAVll) - the most widely used TRICYCLIC ANTI-DEPRESSANT to treat unipolar
disorder (depression). Elavil has the greatest anti-cholinergic effects, while Desipramine (Norpramin)
has the least anti-cholinergic effects.

• Tricyclic antidepressants are the drugs of FIRST choice to treat UNIPOLAR DISORDER (depression).
Tricyclics inhibit neuronal reuptake of NE & Serotonin (5-HT) in the brain, which results in potentiation
of their neurotransmitter actions at post-synaptic receptors.

• The most common CNS adverse reaction is DROWSINESS. Anti-cholinergic adverse effects are dry
mouth (xerostomia), constipation, blurred vision, and tachycardia .

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 NOTES • Tricyclic antidepressants (i.e. ElaviD, Serotonin & NE reuptake inhibitors (Le. Effexor) are
antidepressants with the highest incidence of dry mouth (xerostomia). These drugs induce
significant xerostomia in nearly 75% of patients taking these medications due to their secondary anti-
cholinergic nature. Drug-induced xerostomia must be treated palliatively with artificial salivary
substitutes.

• EPI (vasoconstrictor) in local anesthetic injections must be used cautiously in patients taking
tricyclic antidepressants (Le. Elavil), Serotonin & NE reuptake inhibitors (Le. Effexor) to avoid
transient and significant increases in blood pressure. These antidepressants greatly increase NE
levels in tissues. In the presence of a vasoconstrictor administered via a local anesthetic injection,
the patient can experience a significant elevation of blood pressure due to the vasopressor actions
of the com bination.

• Other Tricyclic Antidepressants: Doxepin (Sinequan) & Imipramine (Tofranil).

MONOAMINE OXIDASE (MAO) INHIBITORS - used to treat depression by antagonizing the action
of monoamine oxidase (MAO) which is responsible for the degradation of the naturally occurring
monoamines (EPI, NE, Dopamine, & Serotonin) . Increased levels of monoamines in the brain is
responsible for the anti-depressant effect of MAO inhibitors.

• MAO inhibitors: Isocarboxazid (Marplan), Tranylcypromine (Parnate), & Phenelzine (Nardil).

• Local anesthetics containing EPI are contraindicated in patients taking MAO inhibitors.

• The major limitation for the widespread use of MAO inhibitors to treat depression is the potential for
serious side effects. MAO inhibitors interact with many drugs and foods containing large amounts
of the amino acid TYRAMINE. Drugs that interact with MAO inhibitors are Meperidine (Demerol), EPI ,
and Ephedrine.

LITHIUM - current drug of choice to treat the MANIC PHASE of bipolar disorder ("manic-depressive
syndrome") . Bipolar disorder ("manic-depressive syndrome) is characterized by cyclical changes in
affective state between the manic &depressive phases of behavior. Bipolar patients cycle between the
two affected states.

• Lithium is used mainly to suppress recurrences of the manic phase of bipolar disorder. It is NOT
useful to treat acute manic episodes. Lithium can prevent the occurrence of the depressive and
manic episodes in some, but not all patients. Anti-depressants are often administered with Lithium
to manage the depressive phase of bipolar disorder, if lithium alone is insufficient.

NEUROLEPTIC AGENTS (ANTI-PSYCHOTIC AGENTS OR MAJOR TRANQUILIZERS) - treat

ACUTE manic episodes. Chlorpromazine (a phenothiazine), & Haloperidol (acts similar to a
phenothiazine) are effective in quelling extreme mania and psychotic behavior.

SElECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIS) - have revolutionized the treatment

of depression. The most important clinical distinction of SSRls from all other anti-depressants is SSRl's
very high specificity for blocking the reuptake of serotonin. These drugs increase the activity of
serotonergic systems in the brain:
1. Fluoxetine (Prozac)- prototype SSRI with the LONGEST half-life. Treats obsessive-compulsive
disorders (OCD) and depression.
2. Paroxetine (Paxil), Sertraline (Zoloft), & Fluvoxamine (Luvox)-have short half-lives, and can be
given once daily. These drugs are also effective for treating PANIC ATTACKS, depression, and
obsessive-compulsive disorders.
3. Citalopram (Celexa) &Escitalopram (Lexapro)-treats depression and anxiety.

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Adverse Effects: nausea, headache, anxiety, agitation, insomnia, and sexual dysfunction. SSRls do not
have secondary anti-cholinergic effects, thus do not cause any significant dry mouth. Selective Serotonin
Reuptake Inhibitors (i.e. Prozac) do not have an effect on NE in tissues and interaction with a
vasoconstrictor like EPI is not a problem.

SEROTONIN & NE REUPTAKE INHIBITORS - Venlafaxine (Effexor), Nortriptyline (Pamelor), &

Desipramine (Norpramin).

SECOND GENERATION MISCELLANEOUS - Bupropion (Wellbutrin), Trazodone (Desyrel), Nefazodone

(Serzone), Mirtazipine (Remeron).

ANTI-PSYCHOTICS
ANTIPSYCHOTIC DRUGS - primarily indicated to treat "PSYCHOSIS" associated with
SCHIZOPHRENIA, PARANOIA, & MANIC symptoms of manic-depressive illness.
1. Phenothiazines-the most widely used and most effective group of antipsychotic agents in
medicine that have antipsychotic effects (improve mood & behavior) and neuroleptic effects
(emotional quieting and development of extrapyramidal symptoms). These effects are due the
phenothiazine's ability to BLOCK OOPAMINERGIC SITES in the brain. Phenothiazines are the
most effective antiemetic agents that depress the chemoreceptor trigger zone (CTZ) to
reduce nausea and/or vomiting.
• Phenothiazines: Chlorpromazine (Thorazine), Thioridazine (Mellaril), Promazine (Sparine),
Fluphenazine HCL (prolixin), Mesoridazine (Serentil), Triflupromazine (Vesprin), Acetophenazine
(Tindal), Trifluoperazine (Stelazine). These act by blocking dopaminergic sites in the brain.
• Phenothiazines pharmacologic actions are sedation, anti-emetic activity, alpha adrenergic
receptor blockage, and potentiate the action of narcotics. It is NOT an anti-convulsant.
• Phenothiazine Contraindications: patients with severe CNS depression or epilepsy, and
given with caution in patients with liver disease.
• Phenothiazine Adverse effects: hypotension, liver toxicity (jaundice), dry mouth
(xerostomia), & extrapyramidal reactions (tardive dyskinesia). Tardive dyskinesia-an
extrapyramidal disease & irreversible side effect of long-term phenothiazine therapy due to
the effect of the basal ganglia. Characterized by involuntary, repetitious movements of the
face, limbs, and trunk.
• Tardive Oyskinesia-a serious, irreversible neurological disorder that can appear at any age. It
is a side effect of antipsychotic/neuroleptic drugs (i.e. phenothiazine). Symptoms can be barely
noticeable or profound. Symtoms are uncontrollable movement of various body parts (body
trunk, legs, arms, fingers, mouth, lips, or tongue) . Once any TO symptoms appear, the
antipsychotic/neuroleptic must be discontinued . 20% of people taking
antipsychotics/neuroleptic drugs for more than 1 year are affected .
• Muscle spasms of oral-facial region is an extrapyramidal syndrome (EPS) caused by
Phenothiazine-type anti psychotics. EPS is a variety of signs and symptoms caused by blockade
of dopamine receptors in specific brain regions. EPS symptoms include Parkinson-like
movements (shuffled gait, pill-rolling effect of fingers), muscle rigidity, spasms of the neck
and facial muscles, tremors, and loss of muscle movement.
• Use caution when administering any sedative drugs to a patient taking Phenothiazines (i.e.
Chorpromazine, Fluphenazine, Prochlorperazine). These drugs will potentiate the action of
sedative drugs.
2. Thioxanthenes-Chlorprothixene & Thiothixene are a less potent group of anti psychotics that
treat Schizophrenia.

3. Butyrophenones-Haloperidol & Droperidol are highly effective antipsychotic drugs (potent

dopamine antagonists) that treat Schizophrenia and Tourette's Syndrome.

4. Diverse Heterocyclic Antipsychotics: newer agents that antagonize dopamine and serotonin in
the brain. Molindone (Moban), Clozapine (Clozaril), Loxapine (Loxitane), Olanzapine (Zyprexa),
Resperidone (Resperdal), & Quetiapine (Seroquel). These drugs effectively treat Schizophrenia
and are more effective & less toxic than the older drugs (i.e. Phenothiazines, Butyrophenones,
& Thioxanthenes), but are much more expensive.
157
 NOTES ANTI-HISTAMINES
ANTIHISTAMINES - antagonizing agents that compete with natural histamine for Hl & H2 receptor
sites. Histamine is found in all tissues. It is stored in the cytoplasmic granules of tissue mast cells and
blood basophils. Histamine is released in response to IgE-mediated (immediate) allergic and inflammatory
reactions to produce a variety of physiologic actions in many tissues. Histam ine plays an important role
in hay fever, urticaria, angioneurotic edema, and in controlling stomach acid secretion (HCLl. There are
2 types of histamine antagonists/receptors:

1. Hl receptor antagonists: competitively block Hi receptors, blocking the effects of histamine at

these receptors. Hi antagonists block vasodilation, block bronchi constriction, and block
capillary permeability that histamine usually causes. Blocking histamine's effects overcomes
the symptoms of seasonal allergies. Hi plays an extremely important role in allergic reactions.
Antihistamines located at the Hl histamine receptor site:
• 1st-Generation (Classic) Hl Blockers: Diphenhydramine (Benadryl), Chlorpheniramine
(Chlor-Trimeton), &Tripelennamine (Pelamine). These agents have a "broad spectrum of
action" that includes anti histaminic, anticholinergic, antiserotonergic, antibradykinin,
and sedative properties.
• 2nd Generation Hl Blockers: Cetirizine (Zyrtec), Fexofenadine (Allegra), Loratidine (Claratin),
& Desloratidine (Clarinex) . Most of these agents due to their poor CNS penetration, cause LESS
sedation and drowsiness than 1st generation agents.
• All Hl blockers do not prevent histamine release, but COMPETE with free histamine from
binding at Hl receptor sites. Binding is usually competitive, but some 2nd-generation agents
bind non-competitively at higher doses.
• Common Adverse Effects: drowsiness, dizziness, anticholinergic effects (dry mouth , nose &
throat), nausea. Both Hl &H2 antagonists can stimulate and depress the CNS.

2. H2 receptor antagonists: important in gastric acid (HCLl secretion by competitively blocking H2

receptors to block histamine's effects at H2 receptors (these antagonists compete with histamine
ONLY at H2 receptors in the GI tract (however, H2 receptors are also located in vascular &
bronchial smooth muscle). H2 antihistamines block stomach acid secretions and treat duodenal
ulcers by inhibiting histamine at parietal cells to interfere with one of several mediators for
signaling parietal cells to secrete acid . H2 blockers reversible competitive antagonists of the
actions of histamine on H2 receptors. They are orally active, and relatively non-toxic, thus can
be given in large doses so the duration of action of a single dose may last 12-24hrs. These agents
treat acid-peptic disease (especially duodenal ulcers and gastric peptic ulcers). H2 antagonists
also treat Zollinger-Ellison Syndrome (hypersecretory disease), and gastroesophageal reflux
disease (GERD). However, for both of these disorders, Omeprazole (Prilosec) which a "proton-
pump" inhibitor is more effective.

• Cimetidine (Tagamet)-an antihistamine H2 receptor blocker that is more likely to provoke

interactions with hepatically metabolized drugs (a potent inhibitor of hepatic drug-metabolizing
enzymes). May cause gynecomastia (male breasts), however, Zantac, Pepcid, &Axid do not
produce these adverse effect.

• Ranitidine (Zantac}-an H2 receptor blocker that treats GERD (heartburn) by blocking the effects
of histamine at H2 receptors.

• Famotidine (Pepcid) &Nizatidine (Axid}-an H2 receptor blocker that blocks the effects of
histamine at H2 receptors.

158
OMEPRAZOLE (PRILOSEC) & LANSOPRAZOLE (PREVACID) - gastrointestinal drugs and proton-
pump inhibitors (H+/K+ ATPase) that reduce stomach acid formation by inhibiting the proton-pump of
the stomach's parietal cells. These drugs inhibit the pump so that no H+ protons are pumped into the
stomach contents, thus no HCL is produced.

• Hydrochloric acid (HCLl is produced by the stomach's parietal cells through a pump within each cell
that pumps H+ protons into the stomach contents. This pump is the H+/K+ ATPase pump. HCL is
used for food digestion, but an abundancy can cause heart burn and acid indigestion.

• Stomach acid is also reduced by inhibiting the effects of histamine in the stomach at the histamine
Type-2 receptors (H2 receptors). Ordinarily, histamine stimulates gastric parietal cells to produce
HCL.

• Proton-pump inhibitors and H2 blockers are used to treat heartburn, indigestion, sour stomach,
active duodenal ulcer disease, and gastroesophageal reflux disease (GERD).

Drugs that Reduce GI Motility to treat DIARRHEA (Anti-diarrhea Is):

1. loperamide (lmodium)-an anti-diarrheal that acts on intestinal muscles to inhibit peristalsis.
It is an OPIOID, that does not penetrate the CNS like other opioids, thus is sold over-the-counter
(OTC) . Imodium has no evidence of drug abuse or dependence (unlike other opioids like Codeine,
Morphine, & Meperidine).

2. Diphenoxylate with Atropine (lomotill-an anti-diarrheal that inhibits excessive GI tract motility
and propulsion. Commercial preparations contain a sub-therapeutic amount of Atropine to
discourage abuse. lomotil requires a prescription, thus is not sold OTC.

Important: laxatives act in the REVERSE manner of anti-diarrheals by increasing GI tract motility to
treat constipation. Laxatives include Magnesium Hydroxide (Milk of Magnesia), Castor oil, Metamucil, &
Methylcellulose.

ANTACIDS - neutralize excess stomach acid by a chemical reaction.

ALUMINUM HYDROXIDE - the MOST POTENT ANTACID, but has less neutralizing capacity than
calcium carbonate or sodium bicarbonate (the only systemic antacid). Gastric antacids are drugs that
directly neutralize the gastric acid (HCLl secreted in the stomach. Antacid therapy is directed at
decreasing the concentration and total load of gastric acid. Common OTC Antacids:
• Sodium bicarbonate product: Alka-Seltzer
• Calcium carbonate products: Amitone &Turns
• Aluminum hydroxide products: Alterna GEl &Amphogel
• Magnesium hydroxide products: Milk of Magnesia (Maalox)
• Bismuth subsalicylate salt products: Pepto-Bismol
• Magnesium & Aluminum products: Maalox &Mylanta

ALUMINUM SALTS USED AS ANTACIDS - hydroxide, carbonate, phosphate, and aminoacetate.

DYSPEPSIA - an impairment of the power or function of digestion.

159
 N ANTI-CONVULSANTS (ANTI-EPILEPTICS)
EPILEPSY - a neurological disorder characterized by sudden, recurring attacks of motor, sensory, or
psychic malfunction with or without loss of consciousness or convulsive seizures. The goal of anti-
convulsant therapy is to reduce or eliminate these seizures.

• Carbamazepine (Tegretol)-used a prophylaxis for partial seizures with complex symptomatology

(psychomotor and temporal lobe seizures) . Also treats tonic-clonic seizures (grand mal), and pain
associated with TRIGEMINAL NEURALGIA by blocking Na+ channels. Adverse effects: diplopia,
ataxia, enzyme induction, and blood dyscrasias, but rarely causes aplastic anemia.

• Diazepam (Valium)-treats STATUS EPILEPTICUS and emergency treatment of seizures. May cause
drowsiness, dizziness, and ataxia.

• Ethosuximide (Zarontin)-the preferred drug for effectively treating absence seizures because it
causes minimal sedation by BLOCKING CALCIUM CHANNELS. Adverse Effects: GI distress, lethargy,
headache.

• Gabapentin (Neurontin)-used as an adjunct to treat partial seizures.

• Phenytoin (Oilantin)-treats tonic-clonic (grand mal) seizures. The rate of gingival hyperplasia is
diminished by proper oral hygiene. Produces Na+ channel blockade. Phenytoin is the most extensively
used of all anti-epileptics, used IV for status epilepticus. Phenytoin-induced gingival hyperplasia
is a common adverse effect, that may partially or completely obscure teeth crowns.

• Valproic Acid (Oepokote or Depakene)-also a preferred drug for effectively treating complex partial
seizures, and adjunctively in patients with multiple seizure types, including absence seizures because
it causes minimal sedation. It functions by causing neuronal membrane hyperpolarization. Adverse
Effects: GI distress, lethargy, headache, blood dyscrasias, hepatotoxicity & liver failure.

• Most of the commonly used anti-convulsants are CNS depressants. Thus, respiratory depression
may occur with overdosage of anti-convulsants.

ANTI-INFECTIVES
SULFONAMIDES ("SULFA DRUGS") - BACTERIOSTATIC agents structurally similar to Para-
aminobenzoic Acid (PABA) which is the basis for their antibacterial actions. Bacteria require PABA to
synthesize folic acid which is needed to synthesize bacteria cellular components for bacterial cell growth.
Due to the structural similarities between sulfonamides and PABA, the sulfonamides COMPETE with
PABA to inhibit PABAs actions, which prevents bacterial folic acid synthesis to inhibit cellular growth.
Sulfonamides are "sulfa drugs" because their molecules contain sulfur atoms and their unique structure
gives them their unique antibacterial mechanism of inhibiting folic acid synthesis and cell growth.

• Sulfonamides DO NOT TREAT dental infections because of a low degree of effectiveness against oral
pathogens. However, they are used primarily in medicine to treat URINARY TRACT INFECTIONS
(UTls).

• Bactrim-the brand name of combining Trimethoprim + Sulfamethoxazole. Bactrim is the drug of

choice for many UTls. Note: Trimethoprim component is an antimicrobial, while Sulfamethoxazole
is a sulfonamide.

160
3 Allergic Reactions to Penicillin: a RASH is the most common sign/manifestation of an allergy to NOTES
PENICILLIN. The most common adverse effect of penicillin therapy is an allergic reaction. These reactions
occur in up to 10% of patients receiving penicillin.
1. Acute/Immediate Onset Reactions (Anaphylactic Shock)-occurs within 30min and are IgE
mediated. Characterized by urticaria, angioedema, bronchoconstriction, GI disturbances, and
shock. Death can result quickly if treatment is not given immediately (parenteral administration
of EPI) . This is rare, but can occur especially with oral dosing.
• Cephalosporins: are definitely contraindicated for penicillin-allergic patients who exhibit
immediate-type reactions.
• Ex: a patient was given penicillin 15min ago and develops laryngeal edema, urticaria (welts
that itch), severe hypotension, GI disturbances, bronchoconstriction (airway constriction), and
shock. This patient is having an anaphylactic reaction (anaphylactic shock).
• An anaphylactic reaction can be fatal if countermeasures like injecting EPI are not taken
promptly. EPI prevents the release of substances from mast cells and antagonizes the actions
of histamine and leukotrienes of smooth muscle.

2. Accelerated Allergic Reaction-occurs 30-48hrs after administration of penicillin. Manifestations

are urticaria, pruritis, wheezing, mild laryngeal edema, and local inflammatory reactions. Not
life-threatening.

3. Delayed Allergic Reaction (Skin Rash)-occurs after 2-3 days. Approximately 80-90% of all
allergic reactions occurring with penicillin are "delayed", manifested by mild skin rashes (the
most prevalent allergic manifestation).

HYPERSENSITIVITY REACTIONS - occur in up to 10% of patients receiving penicillin. Manifestations

range from a mild rash to anaphylaxis. The rash may be urticarial, vesicular, bullous, or maculopapular.
Rarely thrombopenic purpura develops.

PROBENECID (BENEMID) - co-administered with antibiotics to DELAY RENAL CLEARANCE of the

antibiotic to elevate and prolong the antibiotic's serum concentrations when high tissue
concentrations are necessary. In some cases, Probenecid administration can more than double the
drug's serum concentration. The drug's half-life is also prolonged. Given concurrently with natural
penicillins to increase their blood levels.

• Most penicillins are handled by the kidneys as organic acids and excreted by renal tubular secretion.
Probenecid interferes with tubular handling of organic acids inside the nephron. Probenecid affects
most cephalosporins, natural penicillins, and other beta-Iactam related antibiotics like Aztreonam
and Imipenem.

• Probenecid INHIBITS renal tubular cell secretion that raises penicillin blood levels by diminishing
their tubular secretion. Probenecid is sometimes given simultaneously with penicillin to raise
penicillin blood levels for increased activity, and is the DRUG OF CHOICE TO TREAT GOUT.

• Nafcillin, Oxacillin, Cloxacillin, &Dicloxacillin are lipophilic and excreted by BILIARY MEANS
(LIVER). Thus, a combination of Probenecid or dosage adjustment for renal dysnfunction is NOT
necessary for these penicillins.

• Imipenem-beta-Iactam antibiotic derived from Thienamycin, and first drug classified as a

Carbapenem antibiotic. Currently the drug of choice for infections due to Enterobacter, and is
usually combined with Cilastin and treats severe or resistant infections, especially nosocomial
infections.

• Aztreonam-a perenteral synthetic beta-Iactam antibiotic (classified as a monobactam). The spectrum

is limited to aerobic gram (-) rods like Klebsiella, Pseudomonas, &Serratia. It has no gram (+) or
anaerobic activity, and is synergistic with aminoglycosides.

161
 Therapeutic Management of GOUT involves three different aspects of the disease:
1. Colchicine-reduces the inflammation during acute attacks by impairing leukocytic migration to
inflamed areas, and disrupts urate deposition and subsequent inflammatory resposne. Colchicine
is most effective when given 12-36hrs after the symptoms begin. It is NEVER given 1M or
subcutaneously because it causes tissue irriation.
• Adverse Effects: severe liver & kidney damage, and long-term therapy may cause bone
marrow depression.
• Indomethacin (NSAlDs) are important for treating acute gouty arthritis, but may cause
renal damage or bone marrow depression.

2. Allopurinol (Zyloprim)-decreases uric acid production. Drug of choice for managing CHRONIC
GOUT by inhibiting xanthine oxidase (enzyme that converts hypoxanthine xanthine uric acid).
• Adverse Effect: GI disturbances.

3. Probenicid (Benemid) & Sulfinpyrazone (Anturane)-uricosuric agents that enhance uric acid
clearance by acting in the kidney's proximal convoluted tubules, and inhibit secretion of other
weak acids (i.e. penicillin) in addition to inhibiting uric acid reabsorption.
• Important: normal penicillins and cephalosporins must be given in high and frequent doses
due to their high rate of elimination by the kidneys. Probenicid, is given simultaneously to
SLOW THEIR EXCRETION.

PENICILLINS - are BACTERICIDAL by inhibiting cell-wall synthesis. A MAJOR disadvantage of

penicillin is their high incidence of ALLERGIC reactions. -10% of the population is allergic to penicillins.
This incidence probably holds for any of the specific penicillins because there is a cross allergy from one
to another. In non-allergic individuals, penicillin at normal therapeutic doses virtually have no side
effects. Penicillins are BACTERICIDAL by causing death of invading bacteria. Penicillins are NOT active
against viruses, fungi, Rickettsiae, or other nonbacterial organisms.

All penicillins are DERIVATIVES of 6-aminopenicillanic acid and contain a beta-Iactam ring structure
connected to a thiazolidine ring (this beta-Iactam ring is essential for its antibacterial activity). This
basic structure is synthesized by the penicillin mold from 2 amino acids (L-cysteine & L-valine).
Antibiotics containing this beta-Iactam ring are "beta-Iactam antibiotics" which includes penicillins,
cephalosporins, and two newer groups of agents (Carbepenems & Monobactams).

Most penicillins are directly EXCRETED INTO URINE via renal tubular cell secretion. Probenecid
(Benemid)-an inhibitor of renal tubular cell secretion that raises the blood levels of the penicillins
by diminishing their tubular secretion. Probenecid is sometimes given simultaneously with penicillin to
raise the blood levels for increased activity, and is the DRUG OF CHOICE TO TREAT GOUT.
1. Penicillin VK (Pen Vee K, V-cillin K)-the antibiotic/antimicrobial associated with the highest
incidence of drug allergy. However, it the antibiotic of choice for treating non-penicillinase
producing gram (+) staphylococcal infections. It is prudent to use an antibiotic with narrow
spectrum of action and one that is bactericidal to minimize the development of bacterial
resistance. Penicillin VK has these properties. Has a relative limited spectrum of action against
aerobic gram (+) cocci and anaerobes. Penicillin VK is a naturally occurring penicillin preferred
for treating oral infections because it is more acid stable (more reliable oral absorption).
• Can be used in pregnant patients as it is not harmful to the fetus. It is not incorporated into
bony tissue or in the teeth of children unlike tetracyclines.
• Adverse effects: hypersensitivity that causes a skin rash and rare anaphylaxis.

2. Penicillin G(Benzylpenicillin)-the PROTOTYPE penicillin for comparison. By side-chain

substitutions (substituting other groups at "Rn position of the penicillin molecule) of the basic
6-aminopenicillanic acid molecule, the semi-synthetic penicillins are produced (a more acid
stable, broader spectrum, or penicillanse resistant).
• Penicillin GProcaine (Cysticillin)-always given intramuscular (1M) route .
• Penicillin GBenzathine (Bicillin L-A)-always given intramuscular (1M) route to treat SYPHILIS
& PREVENT RHEUMATIC FEVER. It has a longer duration of action than Penicillin GProcaine.

162
 3. Carbenicillin-has the WIDEST (BROADEST) spectrum of antibacterial activity. Other penicillins
with very broad spectrums of action are Ticarcillin & Piperacillin . In addition to being active
NOTES
against gram (+) cocci (streptococci, staphylococci, and pneumococci), and gram (+) rods
(bacillus and others), these agents are active against Pseudomonas, Proteus, Klebsiella, and
Bacteroides. These antibiotics are used to treat URINARY TRACT INFECTIONS (UTls) and other
infections caused by susceptible gram (-) Pseudomonas species and Proteus species.
Degraded in the stomach acid, so must be given parenterally {IV).

Aminopenicillins {Ampicillin, Amoxicillin, Becampicillin)-like other penicillins, aminopenicillins inhibit

bacterial cell wall synthesis. Aminopenicillins are characterized by the amino substitution of Penicillin
G, allowing them to penetrate/work against many gram (-) bacteria more readily than the natural
penicillins or the penicillinase-resistant penicillins. Gram (-) bacteria susceptible to aminopenicillins
are Haemophilus influenzae, some Escherichia coli, &Proteus mirabilis. However, aminopenicillins are
not stable to beta-Iactamases (penicillinase) of either gram (+) or gram (-) bacteria. They are NOT
penicillinase resistant. Aminopenicilins are useful for treating upper respiratory infections.

1. Ampicillin {Polycillin, Onipen)-an aminopenicillin with a broader spectrum of action than

penicillin VK. Given orally or IV to primarily treat infections like otitis media, bronchitis, sinusitis,
and acute bacterial cystitis caused by suspectible organisms. The preferred agent to treat
URINARY TRACT INFECTIONS caused by enterococci (streptococci that inhabit the intestine).
• "Parenteral" ampicillin is the drug of choice for patients unable to take oral medications
and who are not allergic to penicillin for prophylaxis for bacterial endocarditis.

2. Amoxicillin {Amoxil, Larotid)-an aminopenicillin with an extended spectrum of action which

includes aerobic gram (+) cocci and anaerobes, and some gram (-) bacilli (Hemophilus, Proteus,
Salmonella). Only given orally to primarily treat infections like otitis media, bronchitis, sinusitis,
and acute bacterial cystitis caused by suspectible organisms. Compared to ampicillin, amoxicillin
has a higher oral absorption, higher serum levels, longer half-life, and is less likely to cause
adverse GI effects (diarrhea). The preferred agent to treat URINARY TRACT INFECTIONS caused
by enterococci (streptococci that inhabit the intestine).
• Amoxicillin (along with Cephalexin &Cephradine) is a drug of first choice for standard
general prophylaxis medication in a patient NOT allergic to penicillin with a TOTAL JOINT
REPLACEMENT (prosthetic implants). Prophylaxis standard dose/regimen is 2gm orally 1hr
prior to dental treatment.
• "Oral" amoxicillin is the drug of choice for standard general prophylaxis for bacterial
endocarditis in patients undergoing invasive dental procedures. It is the antbiotic of choice
for standard prophylactic regimen of antibiotic coverage to prevent bacterial endocarditis.
• Amoxicillin has a higher oral absorption, higher serum levels, and longer half-life than
ampicillin. Amoxcillin is given orally, while ampicillin can be given orally or IV.
• Methotrexate-has a clinically significant drug interaction with Amoxicillin. In large doses,
amoxicillin inhibits renal tubular secretion of methotrexate, thus causing higher, prolonged
serum levels of Methotrexate. Methotrexate may cause ulceration of the oral tissues.

3. Bacampicillin {Spectrobid)-a n aminopenicillin used to treat upper and lower respiratory tract
infections, urinary tract infections, and skin & skin structure infections. Bacampicillin is
hydrolyzed to Ampicillin during absorption from the GI tract where it has a better absorption than
ampicillin, and less GI side effects.

Afunctional part of the chemical molecule of all the penicillins is the BETA-LACTAM RING (4-membered
imbedded ring structure consisting of 3 carbons and 1 nitrogen atom) that is responsible for the
antibacterial activity of penicillin. Any alteration to the beta-Iactam ring alters the penicillin 's
antibacterial activity.

163
 Current American Heart Association Guidelines
Standard Regimen
Amoxicillin:
• Adults: 2g orally 1hr prior to appointment
• Children: SOmg/kg (not to exceed adult
dose) orally 1hr prior to appointment
Penicillin Allergic Patients
Clindamycin:
• Adults: 600mg orally 1hr prior to appointment
• Children: 20mg/kg orally 1hr prior to appointment
Cephalexin:
• Adults: 2g orally 1hr prior to appointment
• Children: SOmg/kg orally 1hr prior to appointment
Cefadroxil:
• Adults: 2g orally 1hr prior to appointment
• Children: SOmg/kg orally 1hr prior to appointment
Azithromycin:
• Adults: SOOmg orally 1hr prior to appointment
• Children: lSmg/kg orally 1hr prior to appointment
Clarithromycin:
• Adults: SOOmg orally 1hr prior to appointment
• Children: lSmg/kg 1hr prior to appointment

AHA Guidelines were pubished 6/11/97 in JAMA, Vol 277, pp 1794-1801. Premedication requirements for
patients with valvular heart disease or congenital cardiac defects. If in doubt, have the patient consult
their physician as to need.

BETA-LACTAMASES - enzymes produced and secreted by a wide range of gram (+) & gram (-) bacteria
as a defense weapon against cephalosporin and penicillin antibiotics. Beta-Iactamase enzymes destroy
the beta-Iactam nucleus within these antibiotics by splitting open the beta-Iactam ring structure to
render the antibiotic ineffective. Bacterial enzymes that belong to the family of beta-Iactamases are:
• Cephalosporinases-beta-Iactamases that work against cephalosporins.
• Penicillinases-an enzyme secreted by bacteria that splits open the beta-Iactam ring to render the
penicillin molecule ineffective against penicillinase secreting bacteria. They are beta-Iactamases
that work against penicillins.

PENICILLINASE RESISTANT PENICILLINS - Beta-Lactamase Inhibitors: by combining an acid

with the penicillin, the beta-Iactamase enzyme is permanently inhibited by the acid, which maintains the
penicillin's antibacterial activity. These penicillins resist the actions of penicillinase because they have
a protected beta-Iactam ring that prevents the actions of the enzymes. These antibiotics are highly
effective against penicillinase-producing Staphylococcal aureus, but much less effective against other
gram (+) bacteria, and have almost no activity against gram (-) bacteria.
l. Methicillin-a structurally modified penicillin that allows the molecule to remain stable in the
presence of the beta-Iactamase enzyme, but may also narrow its spectrum of action, limiting the
use of such antibiotics only to gram (+) cocci like Staphylococcus bacteria. Degraded in the
stomach acid, so must be given parenterally (IV).
• Methicillin is prescribed primarily to treat severe penicillinase-producing staphylococcal
infections. It is not frequently used due to the incidence of intestinal nephritis and the
availability of equally efficacious alternatives (Nafcillin & Oxacillin). Methicillin is given IV in
severe penicillinase-producing staphylococcal infections.
• Methicillin-Resistant Staphyloccoal Aureus (MRSA)-a group of resistant staphyloccoal
bacteria that can be life-threatening and resist ALL penicillinase-resistant penicillins &
cephalosporins. Such strains are also usually resistant to aminoglycosides, tetracyclines,
erythromycins, and clindamycin. In the past, vancomycin has been used against MRSA bacteria.
However, microorganisms resistant to vancomycin have been reported, and its use has
been curtailed.

164
 2. Augmentin-it is Amoxicillin + Clavulanate potassium which blocks the actions of penicillinase
from reaching the beta-Iactam ring. It is a popular commercial beta-Iactamase inhibitor
preparation used orally as a pill or liquid form.

3. Unasyn-it is Ampicillin + Sulbactam which blocks the actions of penicillinase from reaching the
beta-Iactam ring. A beta-Iactamase inhibitor available for IV & 1M use.

4. Dicloxacillin-similar spectrum of action as penicillin VK, but is active against penicillinase

producing staphylococcus.

• Other Penicillinase-Resistant Penicillins: Nafcillin, Oxacillin, & Cloxacillin.

Penicillinase-Resistant Penicillins
Agent Route of Administration
Methicillin, Nafcillin, Oxacillin,
IV
Ticarcillin/Clavulanate Potassium (Timentin)
Cloxacillin, Dicloxacillin,
Oral
Amoxicillin/Clavulanate Potassium (Augmentin)
Ampicillin/Sulbactam (Unasyn)
IV &1M
PiperacillinlTazobactam (Zosyn)

Important Penicillin Facts:

• Penicillins degraded in stomach acid, thus must be administered PARENTERAllY (by injection):
• Methicillin, Carbenicillin, & Penicillin G.
• Acid Stable Penicillins (given orally):
• Penicillin VK, Amoxicillin, Ampicillin, Nafcillin, Oxacillin, Cloxacillin, & Dicloxacillin.
• Extended Spectrum Penicillins: Aminopenicillins (Ampicillin & Amoxicillin).
• Broad Spectrum Penicillins: Carbenicillin, Piperacillin, Ticarcillin have the WIDEST spectrum of all
penicillins.
• Penicillinase-Resistant Penicillins: Methicillin, Nafcillin, Oxacillin, Cloxacillin, & Dicloxacillin.

CliNDAMYCIN - a BACTERIOSTATIC antibiotic effective against most STAPHYlOCOCCI, AEROBIC &

ANEROBIC STREPTOCOCCI, but is MOST EFFECTIVE in treating infections due to BACTEROIDES SPECIES.

• Clindamycin binds to the 50S ribosomal subunit, blocking bacterial protein synthesis (translocation).
It used is restricted by its adverse side effects (severe diarrhea &abdominal pain/GI upset due to
Pseudomembranous colitis) caused by the overgrowth of the bacteria Clostridium difficile. Thus,
used cautiously because Clostridium difficile always resists Clindamycin.

• Clindamycin is bacteriostatic, and active against most gram (+) and many anaerobic organisms
(including anaerobic gram (-) bacteria Bacteroides fragilis).

• In Oentistry, Clindamycin is an alternate antibiotic when amoxicillin cannot be used to prevent

bacterial endocarditis in patients undergoing dental procedures due to an allergy to penicillins
(Clindamycin is given to penicillin-allergic patients allergic since there is no cross allergenicity
between penicillins &clindamycin), to treat common oral-facial infections caused by aerobic gram
(+) cocci and susceptible anaerobes, and for prophylaxis for dental patients with total joint
replacement.

• Used for prophylaxis of endocarditis in penicillin allergic patients with valvular disease. Treats
oral infections &penetrates into bone (not CSF) .

165
 Bacterial Endocarditis Prophylaxis (Antibiotic) is Recommended:
1. High-Risk Category:
• Prosthetic cardiac valves (i.e. biosynthetic (mechanical) &homograft (pig) valves)
• Previous bacterial endocarditis.
• Complex Cyanotic Congenital Heart Disease (i.e. single ventricle states, transposition of great
arteries, Tetrology of Fallot).
• Surgically constructed synthetic pulmonary shunts or conduits.

2. Moderate-Risk Category:
• Most other congenital cardiac malformations
• Acquired valvular dysfunction (i.e. Rheumatic heart disease).
• Hypertrophic cardiomyopathy.
• MVP with valvular regurgitation and/or thickened leaflets.

3. Dental Procedures: extractions, periodontal procedures (surgery, SRP, probing, and recall
maintenance), implant placements of avulsed teeth, endodontic (RCT) instrumentation of surgery
ONLY past the apex, subgingival placement of antibiotic fibers/strips, initial placement of
orthodontic bands (not brackets), intra ligamentary local anesthetic injections, prophylactic
cleaning of teeth or implants where bleeding is anticipated.

Bacterial Endocarditis Prophylactic Antibiotic is NOT required:

• Isolated atrial or ventricular septal defects, or patent ductus arteriosus.
• Coronary Artery Bypass Graft Surgery (CABG).
• MVP without valvular regurgitation
• Heart murmurs.
• Kawasaki Disease without valvular dysfunction.
• Cardiac Pacemakers (intravascular &epicardial) and implanted defibrillators.

RESTORATIVE DENTISTRY - with or without a retraction cord, local anesthetic injections (non-
intraligamentary), intracanal RCT, post and core placement, placing rubber dams, post-operative suture
removal, placement of RPD and orthodontic appliances, impressions, fluoride treatments, radiographs ,
or shedding of primary teeth.

NO Antibiotic prophylaxiS for patients with non-valvular devices UNLESS 2-3 weeks after surgery and
healing is still occurring. AHA does NOT recommend dental antibiotic prophylaxis AFTER these non-
valvular devices are placed:
• Non-Valvular Devices: PACEMAKERS, implantable cardioverter defibrillators, left ventricular assist
devices (LVAD), total artificial hearts, ventriculoatrial SHUNTS, peripheral vascular STENTS,
hemodialysis prosthetic vascular grafts, intra-aortic balloon counterpulsation CATHETERS, coronary
angiography and percutaneous coronary artery intervention, CORONARY ARTERY STENTS, vascular
closure devices, and vena cava filters.

Antibiotic prophylaxis for dental patients with TOTAL JOINT REPLACEMENTS statement by ADA &AAOS:
• Currently no scientific evidence supports giving antibiotic prophylaxis to prevent HEMATOGENOUS
INFECTIONS PRIOR to dental treatment in patients with total joint prosthesis.
• Antibiotic prophylaxis is NOT indicated for dental patients with PINS, PLATES, & SCREWS, nor is it
routinely indicated for most dental patients with total joint replacements.
• High-Risk Patients with prosthetic joints for Hematogenous Total Joint Infection: ALL patients during
the first 2 years after joint replacement require antibiotic premedication. If more than 2 years after
prosthetic joint replacement pass with no complications, then premedication is NOT required.

If unanticipated bleeding occurs, administer an antimicrobial prophylaxis within 2 hours after the
procedure!

If a series of dental procedures is required: observe an interval of 9-14 days between procedures to
reduce the potential for the emergence of resistant organisms, and allow the mouth to repopulate
with antibiotic susceptible flora .

166
If a patient is taking an antibiotic normally used for endocarditis prophylaxis then SELECT a drug NOTES
from a different class rather than increase the dose of the patient's current regimen, or delay the
procedure for 9-14 days after the patient completes the antibiotic.

Bacterial Endocarditis Prophylaxis:

• Amoxicillin: 4 capsules (each 500mg =2000mg =2g) 1hour before the procedure. Dispense 16 capsules.
• Clindamycin-take if allergic to penicillin. 2 capsules (each 300mg = 600mg) 1hour before appointment.
• Cephalexin-4 capsules (each 500mg =2000mg =2g) 1hour before appointment. Dispense 16 capsules.
• Cefadroxil-4 capsules (each 500mg = 2000mg = 2g) 1hour before appointment. Dispense 20 capsules.

TETRACYCLINES - bacteriostatic antibiotics that exert its antibacterial activity by INHIBITING

BACTERIAL PROTEIN SYNTHESIS in the bacterial cell and the FIRST CHOICE to treat mycoplasma
pneumonia, chlamydia infections, rickettsial infections, &vibrio infections. Tetracyclines treat acne,
gonorrhea, syphilis in patients allergic to penicillin, and exacerbations of chronic bronchitis. They have
limited use for treating oral infections, but are good alternatives to penicillin for patient with ANUG
(acute necrotizing ulcerative gingivitis) who require antibiotics. May be useful in periodontal diseases
(juvenile periodontitis caused by actinobacillus infections) .
1. Minocycline (Minocin)-treats acne, anthrax, and meningococcal prophylaxis. Ex: Arestin used
to treat periodontal pockets causing the pocket to shrink.
2. Doxycycline (Vibramycin)-treats syphilis, rickettsia infections, Chlamydia , & mycoplasma
infections, and is an alternative to mefloquine for malaria prophylaxis.
3. Demeclocycline (Declomycin)

Tetracyclines Indications/Treatments:
• Medical infections causes by susceptible gram (+) &gram (-) bacteria.
• Infections caused by Mycoplasma, Chlamydia , or Rickettsia .
• Exacerbations of Chron ic Bronchitis.
• Acne, gonorrhea, and syphilis in patients allergic to penicillin.
• Periodontitis associated with Actinobacillius Actinomycetemcomitans (AA).

• Tetracyclines ARREST RAPID BONE LOSS associated with juvenile periodontitis via tissue
regeneration & enhanced repair due to their collagenase inhibiting effect. Tetracyclines have
been used as alternatives to penicillin in ANUG patients (Acute Necrotizing Ulcerative Gingivitis)
who require antibiotics.

• Absorption of tetracyclines from the GI tract is inhibited by divalent &trivalent cations (Ca2+,
Mg2+, Fe2+, AI3+. These cations form CHELATION PRODUCTS with the tetracyclines to prevent their
absorption. Thus, tetracyclines are NOT GIVEN with milk or dairy products that contain Ca2+,
iron-containing vitamins (contain Fe2+), mineral supplements containing these ions, or antacids
that contain Mg2+.
• Tetracycline absorption from GI tract is inhibited by divalent & trivalent cations (Ca2+, Mg2+,
Fe2+, AI3+) thus, are not given with milk and dairy products, iron supplements, or antacids.
• The therapeutic effectiveness of tetracyclines is most affected (reduced) by concomitant
ingestion of antacids. Tetracycline chelates with calcium.

Common Tetracyclines Adverse Effects: photosensitivity, nausea, diarrhea, fungal superinfections,

teeth discoloration &enamel hypoplasia in young children.
• LIGHT exposure causes oxidation of tetracyclines into a brown material that permanently
discolors teeth. Tetracyclines are contraindicated in children up to age 8 and in pregnant women,
since they can chelate Ca2+ ions and become incorporated in bony tissues. A greenish-brown
discoloration effect is sometimes seen in newly erupted teeth of infants whose mothers have received
tetracycline during pregnancy.
• Occurrence of opportunistic (superinfections) caused by Candida albicans due to the wide
spectrum of antibacterial actions which alters normal flora (i .e. vaginal and oral candidiasis/vaginal
oral yeast infections). Thus, tetracyclines use to treat odontogenic infections is limited because they
cause "yeast" infections very easily.
• PHOTOSENSITIVITY. The photosensitivity reaction caused by tetracyclines causes the appearance of
red rashes or blotches over the skin in the presence of sunlight.

167
 Tetracyclines are a group of broad-spectrum, bacteriostatic antibiotics that INHIBIT PROTEIN
SYNTHESIS in the bacterial cell wall by binding to the 30S-subunit of the bacterial ribosome. Inhibiting
ribosomal function interferes with the attachment of the growing amino acid chain to prevent complete
formation of peptides from the ribosome. Since no peptides are formed, no proteins are formed. Since
proteins are required for the bacterial cell to metabolically function, the lack of proteins causes a static
state where the bacterium becomes vulnerable to phagocytosis by the body's immune system.

MACROLIDES - inhibit protein synthesis.

1. Erythromycin-the prototype macrolide, and 2nd choice bacteriostatic agent to penicillins to
treat oro-dental infections caused by aerobic gram (+) bacteria and against many oral
anaerobes (not very effective against gram (-) bacteria). However, resistance may develop quickly.
Adverse Effects: GI EFFECTS in -21 % of patients, and OTOTOXICITY (a less common, but
significant adverse reaction to erythromycin (especially after IV admin) manifested as tinnitus
and/or deafness.
• Oral bioavailability of erythromycin is poor. It is readily inactivated by stomach acid, thus
several salts have been developed to overcome this drawback: Erythromycin Stearate
(Erythrocin) & Erythromycin Estolate (Llosone) has the best oral absorption, but can cause
liver toxicity.
• To prevent their destruction by stomach acid, erythromycins are usually ENTERIC COATED
(a special coating applied to tablets or capsules that prevents their release and absorption of
their contents until they reach the intestines. Erythromycin is metabolized in the liver, and
excretion is mainly via bile.
• In penicillin allergic patients, erythromycins are important alternatives, and may be given
prophylactically before dental procedures to prevent BACTERIAL ENDOCARDITIS. It is
second only to penicillins to treat dental infections, since it is effective against most
aerobic gram (+) bacteria that cause orodental infections.
• Erythromycin was previously used as an alternate agent for the penicillin-allergic patient,
but is NO LONGER USED due to GI tract upset (the most common side effect, so is always
taken with food) &complicated pharmacokinetics. However, practitioners who successfully
use erythromycin for prophylaxis, may choose to continue using it.
• Erythromycin is a BACTERIOSTATIC antibiotic that binds to the 50S ribosomal subunit of
susceptible bacteria, causing INHIBITION OF PROTEIN SYNTHESIS.
• Erythromycin Derivatives: Erythromycin base (E-mycin; Eryc), Erythromycin ethylsuccinate
(EES), Erythromycin stearate (Erythrocin), and Erythromycin estolate (Llosone).

2. Clarithromycin (Biaxin) &Azithromycin (Z-Pak, Zithromax)-alternative antibiotics for

prophylaxis against bacterial endocarditis. Their bacterial spectrums of activity are similar to
Erythromycin, but they possess greater intrinsic activity against H. influenzae. These macrolides
concentrate within macrophages like Mycobacterium avium intracellulare. Both cause fewer GI
tract adverse reactions and fewer drug interactions than erythromycin.
• Both agents have significant tissue penetration ability, and a prolonged elimination half-life
of Azithromycin (ll-14hrsl, allows for one daily dose, and twice-daily dosing for Clarithromycin.
• 10% of patients receiving Clarithromycin and 5% of patients taking Azithromycin have adverse
GI effects.

CEPHALOSPORINS - a BROAD-SPECTRUM &BACTERICIDAL antibiotics that inhibits bacteria cell

wall synthesis during cell division so wall closure does not occur (causing cell lyses/death) (just like
penicillin's mechanism). Cephalosporins act against a wide-range of gram (+) & gram (-) bacteria, and
are used in penicillin allergic patients with Staphylococcal infections. There are 4 generations of
cephalosporins. Progression from the 1st to the 4th generation is associated with a broadening of action
against more gram (-) bacteria and a decreased activity against gram (+) bacteria .

1. 1st Generation Cephalosporins: Cephalexin (Keflex), Cephradine (Velosef), Cefadroxil (Duricef),

Cefazolin (Ancef). Used to prevent bacterial endocarditis in patients with a history of non-
immediate allergic reactions to penicillin. -10% of patients with penicillin allergies have cross
allergenicity to cephalosporins. Cephalosporins are contraindicated in patients with immediate-
type hypersensitivity reactions to penicillins (i.e. urticaria, angioedema, & anaphylaxis).

168
 ........

• Cephalexin &Cephradine are drugs of first choice for standard prophylaxis medication in NOTES
a patient NOT allergic to penicillin, with a TOTAL JOINT REPLACEMENT (prosthetic implants).
Prophylaxis dose is 2 grams orally 1hr prior to dental treatment. This is according to the
"Advisory Statement, Antibiotic Prophylaxis for Dental Patients with Total Joint Replacement"
published by the ADA and American Academy of Orthopaedic Surgeons in JADA.

2. 2nd Generation Cephalosporins: Cefaclor (Ceclor), Cefuroxime (Ceftin), Cefoxitin (Mefoxin),

& Cefprozil). Treats oro-dental infections (acute cellulitis) caused by gram (+) &(-) aerobic
bacteria, and against anaerobic bacteria causing periapical abscesses.
3. 3rd Generation Cephalosporins: Cefixime (Suprax) & Cefoperazone (Cefobid).
4. 4th Generation Cephalosporins: Cefepime (Maxi pi me).

AMINOGLYCOSIDES - bactericidal antibiotics with a broad antibacterial spectrum, used primarily to

treat AEROBIC-GRAM (-) infections. They have little action against gram (+) anaerobic or facultative
bacteria. They irreversibly bind to the 30S ribosomal subunit of bacteria to inhibit protein synthesis.

• Am inoglycosides are reserve.d to treat more serious bacterial infections because of their 2 well-known
adverse effects ototoxicity &nephrotoxicity. Aminoglycosides may cause severe neuromuscular
weakness lasting hours-to-days because of their potential curare-like effect. Aminoglycosides may
aggravate muscle weaknesss in patients with muscular disorders like myasthenia gravis, infant
botulism, or parkinsonism, thus are contraindicated or used with great precaution in patients with
these conditions.

• Aminoglycosides are poorly absorbed after oral administration, thus must be administered 1M or IV
to produce a systemic effect. They are rapidly excreted by the normal kidney.

Aminoglycosides:
1. Gentamicin (Garamycin), Amikacin (Amiken), Tobramycin (Nebcin), & Netilmicin (Netromycin).
These aminoglycosides are effective against serous infections cuased by aerobic-gram (-) bacteria
like E. Coli, Enterobacter, Klebsiella, Proteus, Pseudomonas aeruginosa, and Serratia.
2. Streptomycin-the first aminoglycoside effective to treat tuberculosis, but is rarely used today.
3. Neomycin (Mycifradin) &Kanamycin (Kantrex)-due to its toxicity potential, neomycin is used
only topically or locally (i.e. in the GI tract). Kanamycin is rarely used because of its marked
tendency to cause ototoxicity.
4. Spectinomycin-sometimes used to treat gonorrhea .

BACITRACIN - inhibits bacterial cell wall synthesis, gram (+) activity.

• Potentially nephrotoxic if systemic, so only administered topically.
• Sold as a triple antibiotic ointment/Neosporin with polymyxin & neomycin to treat dermatological &
ophthalmic infections.

POLYMYXIN B- cationic basic peptides that (cationic detergents) that SCRUB BACTERIA CELL MEMBRANES.
• Administered topically due to potential nephrotoxicity (its major adverse effect) .
• Only active against gram (-) rods = PSEUOOMONAS (treat corneal ulcers &external otitis).
• Sold as a triple antibiotic ointment (containing bacitracin or neomycin) to treat SUPERFICIAL SKIN
LACERATIONS (dermatological &ophthalmic infections).

CHLORAMPHENICOL (CHLOROMYCETIN) - a broad-spectrum antibiotic that can cause BONE

MARROW DISTURBANCES (aplastic anemia) thus, has LIMITED USE due to its side effects. Effective
against gram (+) & gram (-) bacteria and against anaerobes, used as a 2nd or 3rd line drug in medicine
to treat SERIOUS INFECTIONS due to organisms resistant to less toxic antibiotics. It is a bacteriostatic
antibiotic that reversibly binds to the 50S ribosomal subunits of susceptible organisms, to prevent amino
acids transfer to growing peptide chains, thus INHIBITING bacterial PROTEIN SYNTHESIS.
Chloramphenicol causes 3 Major Toxicities:
1. Aplastic Anemia-
2. Bone Marrow Suppression (anemia & neutropenia may occur during the first week of
antibiotic therapy).
3. Gray Syndrome-characterized by circulatory collapse, cyanosis, acidosis, coma, and death.

169
 PARKINSON'S DISEASE - a slowly progressing, degenerative disorder of the nervous system with
several distinguishing features: tremor (shaking) when at rest, sluggish initiation of movements, and
muscle rigidity. In Parkinson's disease, nerve cells in the BASAL GANGLIA DEGENERATE, causing
decreased dopamine production. It may be treated, bu not cured with various drugs:

1. Carbidopa-a drug used to treat PARKINSON'S DISEASE, but only works when combined with
LEVODOPA (treats Parkinson's Disease to replenish the brain's supply of dopamine, which is
the deficient neurotransmitter in Parkinson's.
• Administering Carbidopa + Levodopa = Sinemet, which reduces the required dose of levodopa
by -75%. When levodopa is given alone, most of the dose is metabolized before it reaches the
brain. Thus, large doses are required and can cause unwanted side-effects.
• Carbidopa inhibits the peripheral decarboxylation of levodopa to simultaneously reduce
peripheral side-effects and to allow more levodopa to reach the brain . Since carbidopa does
not cross the blood-brain barrier (BBB), levodopa is converted into dopamine in the brain.
Thus, co-adminstration of carbidopa + levodopa in the form of SINEMET allows a significant
reduction of levodopa dosage without reducing the desired effects.
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2. Levodopa (L-dopa, Dopar)-in combination with carbidopa, is the precursor of dopamine, and
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3. Bromocriptine (Parlodel) & Pergolide-dopamine agonists often given in addition to levodopa
co
-< early in the treatment process to enhance levodopa's action, or may be given later in treatment
when levodopa's side effects become problematic.
4. Selegiline (Eldepryl)-selective inhibitor of MAO Type B (the enzyme that causes the oxidative
deamination of dopamine in the brain). Selegiline is used as an adjunct to levodopa.
5. Amantadine (Symmetrel)-anti-viral agent that enters the CNS to treat Parkinson's disease by
potentiating dopaminergic responses. Anti-parkinsonian actions are unrelated to its antiviral
effects. Used in the early stages for mild disease.
6. Anticholinergic drugs: includes Benztropine & Trihexyphenidyl, certain anti-depressants, &
anti-histamines like diphenhydramine. These may be given without L-dopa in early stages of the
disease, with levodopa in later stages.

TUBERCULOSIS - a bacterial infection caused by MYCOBACTERIUM TUBERCULOSIS. Anti-tubercular

drugs either inhibit bacterial growth or kill the bacteria. Since Mycobacterium tends to develop resistance
to any single anti-tubercular drug, combination drug therapy is the standard in treating tuberculosis.
TB is ALWAYS treated by MULTI-DRUG THERAPY (minimum of two drugs): Anti-tubercular drugs:
1. Rifampin-given in combination with other agents. Prevents transcription (RNA synthesis) by
inhibiting bacterial DNA dependent RNA polymerase.Treats Mycobacterium tuberculosis (TB),
Mycobacterium leprae (Leprosy). THE MOST POTENT ANTI-LEPROSY AGENT.
2. Isoniazid-often given in a 4 drug regimen along with Rifampin, Pyrazinamide, & Ethambutol.
Adverse Effects: PERIPHREAL NEURITIS (paresthesia) caused by pyridoxine (vitamin B6)
deficiency. Corrected with vitamin B6 supplements, and FATAL HEPATITIS.
3. Pyrazinamide-popular in combination with Rifampin. Enters CSF to treat
TUBERCUOSIS MENINGITIS
4. Ethambutol-given in combination with other agents. Adverse Effects: Optic neuritis,
hyperuricemia, & COLOR VISION DISTURBANCES
5. Streptomycin-given in combination with Isoniazid.
6. Rifabutin-active against MAl complex.

ANTI-MALARIA AGENTS - malaria is a disease due to infection by protozoal genus plasmodium.

Plasmodium falciparum is the most dangerous.
1. Mefloquine (Lariam)-a member of the blood schizonticide anti-malarial drugs that treats
MALARIA caused by Plasmodium falciparum (the most dangerous Protozoan), P. vivax
malariae, and P. ovale. It is active alone against multi-drug resistant Plasmodium falciparum.
2. Chloroquin (Aralen)-eradicates erythrocytic (RBC) forms by inhibiting plasmodial heme
polymerase, and damages parasitic membranes by lysing the RBC and parasite. Also inhibits
parasitic DNA synthesis. Treats erythrocytic forms of Plasm podium falciparum & Plasmodium
vivax. Asystemic amebicide that treats amebic liver abscess and extraintestinal amebiasis.

170
 3. Quinine-back-up agent for chloroquine used in combination with FANSIDAR chloroquine-resistant NOTES
malarial strains. Adverse effect: CINCHONISM (nausea, vomiting, vertigo, tinnitus).
4. Atovaquone + Proguanil (Malarone)
5. Sulfadoxine + Pyrimethamine (Fansidar)
6. Halofantrine
7. Pyrimethamine-folate antagonist (antifolate) active against P. falciparum, P. malariae &
Toxoplasma gondii.

Antibiotic Mechanism of Action on Bacteria

Agents that Affect Agent Inhibiting Bacteria Agents Interfering with Agents that Affect
Cell Walls Protein Synthesis Biosynthetic/Metabolic Cell Walls
Pathways

Aztreonam Am inoglycosides Sulfonamides Quinolones

Bacitracin Chloramphenicol (sulfa drugs) (ciprofloxacin)
Cephalosporins Clindamycin Trimethoprim Metronidazole
Cycloseri ne Erythromycin FI uoroq uinolones (Flagyl)
Imipenem Lincomycin
Penicillins Macrolides
Vancomycin Tetracycline

*The most common clinical cause of bacterial resistance is using antibiotics when they are
not indicated.

Antibiotic Antibacterial Action & Mechanism

Antibiotic Action Mechanism Adverse Effects

Penicillins: Inhibit Cell Wall Synthesis Bactericidal Hypersensitivity

• Penicillin VK, Amoxicillin,
• Augmentin, Ampicillin
Cephalosporins: Inhibits Cell Wall Synthesis Bactericidal Hypersensitivity
• Cephalexin (Keflex)
• Cefaclor (Ceclo
Clindamycin Inhibits 50S Ribosome Bacteriostatic Pseudomembranous
Colitis, Severe GI upset
Macrolides: Inhibits 50S Ribosome Bacteriostatic
• Azithromycin (Z -Pak) None
• Clarithromycin (Blaxin) GI hyperactivity
• Erythromycin GI hyperactivity
Tetracyclines: Inhibits 30S Ribosome Bacteriostatic
• Tetracycline Su peri nfections
• Doxycycline (Vibramycin) None
• Minocycline (Minocin, None
Arestin)
Aminoglycosides: Inhibits 30S Ribosome Bactericidal Ototoxicity &
• Streptomycin Nephrotoxicity
• Gentamycin
Miscellaneous:
• Ciprofloxacin (Cipro) Inhibits DNA Bactericidal Nausea, Headache
• Bacitracin Inhibits Cell Wall Synthesis Bactericidal Nephrotoxicity
• Chloramphenicol Inhibits 50S Ribosome Bacteriostatic Blood Disorders
171
 ANTI-FUNGALS
MYCOSES - chronic fungal infections. Mycotic infections are superficial (involving skin caused by
dermatophytes), or can infiltrate the skin to cause subcutaneous infections. Antifungal agents are drugs
to treat systemic and subcutaneous fungal infections.

CANDIDIASIS - a fungal infection usually found in the oral cavity or vagina (C. Albicans) that causes
an inflammatory, pruritic infection characterized by a thick, white discharge. Common in patients with
an immune deficiency in T-Iymphocytes, receiving chemotherapy, & immunosupressed/AIDS patients.
However, his yeast-like fungi is a normal inhabitant of the oral cavity and vaginal tract, but is usually
held in check by the indigenous bacteria of these areas.

• Angular Cheilitis-bilateral ulcers at the corners of the mouth linked to C. Albicans.

• Nystatin (Mycostatin)-drug of choice (anti-fungal polyene antibiotic) for treating oral cavity
Candidiasis (fungal infection). An anti-fungal used as "swish & swallow" to treat oral cavity Candida
infections. Taken as an oral suspension to be swished around the mouth and swallowed or may also
be prescribed in an ointment form that alters the fungal cell membrane to treat cutaneous and
mucocutaneous Candidiasis.Nystatin is an oral suspension that alters the fungal cell membrane.
Nystatin's mechanism & structure is similar to Amphotericin B.
• Drug of choice for treating Candidiasis in an HIV-infected patient (Le. Hairy leukoplakia).

• Clotrimazole (Mycelex Troche)-anti-fungal taken as a troche (lozenge) that is slowly dissolved in

the mouth and swallowed. Treats oropharyngeal Candidiasis by altering the fungal cell membrane.

• Nystatin & Clotrimazole work by binding to sterols in the fungal cell membrane, increasing
permeability, and permitting the leakage of intracellular components. This leads to death of the
affected fungal cell.

Topical Anti-Fungals (Creams/Ointments):

1. Amphotericin-B (Fungizone): anti-fungal given IV or orally to treat severe systemic fungal
infections caused by fungi like Candida species. Treats cutaneous & mucocutaneous Candidiasis
by altering the fungal cell's membrane.
2. Ketoconazole (Nizoral)-inhibits Ergosterol synthesis to disrupt the fungal membrane. Can
antagonize/inhibit amphotericin B's antifungal effect. Given orally to treat Histoplasmosis,
Nonmmeningeal coccidioidomycosis, Blastomycosis, Dermatomycosis. Can be given in a cream
form to treat cutaneous & mucocutaneous candidiasis by altering the fungal cell membrane.
Adverse Effects: toxicity causes ENDOCRINE EFFECTS by inhibiting cortisol & testosterone
synthesis causing (gynecomastia, decreased libido, and menstrual irregularities).

Systemic Anti-Fungal Agents:

1. Fluconazole (Diflucan)-inhibits erogosterol synthesis. Given orally or IV, crosses BBB (enters
CSF). Drug of Choice: Mucosal candidiasis (oropharyngeal & esophageal), & Coccidiomycosis.
Treats blastomycosis, histoplasmosis, & Cryptococcal meningitis in AIDS patients.
2. Ketoconazole (Nizoral)-used to treat oral, esophageal, and oral esophageal Candida infections
by inhibiting ergosterol synthesis to disrupt the fungal membrane. Adverse Effects: toxicity
causes ENDOCRINE EFFECTS by inhibiting cortisol & testosterone synthesis causing
(gynecomastia, decreased libido, & menstrual irregularities).
3. Amphotericin-B (Fungizone): an anti-fungal of choice (wide spectrum) given IV injection or orally
to treat SEVERE SYSTEMIC FUNGAL INFECTIONS (MYCOSES) caused by fungi like Candida by
binding to ergosterol in the fungal cell membrane. Not is CSF Also treats cutaneous &
mucocutaneous Candidiasis by altering the fungal cell membrane. Adverse Effects: associated
with high incidence of KIDNEY TOXICITY.
4. Itraconazole-inhibits ergosterol synthesis. BROAD spectrum anti-fungal given ORALLY. Drug of
choice for Blastomycosis & Paracoccidioidomycosis. Well distributed in BONE, SPUTUM, &
ADIPOSE TISSUE (Not CSF).
5. Flucytosine-a PRODRUG that inhibits fungal DNA & RNA synthesis and cell division.Given o;2 11y
to treat systemic mycosis by Chromoblastomycosis, Candidiasis, & Cryptococcus. Enters CSF,
excreted by Glomerular Filtration . Adverse Effects: GI, Reversible Bone Marrow Suppression.
172
ANTI-PROTOZOALS
Anti-Protozoal Agents:
1. Nitazoxanide (Alinia)-an oral ANTI PROTOZOAL that treats DIARRHEA caused by GIARDIA LAMBLIA
and protozoal infections caused by Cryptosporidium Parvum. This type of diarrhea is an intestinal
infection called Giardiasis, and is the most common protozoan infection in the U.S. It mechanism
is interfering with the electron transfer reaction within the protozoa that is essential to
anaerobic metabolism.

2. Atovaquone (Mepron)-an anti-protozoal agent that treats Pneumocystitis Carinii Pneumonia

(PCP) in patients intolerant to Co-trimoxazole (formed by the combination of Trimethoprim +
Sulfamethoxazole). Co-trimoxazole is the Drug of choice for Pneumocystis carinii pneumonia
by inhibiting folic acid synthesis.

3. Eflornithine (Vaniqa}-has orphan drug status to treat the meningoencephalitic stage of

Trypanosoma Brucei Gambiense infection (SLEEPING SICKNESS). Also indicated as a facial
cream to reduce unwanted facial hair and areas under the chin .

4. Furazolidone (Furoxone)-antiprotozoal agent that treats DIARRHEA caused by susceptible

Giardias Lamblia and Vibrio Cholerae.

5. Metronidazole (Flagyl}-a synthetic antibacterial & antiprotozoal effective against Trichomonas

Vaginalis that causes Trichomoniasis. It is one of the most effective drugs available against
anaerobic bacterial infections. Metronidazole is not a true antibiotic since it is not found in
natural organisms. It is a synthetic substance produced in a chemical laboratory. Adverse Effects:
dizziness, headache, nausea.

ANTI-VIRALS
VIRUSES - double or single stranded DNA or RNA enclosed in a protein coat (CAPSID). Viruses lack a
cell membrane, wall, and metabolic machinery, thus are OBLIGATE INTRACElLULAR PARASITES.

Anti-Viral Medications:
• Penciclovir (Denavir)-an antiviral agent that is active against Herpes Simplex Virus Type 1 (HSV-
1). It is a cream formulation indicated to treat recurrent herpes labialis (cold sores) in adults. This
condition is caused by HSV-l. Penciclovir is not available for systemic dosing. Penciclovir inhibits viral
action by selectively inhibiting herpes viral DNA synthesis which inhibits viral replication.

• Acyclovir-inhibits viral DNA polymerase/viral DNA synthesis. Available in tablets and creams to treat
HSV-1, HSV-2, &varicella zoster (chicken pox/shingles). Drug of Choice for HSV Encephalitis,
genital herpes, herpes labialis (cold sores) &varicella-zoster virus. Enters CSF, and accumulates
during renal failure.
• Valacyclovir (VALTREX)-PRODRUG of acyclovir given orally that is converted by 1st pass
metabolism into acyclovir. Treats HSV1&2, genital herpes, cold sores (herpes labialis), &herpes
varicella-zoster virus (shingles).

• Ganciclovir-inhibits viral DNA polymerase/viral DNA synthesis. Treats Cytomegalic Retinitis (CMV
retinitis) &CMV prophylaxis in transplant patients (crosses BBB).

• Docosanol cream (Abreva) &Lysine tablets-anti-viral agents that treat Herpes Labialis (cold sores) .

173
 AIDS (ACQUIRED IMMUNODEFICIENCY SYNDROME) - recognized since 1981 as a unique
clinical syndrome caused by an infection with the human immunodeficiency virus 1 (HIV-1) or virus 2 (HIV-
2). The major cellular defect caused by HIV infection is DEPLETION OF T-CELLS (sub-type T-helper cells
CD4 cells) which causes a compromised immune system that is susceptible to opportunistic infections
(i.e. Hairy Leukoplakia, Candidiasis).

• HIV is a RETROVIRUS responsible for the fatal illness from AIDS. A "retrovirus" has RNA as its
nucleic acid and uses the reverse transcriptase enzyme to copy its genome in the DNA of the host's
cell chromosomes. This DNA segment is then permanently incorporated into the host cell's DNA within
the nucleus. The integrated DNA segment can produce new RNA in the host cell's cytosplasm, and
then synthesizes viral proteins that are passed onto other host cells like the immune system
macrophages. Ultimately, enough of the human immune cells are compromised so that immune
function is lost.

• HIV drugs: Didanosine (Videx), Zidovudine (Retrovir), Ritonavir (Norvir), Indinavir (Crixivan) all work
by inhibiting steps in the HIV infection process within the target cells to stop immune system
destruction by the HIV retrovirus.

• HIV Protease Inhibitors: Ritonavir (Norvir), Amprenavir, Indinavir (Crixivan), Nelfinavir (Viracept),
Suquinavir (lnvirase). All inhibit HIV aspartate proteases required to produce the structural proteins
& enzymes necessary for viral replication. Protease inhibitors suppress viral replication by inhibiting
protease (enzyme responsible for cleaving viral precursor peptides into infective virions).
Contraindicated with patients taking Rifampin.

• Nucleoside Reverse Transcriptase Inhibitors: Zidovudine (Retrovir, AlT), Zalcitabine (Hivid, ddC),
Didanosine (Videx), Stavudine & Lamivudine. All are converted into AZT-triphosphate analogs in cells
to inhibit viral DNA synthesis & replication by inhibiting reverse transcriptase (RT). These agents
are nucleosides that inhibit the viral enzyme "reverse" transcriptase" to inhibit HIV viral RNA from
being made into a DNA segment (prevents the HIV virus genome of being copied from RNA). Adverse:
myelosuppression of bone marrow.
• Stavudine (d4T, Zerit)-anti-retroviral drug that treats adults with HIV in combination with other
anti-retroviral agents.

• Non-Nucleoside Reverse Transcriptase Inhibitors: Nevirapine (Viramune), Adefovir (Hepsera),

Efacirenz, & Delavirdine (Rescriptor). Non-competitive inhibitors of HIV reverse transcriptase that
inhibit the catalytic reaction of reverse transcriptase that is independent of nucleotide binding. Does
not cause myelosuppresion.

• Interferon-natural glycoproteins synthesized by recombinant DNA technology to activate host

enzymes to block viral RNA translation, and interfere with ability of viruses to infect cells.
• IFN-a (intron A)-treats Chronic Hepatitis B&C, Genital Papilloma, & Kaposi's Sarcoma in
HIV patients.

Treatment of Viral Respiratory Infections (Influenza A&B, Respiratory Syncytial Virus (RSV):
1. Amantadine (Symmetrel) & Rimantadine-anti-viral agents that inhibit/block viral membrane
matrix protein "M2" ion channel. Used for prophylaxis or early treatment of Influenza "A"
virus. Amantadine enters the CNS to treat Parkinson's disease.

2. Ribavirin-inhibits viral mRNA synthesis. Treats SERIOUS RSV infections in infants/young children,
influenza A&B, Acute Hepatitis C, & SARS. Active orally, IV and as an AEROSOL to treat respiratory
viral infections.

174
NSAID's (NON-STEROIDAL ANTI-INFLAMMATORY DRUGS) NOTES
NSAID'S - have anti-inflammatory effects due to their ability to inactivate the enzyme "prostaglandin
endoperoxide synthase" (cyclooxygenase). Enzyme inactivation inhibits the cyclooxygenase step of the
arachidonic acid cascade, thus reducing local prostaglandin synthesis. NSAID's have anti-
inflammatory, analgesic, &antipyretic actions.
• Prostaglandins are derived from the unsaturated fatty acids in cell membranes.

NSAlDs decrease production of inflammatory mediators possess anti-inflammatory, analgesic, &

anti-pyretic effects. A"ceiling" effect exists for the analgesic properties. Most NSAlDs work best for mild
to moderate pain, although efficacy varies between NSAlDs. Safer than corticosteroids for long-term
use, but some NSAlDs have strong adverse effects, thus contraindicated in specific patient
populations. Traditional NSAIDs "reversibly" reduce platelet aggregation (normal platelet function returns
when the drugs leave the system).
• Aspirin, Cortisol, Ibuprofen (Motrin, Advil, Nuprin, Rufen), & Indomethacin have significant anti-
inflammatory properties.

CYClOOXYGENASE (COX) - the enzyme that produces prostaglandins which comes in two forms
(COX-l &COX-2).

COX-l ENZYME - produces prostaglandins in the GI tract. The prostaglandins formed act as a
protective substance against the formation of GI ulcers. Traditional NSAlDs (Ibuprofen, Naproxen, Aspirin)
inhibit the COX-l & COX-2 enzymes to diminish the formation of the protective prostaglandins. Thus, they
effectively reduce pain and inflammation, but can induce GI ulcers are a potential adverse effect. Since
traditional NSAlDs (ibuprofen, naproxen, and aspirin) inhibit both COX-l & COX-2 enzymes they are "Non-
Selective COX Inhibitors:

• Propionic Acid Derivatives: Ibuprofen (Motrin, Advil, Nuprin, Rufen)-has anti-inflammatory properties
by inhibiting prostaglandin synthesis/production in peripheral tissues at sites of pain and
inflammation. Inhibiting prostaglandin production decreases the inflammatory response at sites of
surgery, injury, or infection which results in a reduction of perceived pain. Ibuprofen is the MAIN
INGREDIENT in OTC Advil, Nuprin, &Medipren (which contains 200mg of ibuprofen). Ibuprofen is also
the main ingredient in Motrin (only sold via prescription) and contains at least 400mg of ibuprofen.
More efficacious analgesics & anti-inflammatory than aspirin. Better for moderate pain . One of the
stronger NSAID analgesics. Patients intolerant to aspirin may not be able to tolerate ibuprofen. GI
ulceration & upset, and drug interactions are common adverse effects. Fenoprofen, Suprofen, Naproxen,
Naproxen Sodium, Ketoprofen, & Benoxaprofen are also NSAlDs propionic acid derivatives.
• Ibuprofen (Motrin, Advii) is a non-narcotic analgesic that may interact with Warfarin (Coumadin)
to cause unnecessary bleeding because it inhibits platelet aggregation.
• Ibuprofen can be given to patients with a history of drug abuse since it has no addictive properties.
Ibuprofen is an NSAID and non-narcotic analgesic which have no liability for abuse or addiction.
They are not controlled substances.

• Naproxen/AnaproxiNaprosyn (Aleve)-potent anti-inflammatory & analgesic. Longer-acting than

ibuprofen, better compliance, relieves pain longer. Does not interact with Warfarin or oral
hypoglycemics, so better for Type" Diabetes Mellitus patients. Inhibit platelet aggregation.

• Flurbiprofen (Ansaid)-inhibit platelet aggregation.

• Ketorolac (Toradoi}-a newer NSAID and more efficacious analgesic than aspirin. Sometimes used
for moderate-to-severe pain after minor dental surgery or painful dental procedure. Suggested
use for no > 5 days. Not for longer-term pain relief, as may be toxic with long-term use.

• Acetic Acid Derivatives (NSAlDs): Indomethacin (Indocin), Sulindac (Clinoril), & Tolmetin (Tolectin).
These NSAIDs can cause GI bleeding, ulcers, and possible stomach perforation .

• Fenamic Acid Derivatives: Meclofenemate (Meclomen) &Mefenamic acid (Ponstel).

175
 Drugs that Increase Bleeding Times: aspirin, non-selective NSAIDs (Ibuprofen, Naproxen, Ketoprofen,
Flurbiprofen), anti-platelet drugs (Clopidogrel (Plavix) &Ticlopidine (Ticlid), and anti-coagulants (Warfarin
(Coumadin) &Heparin) .
• Ibuprofen &other "non-selective" NSAlDs (inhibitors of COXl &COX2 enzymes) inhibit platelet
aggregation. This inhibition enhance/potentiates the anti-coagulant effects of Warfarin
(Coumadin) to increase bleeding risk.
• Clopidogrel (Plavix)-inhibits blood clotting (increases bleeding time) by irreversibly inhibiting platelet
aggregation. Thus, the effects on blood clotting are the same as with aspirin. Clopidogrel does not
cuase gastric ulcers like aspirin, and is the ANTI PLATELET AGENT OF CHOICE FOR PATIENTS WITH A
HISTORY OF ULCERS.

SALICYlATES - interfere with blood clotting mechanisms by irreversibly reducing platelet adhesion
(stickiness or aggregation). Bleeding time is prolonged until new platelets are formed.
• Aspirin (Acetylsalicylic Acid)-prototypical non-selective COX inhibitors (NSAID) that inhibits COX-l &
COX-2 (cyclooxygenase) to inhibit prostaglandin production (prostaglandins are potent inflammatory
mediators). Aspirin's analgesic effects are better if given to prevent prostaglandin production .
Prevents worsening of pain . However, cannot reduce pain already caused by prostaglandin build-up.
Aspirin INACTIVATES the cyclooxygenase enzyme that makes prostaglandins, thus inhibits
prostaglandin synthesis. As a result, aspirin is an analgesic, antipyretic (reduces fever), and anti -
inflammatory. Aspirin is an irreversible platelet inhibitor and can reduce blood clotting, causing
prolonged bleeding. Aspirin may interact with Warfarin (Coumadin) to cause unnecessary bleeding.

• Antipyretic action of salicylates (aspirin) is explained in part by cutaneous vasodilation leading

to increased heat loss.

• Aspirin is an anti-inflammatory, antipyretic, and analgesic used to relieve headaches, toothaches,

minor aches and pains, and to reduce fever. The GI tract rapidly absorbs it.

• Low doses of aspirin taken regularly can have a cardioprotective effect. These low doses reduce
thromboxane production of platelets to result in the inhibition of platelet aggregation. In this way,
aspirin has the ability to inhibit the formation of life-threatening thrombi (blood clots).

• If a patient is taking ibuprofen, ASPIRIN is the analgesic that if given while the patient is taking
ibuprofen will DIMINISH the analgesic effectiveness of the ibuprofen. When aspirin and ibuprofen
are given together, the analgesic efficacy of both is less than that of aspirin or ibuprofen alone.
Aspirin displaces ibuprofen from plasma protein binding sites, thus hastening its disappearance
from the blood stream. It is then quickly eliminated from the body by the kidneys through urine.

• Aspirin inhibits blood clotting by inhibiting platelet aggregation in an irreversible manner.

Inhibiting platelet aggregation prevents the activation of the coagulation pathway, thus no fibrin
(clot) is formed. Asprin does not affect the coagulation pathway. Discontinuation of aspirin for 5-
7 days allows for normal clotting time to reappear due to the synthesis of new platelets.

• Aspirin (NSAlDs) Contra indications:

• Bleeding disorders (aspirin increases BT) & Asthmatics.
• Children with viral infections with or without fever due to a potential association with Reye's
Syndrome (a serious neurological defect).
• Pregnancy, especially the 3rd trimester.
• Peptic ulcers as aspirin may cause GI tract bleeding/ulcerations.
• Adverse effects: GI upset, overdose causes hepatic &nephrotoxic. Death if overdose by
respiratory acidosis.
• Salicylism-describes all of the symptoms caused from ingesting extremely large doses of ASPIRIN
(tinnitus/ringing in ears, vertigo/dizziness, nausea, sweating, vomiting, headache, and
mental confusion).

176
COX-2 ENZYME - produces prostaglandins at sites of surgery, infection, and inflammation. When COX- NOTES
2 enzyme is inhibited, less prostaglandins are produced, and there is less pain and inflammation. COX-2
selective inhibitors reduce pain and inflammation without any risk of GI ulcers. COX-2 Selective Inhibitors-
newer NSAlDs that do not affect blood clotting (do not affect platelet function/aggregation) thus can be
given to patients concomitantly taking "blood thinners" like aspirin, warfarin (coumadin), & heparin.
• Rofecoxib (Vioxx) &Celecoxib (Celebrex) &Valdecoxib (Bextra)-more efficacious analgesic than
aspirin and ibuprofen with less GI side effects, and does not inhibit platelet aggregation, so SAFER
for bleeding disorders. COX-2 selective inhibitors treat signs & symptoms or RHEUMATOID
OSTEOARTHRITIS, acute pain, and pain from dysmenorrhea.
• COX-2 selective inhibitors are not salicylates because they are not aspirin drugs and are not opiates
because they do not work like morphine, and are not steroidal anti-inflammatories because they are
not corticosteroids like hydrocortisone.

HEPARIN - a high MW heteropolysaccharide found especially in the LUNGS and inactivates thrombin
and other coagulation factors to prevent blood clotting. Heparin is contained inside mast cells &
basophils found in C.T. and in extracellular spaces near blood vessels, especially in the lungs. *Heparin
neutralizes tissue thromboplastin and blocks thromboplastin generation. Heparin inhibits blood
clotting by affecting the coagulation pathway to PREVENT FIBRIN FORMATION.

• Administration of heparin causes increased bleeding time due to a potentiation of Antithrombin

III, thus inactivating thrombin. This prevents the conversion of fibrinogen fibrin .

• Heparin acts as an anticoagulant by enhancing the inhibition rate of clotting proteases by

Antithrombin III impairing normal hemostasis and inhibiting factor Xa . low MW heparins have a
small effect on partial thromboplastin time (PIT), but STRONGLY inhibit factor Xa.

• Heparin inactivates thrombin and prevents the conversion of fibrinogen to fibrin (blood clot).

• Heparin is used for prophylaxis and treatment of thromboembolic disorders.

• Standard heparin consists of components with MW ranging from 4000-30,000 daltons (average is
16,000 daltons). Low MW heparins range from 2,000-8,000 daltons.

• low MW heparin anticoagulant agents: (Enoxaprin/lovenox, Dalteparin/Fragmin, &

Tinzaparinllnnohep) are used to treat acute symptomatic deep vein thrombosis (DVT) and to prevent
deep vein thrombosis after knee or hip surgery. These are administered subcutaneously since they
cannot be absorbed from the GI tract.

• Thrombin-Inhibitor Type Anticoagulants: administered IV to prevent post-operative deep vein

thrombosis (DVT) after elective hip replacement surgery, and for prophylaxis or treatment of
thrombosis in adults with heparin-induced thrombocytopenia. Their mechanism of action is directly
inhibiting thrombin within the coagulation pathway, thus inhibiting fibrin formation. lepirudin
(Refludan), Argatroban, Danaparoid (Orgaran).

WARFARIN (COUMADlN) & DlCUMAROL - anticoagulants that ANTAGONIZE VITAMIN Kto prolong
blood clotting time, causing decreased liver synthesis of vitamin-K dependent factors (II, VII, IX, & X).
Warfarin inhibits blood clotting by affecting the coagulation pathway to PREVENT FIBRIN FORMATION.

• Used after an myocardial infarction to prevent coronary occlusion, treat pulmonary embolism, and
venous throm bosis.

• Enhanced anticoagulant effects are seen when Warfarin or Dicumarol are combined with aspirin. Thus,
use acetaminophen (Tylenol) for pain control rather than aspirin for patients taking anticoagulants.

• Warfarin interferes with the hepatic synthesis of vitamin-K dependent coagulation factors (II, VII, IX,
X) resulting in the inability of the coagulation pathway to form fibrin (blood clot).

• Vitamin K-a group of fat-soluble vitamins essential for the synthesis of coagulation factors II, VII,
IX, X, &prothrombin in the liver. Vitamin Kenhances (improves) blood clotting.
177
 PROTHROMBIN TIME (PT) - the most valuable test used to evaluate if a patient taking
anticoagulants is a surgical risk. PT test is a one-stage test to detect certain plasma coagulation
defects owing to a deficiency of Factors V, VII, or X. Thromboplastin and calcium are added to a sample
of the patient's plasma and simultaneously to a sample from a normal control. The length of time required
for clot formation in both samples is observed. Thrombin is formed from prothrombin in the presence of
adequate calcium, thromboplastin, and the essential tissue coagulation factors. Aprolonged PT indicates
a deficiency in one of the factors (as in liver disease, vitamin Kdeficiency, or anticoagulation therapy
with the drug Coumarin).

After prothrombin times (PT) are determined, they are expressed as an INR value (international Normalized
Ratio). INR is the ratio of the prothrombin time measured in the patient divided by a standard
prothrombin time value, and multiplied by a constant.

Patients on anticoagulant therapy may have excess bleeding after dental treatment. Always check the
patient's medical history. If the patient is on anticoagulants, have their physician provide documentation
of their INR (International Normalized Ratio) values to assess anticoagulant effects. INR is the ratio of
the prothrombin time measured in the patient divided by a standard prothrombin time value multiplied
by a constant. The higher INR, the greater the anticoagulant effect (greater clotting).
• INR value of 1: means normal prothrombin times of -12sec; normal blood clotting would be present.
• INR> 1: indicates an anticoagulant effect exists.
• Many patients taking anticoagulants have INR values of 2, 3, 4, 5, and even 6.
• For surgical procedures, an INR of 1-1 .5 indicates a normal prothrombin time (-12-18 seconds).
This is within a safe range.

GLYCOPROTEIN liB/IliA INHIBITOR ANTI PLATELET AGENTS - these intravenous agents are
reversible anti-platelet agents used to prevent acute cardiac ischemic complications and used in patients
with acute coronary syndrome. These agents block the platelet glycoprotein lib/Ilia receptor (the binding
site for fibrinogen, von Willebrand factor, and other ligands) . Inhibiting binding at this final common
receptor REVERSIBLY BLOCKS PLATELET AGGREGATION to prevent thrombosis. Platelet aggregation
inhibition is reversible after cessation of the IV administration of the drugs.
• Abciximab (Reopro), Eptifibatide (Integrilin), Tirofiban (Aggrastat).

Conditions Managed by Anticoagulants (Warfarin/Coumadin) & Anti-platelet Agents (Aspirin &

Clopidogrel (Plavix):
1. Coronary Artery Disease (CAD) by helping prevent threat of myocardial infarction in these patients.
2. Angina Pectoris (Unstable Angina) by preventing a thrombus from forming in the coronary arteries.
3. Myocardial Infarction (MI): drugs that prevent blood clotting prevent the threat of future infarcts.
4. Stroke: helps prevent a thrombus from forming, thus preventing the threat of a cerebral embolism .

Hypertension IS NOT MANAGED with anticoagulants or anti-platelet drugs, unless it is accompanied by

the above cardiovascular problems, because these drugs DO NOT LOWER BLOOD PRESSURE.

RHEUMATOID ARTHRITIS (RA) - a chronic inflammatory disease of the joints causing joint pain,
swelling, and destruction . RA is characterized by chronic inflammation of the synovium that lines the
joints. With disease progression, there is an accumulation of prostaglandins, leukotrienes, and other
mediators in the inflammatory changes and tissue destruction in the synovial lining.

These RA drugs (except gold injections) also treat Osteoarthritis (OA), characterized by progressive loss
of articular cartilage. This may be the result of excessive loads on the joint or other factors. Agents that
treat OA provide an analgesic and anti-inflammatory action to reduce pain within the joint. Anti-
Rheumatic Agents:
1. Etanercept (Enbrel)-used to reduce signs and sym ptoms of active rheumatoid arthritis in patients
who have had an inadequate response to one or more disease-modifying anti-rheumatic drugs
(DMARDs). It is a recombinant DNA-derived protein that binds to tumor necrosis factor (TNF). TNF
plays an important role in the inflammatory processes or rheumatoid arthritis (RA) and the
resulting joint pathology.

178
 2. Infliximab (Remicade)-a chimeric monoclonal antibody that binds to TNF-a to reduce the NOTES
inflammatory actions of this endogenous compound. Used to treat Crohn's Disease &
Rheumatoid Arthritis.

3. Prednisone-a corticosteroid that decreases the inflammatory response due to its anti-
inflammatory actions. Treats a wide variety of inflammatory diseases, including rheumatoid
arthritis and osteoarthritis.
• Short-term side effects: insomnia, indigestion, and arthralgia .
• Long-term side effects: edema (abdominal distension), psychological disturbances, peptic
ulcer, osteoporosis, and muscle weakness.

4. Piroxicam (Feldene)-NSAlOs drug that inhibits prostaglandin synthesis. Used to manage

inflammatory disorders and for the symptomatic treatment of acute and chronic rheumatoid
arthritis and osteoarthritis. Common Adverse Effects: gastric irritation, heart burn, and nausea.

5. Gold Injections-decreases prostaglandin production.

6. Methotrexate-may affect immune function .

7. Nabumetone (Relafen)

Aspirin &NSAlOs (Ibuprofen, Naproxen) inactivate "cyclooxygenase" enzyme. Since COX synthesizes
prostaglandins, inhibiting this enzyme inhibits prostaglandin synthesis. NSAlDs are also called COX
inhibitors. Thus, NSAlOs have analgesic, antipyretic, and anti-inflammatory actions (can treat acute
inflammation). NSAlOs must be used cautiously in patients with PEPTIC ULCER DISEASE.
• NSAlOs reduce the production of PROSTAGLANDINS associated with pain and inflammation. The
mechanism of action of NSAIDs is they inhibit the cyclooxygenase step of the arachidonic acid
cascade, thus inhibit the activity of prostaglandin synthetase. Prostaglandins-a group of hormone-
like substances that mediate a range of physiological function like metabolism and nerve
transmission. NSAlDs are used for pain control , arthritis, and painful menstruation.
• NSAIO Adverse Effects: GI upset (possible ulcers), prolonged bleeding time (due to reduced
platelet aggregation).
• NSAlOs Contraindications: patients with impaired renal function, pregnancy, and GI
disease (ulcers).

Drugs Without Anti-Inflammatory Properties:

1. Acetaminophen (Tylenol)-a WEAK inhibitor of prostaglandin synthesis in peripheral tissues, thus
does not greatly affect the inflammatory response. Tylenol reduces pain by non-inflammatory
mechanisms. It is unclear exactly how it works to reduce pain. Lacks anti-inflammatory effects
of aspirin, but is a good analgesic when aspirin or ibuprofen are contraindicated. Better to
use in GI, bleeding disorders, asthma, young children, and pregnancy. Less drug interactions
than aspirin, but overdose can be hepatotoxic, if mixed with alcohol. Acetaminophen is NOT an
NSAIO, but an alternative used for patients who cannot tolerate NSAIDS. Disadvantage: no
peripheral anti-inflammatory effects since lacks anti-inflammatory properties.
• Pregnant or nursing females: for mild-to-moderate pain, acetaminophen is the accepted
choice for short-term use (long-term effects unknown in pregnant women), and safe for
breast feeding, but acetaminophen lacks anti-inflammatory properties).
• Acetaminophen does not hasten the elimination of ibuprofen . The analgesic efficacy of
combining acetaminophen and ibuprofen is greater than either acetaminophen or ibuprofen
alone. The combination provides effective pain relief.
• Acetaminophen is a non-narcotic analgesic that DOES NOT AFFECT PLATELET AGGREGATION
or the coagulation pathway. Thus, it does not affect the anticoagulant nature of Warfarin
(Coumadin), so is safe in warfarin patients.
• Acetaminophen has no effect on platelets nor the coagulation pathways, and does not affect
bleeding times, even with high doses. Thus, acetaminophen is a non-narcotic analgesic that
is the best choice to relive mild-to-moderate pain in a patient taking anti-coagulant
medication (warfarin, heparin) because it does not effect blood clotting .
• Acetaminophen's 2 Major Pharmacological Actions: analgesic &antipyretic (fever reducer)
effect. While it is not effective enough to reduce severe pain, it is effective in reducing mild-
to-moderate pain. Acetaminophen is a weak inhibitor of prostaglandin formation . Thus, for
mild-to-moderate pain, use acetaminophen (never NSAID's aspirin or ibuprofen). 179
 N • Acetaminophen has little value in treating acute inflammation. Acetaminophen inhibits
CENTRAL prostaglandin synthesis (it is an analgesic for low intensity pain and antipyretic).
Because it is less effective than salicylates (aspirin) in blocking peripheral prostaglandin
synthesis, it does not have anti-inflammatory activity and does not affect platelet function,
thus does not affect clotting time. In large doses, acetaminophen can cause hepatic necrosis.
• Large doses of acetaminophen can cause liver toxicity. Alcohol can seriously increase the
hepatotoxic potential of acetaminophen. There are -100 deaths annually due to liver toxicity
caused by ingesting large continuous doses of acetaminophen. However, it rarely causes drug
sensitivities, and can be given to patients will an allergy to aspirin.
• Acetaminophen (Tylenol) is the only OTC non-inflammatory analgesic commonly available in
the U.S. It is a weak cyclooxygenase inhibitor in peripheral tissues, thus accounting for its lack
of anti-inflammatory effect. It may be a more effective inhibitor of prostaglandin synthesis in
the CNS, resulting in analgesic and antipyretic action. Acetaminophen is a relatively safe
ANTIPYRETIC drug with NO INFLAMMATORY ACTION.
• The combination of acetaminophen and propoxyphene (Darvocet-N or Wygesic) treats
moderate-to-severe pain due to dental procedures. *Propoxyphene (Darvon) is an oral
synthetic opioid analgesic structurally similar to Methadone. Darvon compound-65 is a
combination of aspirin , caffeine, and propoxyphene.
• Acetaminophen does NOT effect clotting time (unlike aspirin) . It does not have significant anti-
platelet effects. It is effective for the same indications as an intermediate-dose aspirin, thus
is a useful aspirin substitute, especially in children with viral infections who are at risk for
Reye's Syndrome if they take aspirin.

Acetaminophen (Tylenol) vs. Aspirin

Acetaminophen (Tylenol) Aspirin
Affects Blood Clotting No Yes
GI Ulcers No Yes
Causes Reye's Syndrome No Yes
Anti-inflammatory Effects No Yes
Analgesic Effects Yes Yes

2. Combination Analgesics: narcotic analgesics (pain killers) that effectively REDUCE PAIN (not
inflammation) by working in the brain to block ascending pain impulses that travel from the
periphery (PNS) into the brain (CNS). Codeine & hydrocodone are narcotic analgesics that can be
given in combination with ibuprofen and other NSAlDs to provide effective analgesia. The narcotics
work in the brain (CNS), while ibuprofen and other NSAIDs work in peripheral tissues (PNS). These
two different mechanisms complement each other to provide effective pain reduction . Narcotic
analgesics DO NOT AFFECT BLOOD CLOTTING, thus do not enhance the anticoagulant effects
of Warfarin (Coumadin). Narcotics with acetaminophen can be given safely to Warfarin patients.

CODEINE - codeine preparation is a LESS efficacious opioid analgesic with moderate abuse liability.
Codeine is a narcotic analgesic and antitussive (cough suppressant), that is weaker than morphine, less
addictive, and less constipating. Codeine is usually combined with other drugs (Empirin, Tylenol #2, #3, #4)

• Codeine + Aspirin (Empirin)-an analgesic/anti-inflammatory. Avoid in asthmatics and patients

who cannot take aspirin as codeine precipitate acute asthma attacks.

• Codeine + AcetaminophenlTylenol (TylenoI3)-poor anti-inflammatory agent, but better than Empirin

if the patient has GI problems, pregnant, or patients who cannot take aspirin.

180
HYDROCODONE (VICODIN, LORCH, NORCH, LORTAB) - a combination analgesic more NOTES
efficacious than codeine, but potentially greater abuse liability. Avoid in asthmatics. Has poor anti-
inflammatory, but good analgesic (stronger than Tylenol) .

• Hydrocodone + Ibuprofen-a strong analgesic for mOderate-to-moderately severe pain, with good
anti-inflammatory properties. Ibuprofen has similar contra indications to aspirin , with GI problems
being the most common side effect (take with milk or food to limit). Better for patients who cannot
take aspirin or ibuprofen.

• All combine a narcotic analgesic and cough rel iver (hydrocodone) with a non-narcotic analgesic
(acetaminophen) to relieve moderate-to-severe pain.

OXYCODONE - a combination analgesic that is more efficacious than codeine, but avoided in
asthmatics. Treat moderately-to-severe pain. Oxycodone has the HIGHEST DEPENDENCY LIABILITY
when compared to drugs like codeine, propoxyphene, and pentazocine. Oxycodone is contained in
Percodan , Percocet.
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• Oxycodone + Aspirin (Percodan)-good analgesic with anti-inflammatory properties. The strongest ::cI

pain medication you can prescribe on an outpatient (ambulatory) basis. Do not take it on an empty ...,....
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• Oxycodone + Acetaminophen (Percocet}-better if the patient cannot take aspirin or ibuprofen , but
lacks strong anti-inflammatory effects.

The body contains 3 naturally occurring endogenous opioids peptides that produce morphine-
like effects to reduce pain. Opioid receptors are activated by endogenous chemicals under
physiologic conditions.
1. Beta-endorphins-bind to opioid receptors in the brain and have potent ana lgesic activity.
2. Enkephalins-bind to opioid DELTA receptors in the brain and are more widely distributed in the
brain than beta-endorphins. Playa role in pain perception, movement, mood, and behavior.
3. Dynorphins-the MOST POWERFUL opioids found throughout the CNS &PNS that bind to KAPPA
receptors. Dynorphins may regulate pain at the spinal cord level, influence behavior at the
hypothalamic level, and function with other endogenous opioids to regulate the
cardiovascular system .

Opioid Receptors:
1. Mu (}-the prototypical opioid agonist for this receptor is MORPHINE (its analgesic activity depends
on its binding to the mu receptor). The supraspinal analgesic activity of morphine is mediated
primarily through its influence on the Mu opiod receptor.
2. Delta ( }-enkephalins are the typical agonist for the delta receptor.
3. Kappa ( }-dynorphins are the typical agonist for the kappa receptor.

OPIOIDS (NARCOTICS) - drugs WITHOUT ANTI-INFLAMMAOTRY PROPERTIES used as very effective

analgesics to relieve moderate-to-severe pain, antitussives, anti diarrhea Is, preanesthetic
medications, and as analgeSic adjuncts during anesthesia.

• Opioids suppress the cough reflex (antitussive), cause constipation (antidiarrheal), and when used
as preanesthetic medications, opiates reduce the amount of general anesthetic required for surgical
anesthesia . Opiates are administered with caution to patients with HEAD INJURY or with a history
of drug abuse and dependency.

• Opioids are the most powerful drugs available for pain relief. Strong agonists (those with the highest
analgesic efficacy) are Morphine, Meperidine, Fentanyl, and Methadone.

• Codeine, Hydrocodone, and Oxycodone are mild-to-moderate agonists (analgesic efficacy).

• The most appropriate time to administer the initial dose of an analgesic to control post-operative
pain is BEFORE the effect of the local anesthetic wears off.

181
 N • Opioid Analgesics (i.e. morphine, codeine, meperidine, propoxyphene) MIMIC the body's endogenous
opioids at CNS opiate receptors to raise the pain threshold and increase pain tolerance. Opioids
also cause chemoreceptor trigger zone stimulation and decrease alpha-adrenergic receptor
responsiveness.

• Common Side Effects: sedation and drowsiness (by depressing the conscious centers of the brain),
dizziness, &nausea. The MOST common side effect of the narcotic (opiate) analgesics is NAUSEA.
Narcotic analgesics DO NOT cause peptic ulcers or insomnia.

• less Common Adverse Effects: vomiting, hypotension, irregular/labored breathing (dyspnea),

lightheadedness, nightmares, and insomnia. *Respiratory depression is dose related and causes
death in narcotic drug overdose. It can occur with any of the narcotics. Respiratory depression is
the MAJOR disadvantage of using opioids and is the most significant and well-known adverse
reaction . Death secondary to opioid overdose is usually always due to respiratory depression. When
opioids are used correctly, the risk of severe respiratory depression is small as tolerance rapidly
develops to this effect. The MOST SERIOUS side effect is respiratory depression. The cause of death
from overdose of narcotics is respiratory depression and shut down of the respiratory system .

• Abuse can and does occur with all narcotics. Narcotics are controlled substances under DEA
Schedules II or III. ADEA number/license is required to prescribe narcotics/opioids like Hydrocodone
(Vicodin), Meperidine (Demerol), and Codeine.

Opiates are contraindicated in patients with severe head injuries, but not for patients with bronchial
asthma, renal dysfunction, or acute myocardial infarcations.

MORPHINE (OPIATES) - the standard drug to which all opiates (narcotics) are compared. Morphine
influences the MU OPIOID receptor subtype.

• Morphine Pharmacological Effects: analgesia, drowsiness, euphoria, mental clouding, miosis

(pupillary constriction), constipation, nausea, vomiting, and respiratory depression. Morphine is an
opium alkaloid.

• length of Effectiveness: IV or 1M (2-3hrs), oral (3-4hrs). Sustained release is 8-12hrs.

• Morphine starts to work quickly. The oral form of morphine can be very effective for cancer pain.

• Synthetic Morphine Derivatives: Hydromorphone (Dilaudid), Oxymorphone (Numorphan), &

Nalbuphine (Nubain).

• MORPHINE IS NOT USED IN DENTISTRY DUE TO ITS HIGH ADDICTIVE LIABILITY.

PENTAZOCINE (TAlWIN) - equally as strong as codeine. Chemically related to morphine, but has
weaker analgesic properties. Given orally it lasts up to 4hrs. Not used intravenously to produce
conscious sedation. Can block painkilling action of other opiods. Can cause confusion and anxiety,
especially in elderly patients. Has abuse liability. Talwin compound combines the strong analgesic
properties of Pentazocine and the analgesic, anti-inflammatory, and fever-reducing properties of aspirin.
It is used to relieve MODERATE PAIN, and does not produce euphoria.

CODEINE - an opium alkaloid weaker (less potent) & less addictive opioid than morphine (a mild-to-
moderate agonist). When combined with acetaminophen it is (Tylenol #3). length of Effectiveness: by
mouth (3-4hrs) taken with aspirin or acetaminophen. Synthetic Codeine Derivatives:
• Oxycodone (OxyContin)-an opiate analgesic with similar potency to morphine. When combined with
acetaminophen (Roxicet, Percocet, Percodan, &Tylox). Given orally it lasts 3-4hrs. Usually
combined with aspirin or acetaminophen. Adverse Effects: nausea &constipation. It is a mild-to-
moderate agonist.
• Hydrocodone-similar potency as morphine. When combined with acetaminophen it is called (Vicodin,
lorcet, lortab, Maxidone, & Zydone) . Given orally it lasts 4-6hrs. Usually combined with
acetaminophen. When combined with ibuprofen it is (Vicoprofen). Among the opiates available for
dentistry, hydrocodone products are the drugs of choice. It is a mild-to-moderate agonist.
182
MEPERIDINE (DEMEROL) - a SYNTHETIC narcotic (opioid) agonist that is weaker than morphine, NOTES
but equally addictive. It's duration of action is shorter than morphine, and it is the only narcotic agent
that does NOT cause miosis (pupillary constriction). Demerol is used as an IV supplement during
conscious sedation procedures, but is less potent than morphine and much less potent than fentanyl.
Demerol is also used as an oral medication to control pain after dental surgery. Oemerol treats moderate-
to-severe pain (acute dental pain) and may be used as a preoperative medication to relieve pain and
allay anxiety.
• Length of Effectiveness: IV or 1M (3hrs) and not very effective given orally.
• When combined with promethazine it is know as Mepergan Fortis.
• Meperidine can cause seizures, tremors, and muscle spasms.

Synthetic Meperidine Oerivatives:

• Fentanyl (Sublimaze)-a synthetic potent opioid analgesic used primarily as an IV sedative during
conscious sedation procedures or procedures requiring general anesthesia. It is 80-1 OOx more potent
than morphine. In a fixed combination with the neuroleptic drug Droperidol , fentanyl is available as
("Innovar").
• Innovar-produces a syndrome called "neurolepanalgesia". The neuroleptic action (major
tranquilizing action) is produced by the Droperidol component, and the analgesic action by
the Fentanyl component.
• Fentanyl is also available as a lollipop-type lozenge ("Actiq") for transmucosal absorption and as
a transderma l patch ("Ouragesic") for delivery through a patch applied to the skin.
• Alphaprodine (Nisentil) & Alfentanil (Alfenta)
• Sufentanil (Sufenta)
• Oiphenoxylate (in Lomotil) &Loperamide (in Imodium)

METHADONE (DOLOPHINE) - length of effectiveness given orally is 4-6hrs or longer. Also treats
HEROIN WITHORAWL.

PROPOXYPHENE (DARVON) - synthetic opioid derivate of Methadone, that in the form of

propoxyphene napsylate with acetaminophen is called "Oarvocet-N 100" (low abuse liability). Used for
MILO pain control after dental surgery. Taken orally (not IV). Length of effectiveness given orally is 3-
4hrs. Taken with aspirin or acetaminophen to treat mild pain. Propoxyphene is a very weak agonist drug.

LEVORPHANOL - lasts 4 hours given by IV, 1M or orally. The oral form is strong and can be used instead
of morphine.

NARCOTICS (OPIATES) USED IN DENTISTRY FOR PAIN RELIEF AFTER DENTAL SURGERY -
Hydrocodone (Vicodin), Oxycodone (Percocet, Tylox), Meperidine (Oemerol), Codeine, & Fentanyl.

Codeine, Morphine, & Meperidine (Demerol) are analgesics that can produce drug-dependence and
addiction. These are narcotic analgesics since the actions of this opioids is to produce DROWSINESS &
SLEEP as a side effect.

Opioid (Narcotic Analgesic) Antagonists: these agents reverse respiratory depressive effects caused by
an overdose of Codeine, Morphine, Hydrocodone, Oxycodone, Meperidine (Demerol), & Fentanyl.
1. Naloxone (Narcan)-the prototype/pure opioid/narcotic competitive antagonist given IV, 1M, or
subcutaneously in medical emergencies to reverse narcotic overdose which results in respiratory
depression and death due to respiratory shut down . Naloxone reverses the respiratory
depressant effects of narcotics to counteract their lethal effects. Naloxone is the antagonist
of choice to treat opioid overdose.
2. Nalmefene (Revex)-narcotic reversal agents that reverses respiratory depressive effects of
narcotic analgesics.
3. Naltrexone (ReVia)-narcotic reversa l agent that reverses respiratory depressive effects of
narcotic analgesics and is used to treat alcohol dependence.

Opiates produce drug dependence leading to addiction. Psychic dependence, physical dependence, and
tolerance can develop upon repeated administration.

183
 ADDICTION - a compulsive, uncontrollable dependence on a substance, habit, or practice to such a
degree that cessation causes severe emotional, mental, or physiological reactions.

HABITUATION - an acquired tolerance from repeated exposure to a particular stimulus.

Psychological and emotional dependence on a drug, tobacco, or alcohol result from the repeated use of
the substance, but without the addictive, physiological need to increase dosage.

TOLERANCE - the phenomenon of decreased responsiveness to a drug after chronic administration.

As a patient becomes tolerant to a drug, the dosage required to produce the usual effect is increased.
Occurs when increasingly large doses of opiate are required to produce the same degree of analgesia.

PSYCHIC DEPENDENCE - unlikely if an opiate is taken for a short period for pain relief.

Physiological dependence is common to all forms of drug dependence and abuse. These drugs of
abuse all have the ability to change a person's mood and sensory perception .
..."
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PHYSICAL DEPENDENCE - a condition in which continued drug administration is required to prevent
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unpleasant withdrawal symptoms.
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-< TOXICITY - a condition that results from exposure to a toxin or toxic amounts of a substance that does
not cause adverse effects in smaller amounts.
• Toxicity is both dose-dependent and time-dependent.
• Toxicity is often an extension of the desired drug effect.
• Toxicity can range from nausea to death, and can be caused by even minimal concentrations of a drug.

A drug with a high LD50 and low ED50 has a HIGH therapeutic index, thus is relatively SAFE. The
purpose of an acute toxicity test is to determine the nature and extent of the untoward reactions that might
follow the administration of a single dose (or an overdose) of a drug. A quantitative aspect of acute
toxicity testing is to determine a drug's lethal dose (LD) which is expressed as LD50. Standing alone, it
conveys less information than the ratio of the lethal to the effective doses (LD50: ED501, a quantity that
is called the "Therapeutic Index". The greater a drug's therapeutic index, the LESS likely fatalities will
follow an accidental overdose. In the ideal situation, the therapeutic index would be 100, but this never
happens. The ratio LD50: ED 50 gives a drug's SAFETY.

• Therapeutic Dose-the amount of a drug that usually lies between the minimal and maximal doses
of the drug.

• Effective Dose (ED)-the effective dose at which 50% of people will respond.

• Lethal Dose (LD)-the dose that kills 50% of the people who receive the drug, as determined by mice
experimentation.

• Fatal Dose-a drug dose that kills.

DRUG EFFICACY ("INTRINSIC ABILITY", "MAXIMAL" OR "CEILING EFFECT") -the ability

of a drug to produce a desired therapeutic effect regardless of dosage. Efficacy is the maximum
effect a drug can cause, regardless of the dose.

184
DRUG POTENCY - the relative concentration of two or more drugs that produce the same drug NOTES
effect. The effect usually chosen is 50% of the maximal effect and the dose causing this effect is the
EG50. Potency is mainly determined by the affinity of the receptor for the drug. The smaller the EG50, the
greater drug potency. Potency is a comparative term (one drug is more potent than another drug).
• Ex: Drug A in a dose of 10mg produces the same magnitude of response as Drug B in a dose of 50mg.
The following is true: Drug A is 5x as potent as Drug B, but Drug A is not potent in and of itself. Also,
if Drug Ahas a greater efficacy than Drug B, then Drug Ais capable of producing a greater maximum
effect than Drug B.
• When comparing drugs with respect to intensity of response, the drug that produces the greatest
maximum effect is the drug with the highest efficacy.

ADDITIVE EFFECT - occurs when two drugs with similar effects are administered in combination,
and the resulting response is the sum of the individual actions of each drug when given alone. An additive
effect occurs when additive drugs are administered. The response is no greater than that which would
be expected had the drugs been given one at a time. There is no enhancement of potential of the individual
drugs as a result of being used in combination.

ANTAGONISTIC EFFECT - occurs when the combined actions of two drugs with similar
pharmacological effects are LESS than the sum of the drug's individual effects. The effect of aspirin
and ibuprofen (Motrin) in combination is less than the sum of their individual actions.

CUMULATIVE ACTION - an excssive accumulation effect that occurs if a drug is administered

repeatedly and a higher concentration of the drug than is desired may be achieved .

IDIOSYNCRASY - a response to a drug that is unusual or abnormal, or one that grossly deviates from
the routi ne reaction .

SYNERGISTIC RESPONSE - occurs when the combined action of two drugs with similar
pharmacological effects is GREATER than the sum of the individual actions. Alcohol is synergistic
with the valium-family (valium/diazepam, xanax, halcion), narcotics, and barbiturates. Alcohol must be
avoided when taking these medications.

4 Criteria to Select an Analgesic Agent for a Patient:

1. Type of Pain: severe, mild, moderate
2. Patient's Age:
• Infant &child: when calculating dosage, height. weight. body surface area. and renal
hepatic function must be considered .
• Adult
• Elderly: drug response is affected by age-related changes in physiology and pharmacokinetics.
3. Concurrent Medications: consider unwanted drug interactions (especially with elderly).
4. Pregnancy: because virtually any drug a pregnant women takes can cross the placenta and enter
fetal circulation , drug use in pregnant patients is a source of special concern. Thus, check with
the patient's OB-GYN prior to prescribing an analgesic.

185
 Household Measures & Weights
Teaspoons Tablespoons Cups or Glasses Fluid Ounces Milliliters Grams
1 0.125 5 5
3 1 0.50 15 15
48 16 1 8 237 240

ORAL CONTRACEPTIVES (BIRTH CONTROL) - block ovulation by inhibiting the anterior pituitary
hormones FSH (Follicle Stimulating Hormone) & LH (Luteinizing Hormone). Oral contraceptives also
produce alterations in the genital tract, including changes in cervical mucus, rendering it unfavorable
for sperm penetration even if ovulation occurs. Changes in the endometrium may also occur, rendering
it unfavorable for nidation (implantation of the fertilized ovum).

• Oral contraceptives usually contain BOTH an estrogenic agent (ethinyl estradiol or mestranol) and
progestational agent (Ievonorgestrel, norethindrone, norgestimate, and norgestrel).

• Oral Contraceptive Precautions: the risk of cardiovascular side effects increases in women who
smoke cigarettes, especially women over age 35. The risk of a thromboembolism also increases.
Women with hypertension are encouraged to use a non-hormonal form of contraception. The highest
risk associated with use of oral contraceptives is thromboembolic disorders.

• Antibiotics have the potential to reduce the effectiveness of oral contraceptives. Thus, advise
patients to use additional methods of birth control when taking antibiotics and oral contraceptives
concurrently.

Pain:
1. Pain Threshold-the LOWEST level of pain a patient will detect.
2. Phantom Pain-pain that has no organic basis and is fixed upon some portion of the anatomy
(i.e. the sensation of pain felt in a limb, although the limb has been amputated) .
3. Psychogenic Pain-pain produced or caused by psychic or mental factors, not organic factors.
4. Intractable Pain-pain that is resistant or refractory to ordinary analgesic agents.
5. Referred Pain-pain felt in an area other than the site of origin, like pain near the shoulder
associated with biliary disease.

Drugs that cause XEROSTOMIA by inhibiting SALIVA production & secretion. The xerostomia action
produced by these drugs is reversible as normal salivary flow is regained after discontinuing the drug.
1. Amitriptyline (Elavil}-a tricyclic antidepressant (a drug class that causes significant xerostomia).
They probably work through an anticholinergic action.
2. Diphenhydramine (8enadryl)-a sedating-type antihistamine (a drug class that causes significant
xerostomia). They probably work through an anticholinergic action.
3. Atropine-a powerful anticholinergic that blocks saliva production in the salivary glands. Other
anticholinergics have a similar action.
4. Diazepam (Valium)-a benzodiazepine tranquilizer that has moderate anticholinergic action to
reduce the outflow of saliva.

Drugs that Control Salivary Secretions (Anti-Sialogogues) to help obtain a dry field:
• Atrophine Sulfate, Glycopyrrolate (Robinul), Belladonna derivatives, & Propantheline Bromide
(Pro-banthine).
• Anti-Sialogogues are anti-cholinergics. They block post-ganglionic cholinergic fibers.
• Anti-sialogogues Contraindications: patients with glaucoma, cardiovascular problems, GI tract
obstruction, and asthma.
• Anti-sialogogues also REDUCE SPASMS of smooth muscle in the bladder, bronchi, and intestine. They
relax the iris sphincter, decrease gastric, bronchial, salivary secretions, and perspiration. They
accelerate impulse conduction through the myocardium by blocking vagal impulses.

186
Drugs that treat GLAUCOMA (an increase in intraocular pressure caused by poor drainage of the aqueous
humor (fluid in the eye) and can cause blindness.
1. Pilocarpine {Isopto-Carpine or Salvogen)-eye drops that cause causes papillary constriction
to allow aqueous humor drainage which reduces intraocular pressure.
2. Latanoprost (Xalatan)-a prostaglandin analog. Eye drops reduces intraocular pressure by
increasing aqueous humor outflow/drainage.
3. Betaxolol (Betoptic)-a beta blocker. Eye drops reduces intraocular pressure by reducing aqueous
humor production.
4. Bimatoprost (Lumigan)-eye drops reduces intraocular pressure by increasing aqueous
humor outflow/drainage.

CANCER CHEMOTHERAPY (ANTI-NEOPLASTIC DRUGS)

8 Classes of Chemotherapy Drugs:
1. Alkylating Agents-are most effective in treating chronic leukemias, lymphomas, myelomas, and
carcinomas of the breast & ovary. These agents alkylate DNA so it cannot replicate. Alkylating
agents contain a diverse group of compounds that form alkyl bonds to nucleic acids. All
alkylating agents share a similar mechanism of action and mechanism of resistance, and form
covalent bonds with nucleic acids and proteins. N-7 position of GUANINE is a common bonding
site. Major Alkylating Agents:
• Nitrogen Mustards: Mechlorethamine (Mustargen), Cyclophosphamide (Cytoxan), Chlorambucil
(Leukeran), & Melphalan (Alkeran) . Treats Hodgkin 's Disease & other lymphomas, and Chronic
Lymphocytic Leukemia.
• Nitrosoureas: Carmustine (BiCNU), Lomustine (CeeNU), & Semustine (Methyl-CeeNU). Treats
Hodgkin's disease, other lymphomas, and Myeloma.
• Bisulfan (Myleran)-treats Chronic Granulocytic Leukemia .
• Cisplatin (Platinol)-a chemotherapeutic drug (Alkylating Agent) with adverse effects of nausea
and vomiting (75%-100%; dose-related), alopecia, xerostomia, and changes within the oral
cavity tissues (i .e. mucositis).
• Mucosititis-a common reaction to cancer chemotherapy involving inflammation of the
mucous membranes. During chemotherapy and radiation therapy, mucosal tissues begin to
desquamate and ulcerate. The mucosal integrity is broken and is secondarily infected by
oral flora . Palliative treatment is indicated for mucosititis.
2. Anthracyclines-these agents destroy DNA so the cell cannot replicate. Daunorubicin &
Doxorubicin. Commonly associated with the development of oral mucosititis.
3. Antibiotics-these antibiotics are not used for antibacterial therapy, but are specifically designed
for cancer chemotherapy. Dactinomycin.
4. Antimetabolites-cell cycle-specific drugs that act primarily in the "S" Phase of the cell cycle
(DNA synthesis). Antimetabolites interfere with selected biomechanical reactions necessary for
cell growth. Antimetabolites are one of the oldest and most important classes of anti-neoplastic
agents. Antimetabolites attack cells during the "S" period of the reproduction cycle by
interfering with the biosynthesis of the PURINE & PYRIMIDINE BASES.
• Folic Acid Analogs: Methotrexate (Amethopterin). Treats acute lymphoblastic leukemias in
children. Adverse Effects: commonly associated with the development of oral mucosititis.
• Pyrimidine Analogs: 5-Fluorouracil (5FU), Floxuridine (FUDR), Cytosine Arabinoside (Cytosar-
U), 6-Mercaptopurine, & Methotrexate. Treats carcinoma of the breast, GI tract, ovary, cervix,
and prostate. Induction of remission in acute leukemia in children and adults. Adverse Effects:
commonly associated with the development of oral mucosititis.
• Purine Analogs: Mercaptopurine (Purinethol) & Thioguanine (TG). Treats leukemia in children
and adults. Acute leukemia and induction or remissions in acute granulocyctic leukemia.
5. Antimicrotubulars-affect microtubular assembly with cells to inhibit cell mitosis. Paclitaxel (Taxol).
6. Antiestrogens-block the tumors on which estrogen has a stimulatory effect. Tamoxifen (Nolvadex).
7. Vinca Alkaloids-these are mitotic spindle poisons. Vinblastine & Vincristine.
8. Gonadotropin Hormone-Releasing Antigens-these agents inhibit gonadotropin secretion
(an action effective in reducing certain carcinomas). Leuprolide.

Anti-cancer drugs Asparaginase (deprives tumor cells of certain amino acids to protein production is blocked)
& Interferons (boost the immune system) do not fall within any category, but do treat certain cancers.

187
 ALOPECIA (HAIR LOSS) - the most common complication seen with chemotherapy treatment.
Alopecia occurs with administration of most chemotherapeutic agents 1-2 weeks after treatment. GI
upset, increased incidence of infection (especially Candidiasis), and degeneration of lymphatic tissue
are other common site effects of chemotherapy.

Most chemotherapy drugs are TERATOGENIC in humans, and should be avoided in pregnant women.

HYPOGlYCEMICS (ANTI-DIABETICS)
HYPOGLYCEMIA - the most serious and common complication of insulin therapy. Symptoms: sweating,
weakness, confusion, slurred speech, & blurred vision. Administration of a concentrated glucose source
relieves mild hypoglycemia .
• Humulin-the brand name for the human form of insulin.

INSULIN - a pancreatic hormone secreted by pancreatic beta-cells of ISLETS of LANGERHANS. Insulin

is essential for glucose metabolism and for homeostasis of blood glucose. Insulin is usually administered
by subcutaneous injection. Various insulin preparations are prepared from beef or pork pancreas, and
differ mainly in their onset and duration of action. Effects of Insulin: gluconeogenesis & triglyceride
storage, glycogen synthesis, & protein synthesis.

Insulin preparations mimic the activity of endogenous insulin, which is required for the proper utilization
of glucose in normal metabolism. Insulin preparations are used in Type 1 & Type 2 diabetes that cannot
be completely controlled by the oral anti-diabetic drugs or by diet alone. Insulins differ in their onset and
duration of action:
1. Ultra-rapid acting insulin (Insulin lispro): peak onset of action is .25-.5hrs. Duration of
action is 3-4hrs.
2. Short/Rapid-acting Insulin-peak onset of action of .5-3hrs, with a duration of action of 8-12hrs.
Ex: Regular Insulin Injection & Prompt Insulin Zinc Suspension (Semilente Insulin).
3. Intermediate-acting Insulins-peak action 8-12hrs. Duration of action of 18-24hrs. Insulin Zinc
Suspension (Lente Insulin) & Isophane Insulin Suspension (NPH).
4. Long-acting Insulins-duration of action is> 36hrs. Protamine Zinc Insulin (PZI) and
Ultralente Insulin.

ANTI-DIABETIC AGENTS (ORAL HYPOGLYCEMICS) - Glyburide (DiaBeta), Metformin

(Glucophage), Pioglitazone (Actos), Chloropropamide (Diabinese), Tolbutamide (Orinase). These drugs
are used as adjuncts to diet to treat non-insulin dependent diabetes mellitus (Type 2 Diabetes) that
cannot be controlled by diet alone.

• Glyburide & Chloropropamide-stimulate insulin release from the pancreas, and work by reducing
glucose output from the liver and by increasing insulin sensitivity at peripheral target sites.

• Metformin & Pioglitazone-increase insulin sensitivity at peripheral target sites.

• Tolbutamide-a sulfonylurea that stimulates the synthesis and release of insulin from the pancreas,
increases the sensitivity of insulin receptors, and improves peripheral utilization of insulin .

TERMS TO REMEMBER:
• Half-life - the time it takes a plasma concentration of a drug to decrease 50% for potentially toxic
levels to accumulate and adversely affect the cardiovascular, respriatory, and CNS.

• Efficacy - a substances ability to produce an intended result. A drug's potential performance

compared to other drugs, usually of the same class. In dentistry efficacy often describes
the relative performance of available local anesthetics for regional infiltration and nerve block.

• Paresthesia - abnormal or inappropriate sensation characterized by burning, prickling, or tingling.

The absence of feeling or sensation. In dentistry it is a prolonged numbness in the circumoral
or intra-oral har and/or soft tissues.

• Dysesthesia - a heightened, uncomfortable or painful sensation. In dentistry, it often manifests

188 as a post-operative sequela to regional administration of local anesthesia.
 -

CHAPTER 5

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ORAl I
1 PATHOlOGY

189
 N METABOLIC & GENETIC DISEASES IN DENTISTRY
OSTEOGENESIS IMPERFECTA {"BRITTLE BONES"} - caused by a rare genetic
defecUdisorder that affects the body's production of COllAGEN (major protein of the body's C.T.).
The person either has less collagen than normal, or poorer quality of collagen than normal causing
WEAK BONES THAT FRACTURE/BREAK EASILY often from little or no apparent cause.

• While the characteristics vary greatly, and not all are evident in each case, the main clinical
characteristic is EXTREME FRAGILITY &POROSITY OF BONES with a proneness to fracture due to
the effects of inadequate osteoid production.

• Additional Clinical Features: pale blue sclera, deafness due to otosclerosis, loose joints, low muscle
tone, triangular face, and a tendency toward spinal curvature.

• Teeth have bulbous crowns with a cervical constriction, partially or completely obliterated pulps, and
narrower & shorter roots. Deciduous (primary) teeth are more severely affected than permanent teeth.
Teeth are poor and abnormal due to dentin malformation (Type 1 Dentinogenesis Imperfecta); may
be linked to DENTINOGENESIS IMPERFECTA.

• Treatment: there is NO KNOWN CURE, but treatment is directed toward preventing/controlling

the symptoms.

HYPOPHOSPHATASIA - one of several disorders that resembles OSTEOGENESIS IMPERFECTA. It is

an inherited metabolic (chemical) bone disease that results from low levels of the enzyme alkaline
phosphatase (enzyme is essential to the calcification of bone tissue). Loosening, hypo calcification,
and premature loss of deciduous teeth are characteristic. Radiographically, large pulp chambers
and alveolar bone loss are observed.

• Hypophosphatasia's severity greatly varies from patient to patient. Some patients have blue sclera
that resembles osteogenesis imperfecta. Others have deformity of the arms, legs, and chest and/or
frequent bouts of pneumonia and recurrent fractures. Patients are classified as having either:
1. Perinatal Hypophosphatasia-fails to form a skeleton in the womb and are stillborn.

2. Infantile Hypophosphatasia-manifested by severe rickets, hypercalcemia, and bone

abnormalities. Most cases are lethal.

3. Childhood Hypophosphatasia-involves premature exfoliation of deciduous teeth, increased

infection, numerous skeletal abnormalities. Children that survive are dwarfs.

4. Adult Hypophosphatasia-manifested by spontaneous fractures, prior history of rickets

and osseous radiolucencies.

PAGET'S DISEASE OF BONE {OSTEITIS DEFORMANS} - a common, chronic, non-metabolic

bone disorder characterized by an INCREASE in serum alkaline phosphatase levels. Bones become
enlarged &deformed, and become dense, but fragile due to excessive breakdown and formation of
bone. Has potential to undergo "spontaneous" malignant transformation. There is excessive bone
destruction and unorganized bone repair.

• Paget's effects males and females, but is rarely found in people < 40yrs (affects middle-aged &
elderly people).

• Cause is unknown, but appears to be hereditary. Patients are predisposed to developing

OSTEOSARCOMAS.

• Signs &Symptoms: pain in affected area, bone deformity & susceptibility to fractures in the affected
area, headache, and hearing loss if the affected area is the skull. These symptoms develop SLOWLY.

190
• Clinical Features:
• Patients may give a history of progressively increasing size of hats or new dentures being
made at progressively more frequent intervals due to bony changes.

• Bones are warm to touch due to increased vascularity.

• Radiographs of skull &jaws show typical "COTTON-WOOL" appearance, and teeth have
pronounced hypercementosis and often loss of lamina dura.

• Lab tests reveal drastically increased serum alkaline phosphatase, urinary calcium &
hydroxyproline. However, serum phosphate & calcium are normal.

• Treatment: Administer anti-metabolites or CALCITONIN to decrease bone resorption, or treat with a

high-protein & high calcium diet.

OSTEOMALACIA - SOFTENING of bones in adults (Adult form of Rickets) that occurs because
osteoid tissue in bones failed to calcify due to a lack of vitamin D. More common in women, and may
be asymptomatic until a bone fracture occurs.

• Steatorrhea is one of the most common causes of Osteomalacia due to fat malabsorption where
the body cannot absorb fats, so the fats are passed directly out of the body in stool which results in
poor absorption of vitamin D(fat soluble) and calcium. Osteomalacia affects ALL BONES, specifically
at their epiphyseal growth plates.

• Signs &Symptoms: pain in the bones of the arm , leg, spine, and pelvis.

RICKETS - osteomalacia in children causing skeletal deformities, and usually accompanied by

listlessness, irritability, and generalized muscle weakness. Bowlegs, pigeon breast, and protruding
stomach are signs. Teeth are affected by delayed eruption, malocclusion, and developmental
abnormalities of dentin and enamel, with a higher caries rate.

DWARFISM (Pituitary Dwarfs) - characterized by arrested growth caused by undersecretion of

growth hormone. These people often have limbs and features not properly proportioned or formed.

• Oral Manifestations: delayed eruption rate & shedding of teeth, clinical crowns & roots appear
smaller, dental arch is smaller causing malocclusion, and an underdeveloped mandible.

• ACHONDROPLASIA-the most common type of DWARFISM. Clinically, the child appears very short
(-50 inches), fingers are stubby, bowed legs, bulging of the forehead, bossing of the frontal bones,
saddle-like nose, and mandibular prognathism.

CEREBRAL PALSY - a group of disorders affecting body movement and muscle coordination due to
an insult or anomaly of the brain's motor control centers. This damage interferes with messages from
brain body & body brain. The effects vary greatly among people.

• Cerebral palsy is mainly characterized by SPASTIC PARALYSIS or impairment of control or

coordination over voluntary muscles. Often accompanied by mental retardation, seizures, &
disorders of vision/communication.

• There are NO intra-oral anomalies (oral manifestations) unique to people with cerebral palsy, but
several conditions are more common or more severe than in the normal population:
• Higher incidence of periodontal disease, caries, bruxism, and malocclusion .
• Prone to gingival hyperplasia if Dilantin is used to control seizures.
• More susceptible to trauma, especially the maxillary anterior teeth.

191
 NOTES DOWN SYNDROME - a congenital defect caused by a chromosomal abnormality (TRISOMY 21),
marked by various degrees of mental retardation and characteristic physical features (short, flattened
skull, slanting eyes, thickened tongue/fissured, broad hands/feet, etc.)

• Oral Manifestations: mandibular prognathism, increased periodontal disease, thickened

tongue/fissured delayed teeth eruption, higher incidence of congenitally missing teeth,
malocclusion, & enamel dysplasia.

MUSCULAR DYSTROPHY - a group of genetic diseases marked by progressive weakness &

degeneration of skeletal or voluntary muscles that control movement.
• Oral Manifestations: increase in dental disease if oral hygiene is neglected, weakness in muscles
of mastication causing decreased maxillary biting force, higher incidence of mouth breathing,
and open bite.

FIBROUS DYSPLASIA - also demonstrates typical "ground-glass" appearance of bone, thus if

this appearance is seen, additional tests like a skull radiograph &blood chemistries are performed
to aid in the diagnosis. Characterized by normal bone replaced by fibrous tissue. There are 3 types
depending on the extensiveness of skeletal involvement:

1. Monostotic-involves one bone.

2. Polyostotic-involves more than one bone.

3. Polyostotic with Endocrine disturbances (Albright's Syndrome)-pathologic fractures is the

chief complaint.

Fibrous Dysplasia is a genetic disease of very young people (15-30yrs), asymptomatic alteration of
bone (SWELLING MASS OF BONE OCCURS). Bone is replaced by fibrous tissue & non-functional bone
trabeulae. Demonstrates typical "ground-glass" appearance of bone, thus if this appearance is
seen, additional tests like a skull radiograph &blood chemistries are performed to aid in the
diagnosis. Characterized by normal bone replaced by fibrous tissue. Teeth may appear like they are
moving (teeth displacement) due to the bone growing.

• Treatment: cannot treat except with surgery to remove the area when the lesion stops growing. Benign
osseous lesions used to be treated with radiotherapy, but this may produce osteogenic sarcoma (bone
cancer) (so cannot radiate benign bone).

• Radiographic: when mature it has a radiopaque "ground-glass" appearance (d iffuse/not well-

defined homogenous radiopacity) . You can never the borders of the lesions (it blends with the
bone)-this is the main characteristic

ECTODERMAL DYSPLASIA - hereditary condition characterized by abnormal development of the

skin and associated structures (hairs, nails, teeth, & sweat glands). It involves all structures derived
from ECTODERM, affecting males more than females.

• Clinical Signs: hypothrichosis (decrease in hair (fine sparse hair), anhidrosis (no sweat or sebaceous
glands, causing heat intolerance), anodontia (complete absence of teeth), oligodontia (partial
absence of teeth), no tooth buds of the primary or permanent dentition (edentulous), depressed nose
bridge, lack of salivary glands, and child appears much older than their true age.

• Treatment: there is no treatment, but dentures can be fabricated for these patients, but will need
to be replaced periodically to accommodate the patient's jaw growth.

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CLEIDOCRANIAL DYSOSTOSIS - an inherited disorder of bony development characterized by
absent or incomplete formed COLLAR BONES, heavy protruding jaw & wide nasal bridge, and dental
abnormalities (mala ligned teeth, presence of multiple supernumerary teeth, and unerupted teeth) .
The dentition alone (observed by radiographs alone) often suggest the diagnosis.

PIERRE-ROBIN SYNDROME - an inherited disorder with the following findings in the NEONATE:

• Micrognathia-smallness of the jaws.

• Glossoptosis-downward displacement or retracted tongue.

• Breathing problems & Cleft Palate.

LATERAL CLEFTING OF THE LIP - results from the failure of the MAXILLARY & FRONTAL NASAL
PROCESSES TO MERGE. Cleft lip occurs during the 5th _6 th week of embryonic life. It can be bilateral
or unilateral, more common in males, and involves the LEFT SIDE more than the right side.

CLEFT PALATE - occurs in 6th _8th week of embryonic life. Isolated cleft palates are more common
in females, characterized by a fissure in the midline of the palate due to the failure of the two sides
to fuse during embryonic development. The most severe handicap caused by cleft palate is an
impaired mechanism PREVENTING NORMAL SPEECH & SWALLOWING.

Important: Speech problems associated with Cleft lip & Cleft Palate are usually due to the inability
of the soft palate to close airflow into the nasal area.

EXOSTOSIS - slow-growing, benign knots of bone on the hard palate (palatal or mandibular tori).
Exostosis are the most common exophytic lesions.

CHERUB ISM - a BENIGN inherited autosomal dominant disease of the maxilla & mandible, typically
found in children by age 5 (affects males 2: 1). Most cases occur in the MANDIBLE. The jaws are firm
and hard to palpation, and regional lymphadenopathy may be present. BILATERAL expansion of the jaws
gives the child a very round face, reminding one of cherubs (cupids) in paintings. The tumors stop
growing shortly after puberty. As the patient's age and size increases, the deformity is less noticeable.

• Histologically, cherubism lesions closely resemble central giant cell granulomas lesions. Histology
shows a giant cell lesions with some reactive bone formation. However, perivascular collagen cuffing
is pathognomonic for cherubism.

• Radiographically, the lesions appear as multiple, well-defined, multi-locular radiolucencies

of the jaw.

• There are no associated systemic manifestations. However, the deciduous dentition may be
spontaneously shed prematurely, starting as early as age 3. There is often delayed eruption of the
permanent dentition, which is often defective with the absence of numerous teeth and displacement
of those teeth present.

• Treatment: cautious waiting as Cherubism tends to regress in early adulthood. Do not treat with
radiation therapy.

ACROMEGALY - a hormonal disorder that occurs when the pituitary gland produces EXCESS
GROWTH HORMONE due to a BENIGN TUMOR after adolescence (fusion of epiphyses). Most
commonly affects MIDDLE-AGED ADULTS and can cause serious illness and premature death.

• In > 90% of acromegaly patients, GH overproduction is caused by a BENIGN TUMOR of the

pituitary gland (ADENOMA). Whether or not the epiphyses of the long bones have fused with the shaft
is the main determinant of whether gigantism or acromegaly will occur when there is oversecretion
of GH by the pituitary gland .

193
 • Clinical Signs: soft tissue swelling of the hands & feet is an early feature, with patients noticing a
change in ring or shoe size. Gradually, bony changes alter the patient's facial features (i .e. brow &
lower jaw protrude, nasal bone enlarges, and teeth spacing increases).

• Oral Manifestations of Acromegaly &Gigantism: enlarged tongue, mandibular prognathism,

teeth are tipped to the buccal or lingual side due to an enlarged tongue, and roots may be longer
than normal.

• Gigantism-caused by a benign tumor BEFORE adolescence (non-fusion of epiphyses).

CYSTIC FIBROSIS - a congenital/heredity metabolic disorder that causes EXOCRINE GLANDS

(glands that secrete fluids into a duct) to produce ABNORMAL SECRETIONS mainly affecting GI and
respiratory systems. CF results in several symptoms (the most important symptom affects the
digestive tract and lungs). In some glands (glands in the pancreas & intestines), the secretions are
thick or solid excessively viscous mucous that can completely block a gland. Mucous-producing
glands in the lung's airways produce abnormal secretions that clog the airways allowing bacteria to
multiply. CF is the most common inherited disease causing death among white people in the U.S.
and is equally common in boys &girls.

• CF is usually characterized by COPD, exocrine pancreatic insufficiency, and abnormally high

sweat electrolytes (sweat glands secrete fluids that have a high sodium & chloride content.
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:!:j of tetracyclines during childhood. Ahigh % of children with CF have dark-colored teeth (yellowish gray
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to dark brown). There is a greatly reduced caries rate in CF patients, probably due to saliva
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." alterations and long-term use of antibiotics.
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• CF Signs &Symptoms: poor growth despite good appetite, malabsorption & foul, bulky stools
(steatorrhea), chronic bronchitis (COPD) with cough, recurrent pneumonia with respiratory infections,
clubbing of fingers/toes, & barrel-chested appearance.

INFLAMMATORY JAW LESIONS

OSTEOMYELITIS - the inflammation or infection of the bone marrow and adjacent bone, usually
caused by bacteria (Staphylococci) due to trauma or surgery by a direct extension from a nearby
infection, or via the bloodstream.

• Signs & Symptoms: pain, redness, swelling in the infected area, fever, and general malaise.
Radiographically, poorly circumscribed radiolucency with a central sclerotic nidus may be evident.

CONDENSING OSTEITIS (CHRONIC FOCAL SCLEROSING OSTEOMYELITIS) - an unusual

bone reaction to an infection (most often associated with a long-standing periapical infection),
occurring in instances of extremely high tissue resistance or in cases of low-grade infection. There may
be no signs or symptoms of the disease, other than mild pain associated with an infected pulp.
Mandibular 1st molar is the tooth most commonly involved. Most often occurs in young patients.

• Radiographic Findings: periapical radiographs show a pathognomonic, well-circumscribed

radiopaque mass of sclerotic bone surrounding and extending blow the apex of one or both roots.
The entire root outline is almost always visible (important feature that radiographically
distinguishes it from a benign cementoblastoma).

• Atooth with this lesion can be treated with RCT or extracted, since the pulp is infected, and the infection
has spread past the immediate periapical area. The sclerosing bone constituting the osteomyelitis is
NOT attached to the tooth, thus remains after the tooth is treated or removed.

194
PERIAPICAL ABSCESS - usually arises from a pulpal infection of a tooth. This pulpal infection NOTES
follows the carious involvement of the tooth. The cellular debris and/or infection that caused the
tooth pulp to become necrotic, slowly filters out of the root tip, producing an inflammatory reaction
around the root tip. A periapical abscess can also occur after traumatic injury to a tooth , causing
pulpal necrosis, and in cases of irritation of the periapical tissues (either my mechanical manipulation
or application of chemicals) in endodontic procedures.

• Clinical Features:
• Acute Abscess: tooth is extremely painful to percussion (may feel slightly extruded from its socket),
and tooth will exhibit mobility. Radiograph presents only a slight thickening of the
periodontal membrane.
• Chronic Abscess: presents as a granuloma or cyst (radiolucent area at the root apex), but there
are usually no clinical features or symptoms (asymptomatic).

• Treatment: establish DRAINAGE by opening the pulp chamber or extracting the tooth. If a periapical
abscess is not treated, it can cause serious complications (Le. osteomyelitis, cellulitis,
&bacteremia).

OSTEONECROSIS - death of bone.

OSTEOPOROSIS - a reduction of total skeletal mass due to INCREASE BONE RESORPTION,

causing predisposition to pathologic fractures caused by calcium or estrogen hormone deficiencies
over a long time period.
• Most common in thin, elderly white women. Treatment: estrogen therapy, calcium &vitamin D
supplements.

OSTEOPETROSIS (" Albers-Schonberg Disease" or "Marble Bone Disease") - an

uncommon hereditary/congenital disorder that manifests in infancy characterized mainly by an
OVERGROWTH &DENSENESS OF BONES due to a defect in osteoclasts which are needed for bone
marrow formation. The long bones become dense and hardened to the extent that BONE MARROW IS
OBLITERATED (prevents bone marrow formation).
• Clinical Signs: abnormal bone & dental development, fragile bones, stunted growth anemia, spleen
& liver enlargement, blindness, and progressive deafness.

CONNECTIVE TISSUE LESIONS

VON RECKLINGHAUSEN'S DISEASE (NEUROFIBROMATOSIS) - the most outstanding feature
is NEUROFIBROMATOSIS (condition of multiple tumors of nerve tissue origin) . VRD is a relatively
common inherited autosomal dominant trait characterized by multiple neurofibromas, cutaneous
cafe-au-Iait macules, bone abnormalities, &CNS changes.

• Clinical Signs: presence of 6 or more cafe-au-Iait macules > 1.5cm in diameter indicates VRD
unless proven otherwise.

• Treatment: there is no satisfactory treatment. The lesions run a high-risk of transforming into a
malignancy.

• Asingle neurofibroma presents at any age as a non-inflamed, asymptomatic nodule that occurs on
the tongue, buccal mucosa, &vestibule. This single nodule is removed by surgical excision , and
rarely occurs.

SCLERODERMA - a relatively rare autoimmune disease affecting the blood vessels &C.T.
characterized by hardness &rigidity of the skin and subcutaneous tissue. The continuous deposition of
collagen in major organs can cause dysfunction and potential failure of these organs.

• Clinical Features: systemic scleroderma usually appears during middle-age (30-50yrs), mainly in
females (4:1). The skin is usually affected first and becomes indurated .
195
 • Oral Radiographs: show abnormal widening of the PDL (abnormal widening of the periodontal-
membrane space is also a radiographic finding in osteosarcomas). The space is created by a
thickening of the periodontal-membrane due to an increase in size & number of collagen fibers. The
enlarged space is almost uniform in width, surrounds the entire tooth root, making the tooth appear
as if it is being extruded rapidly from its socket. Other oral radiographic features may include bilateral
resorption of the angle of the mandible's ramus, or complete resorption of the mandibular condyles
and/or coronoid process.

• Treatment: other than supportive therapy, there is no satisfactory treatment for scleroderma.

ORAL TRAUMATIC NEUROMA - a lesion (soft tissue tumor) caused by trauma to a peripheral
nerve, usually appearing as a very small nodule/swelling « O.5cm in diameter) of the mucosa
near/over the mental foramen on the alveolar ridge in edentulous areas, lips, &tongue. MOST
COMMON SITE IS OVER THE MENTAL FORAMEN IN EDENTULOUS PATIENTS, but they can occur
wherever a tooth has been extracted. Extraction sites in the anterior maxilla & posterior mandible
are common sites.

• In the oral cavity, the traumatic neuroma may be due to trauma from a surgical procedure (i.e. tooth
extraction, from a local anesthetic injection, or accident). A nodule or swelling PAINFUL WHEN
PALPATED, as applied digital pressure elicits a response described as an "electric shock" .

• Multiple neuromas on the lips, tongue, or palate may indicate the patient may have MEN III (Multiple
Endocrine Neoplasia Syndrome).

• Treatment: surgical excision of the nodule with small proximal portion of the involved nerve.
Recurrence is uncommon .

NEURILEMOMA (SCHWANNOMA) - a benign soft tissue tumor (encapsulated mass) of Schwann

cells around the nerve that presents as an asymptomatic lump most commonly found on the
tongue. Bony lesions may cause pain or paresthesia. Derived from a proliferation of Schwann cells
of the neurolemma that surrounds peripheral nerves. Covered by normal mucosa, sessile & does not
metastasize but still do biopsy.

• Treatment: conservative excision. Recurrence is rare.

Neurofibroma-may be derived from the Schwann cell or Perineural Fibroblast and can occur in
two forms:

1. Solitary neurofibroma-an asymptomatic nodule on the tongue, buccal mucosa, or vestibule.

Treat with surgical excision.

2. Multiple lesions as part of the Neurofibromatosis syndrome. Removing the lesions is

impractical, but mon itor due to the high risk/rate of malignant transformation.

FIBROMA ("IRRITATION FIBROMA OR "TRAUMATIC FIBROMA") - most common intra-oral

BENIGN neoplasm of CONNECTIVE TISSUE (soft tissue) origin that occurs in people of all ages and
with equal frequency in both sexes. It's the most common tumor in the oral cavity and is reactive.
Fibromas can arise from almost any soft tissue in the mouth, but are most common on the buccal
mucosa, lateral border of tongue, and lower lip.

• Clinical Features: usually pink (same color or lighter than normal buccal mucosa, painless, smooth,
elevated, well-demarcated masses. Smooth, sessile, soft-to-firm nodule found on buccal mucosa,
lips, and tongue.

• Microscopic Features: bundles of collagen interspersed (interlacing) with fibroblasts and small
blood vessels.

• Histogenesis: fibrous C.T. (C.T. origin) .

196
• History is helpful in diagnosing a fibroma, since in most cases the tumor is reported present for NOTES
months or years with a slow-growing behavior pattern.

• Some feel "true fibromas" of the oral cavity are rare, and are merely localized hyperplasia due to
long-standing irritation or trauma ("irritation fibroma or "traumatic fibroma "). These fibrous nodules
are comparable to hyperplasias from denture irritation ("epulis fissuratum"). The only difference
between a "true fibroma (a true neoplasm) and "irritation fibroma" (not a true neoplasm), is the
hyperplastic tissue may regress after removing the irritant, while a true fibroma will not regress.
Treatment: conservative surgical excision. Recurrence is rare.

PERIPHERAL FIBROMA - a well-demarcated focal mass of hyperplastic tissue with either a

sessile or pedunculated base. Similar in color to surrounding C.T., and may be ulcerated. Treatment:
local excision & recurrence is RARE. 3 forms of peripheral fibroma:

1. Peripheral Ossifying Fibroma-a gingival mass with visible characteristic calcified islands of
bone and an ulcerated surface. The gingiva anterior to the permanent molars is most often
affected. Histologically, in its high degree of cellularity, it exhibits bone formation (in contrast to
peripheral fibroma). Vascularity is NOT a prominent feature as it is with a pyogenic granuloma .

• POF is a subtype or variant form of a peripheral fibroma . However, both originate from an
interdental papilla and both occur more frequently in young adult females (but can occur at
any age, although more common in children &young adults).

• Usually presents as a well-demarcated focal mass of hyperplastic tissue on the gingiva with
a sessile or pedunculated base. It is usually the same color as normal mucosa or slightly
reddened . May demonstrate bone radiographically and often demonstrates bone
formation histologically.

• Treatment: local excision of the mass. POF lesions may recur (peripheral fibroma lesions do
not recur) .

2. Peripheral Odontogenic Fibroma-a gingival mass composed of well-vascularized, non-

encapsulated fibrous C.T.

3. Giant Cell Fibroma-a fibrous hyperplasia composed of multi-nucleated C.T. cells.

GIANT CELL TUMOR - a bone tumor of multinucleated giant cells that resemble osteoclasts
scattered in a matrix of spindle cells. Myelomas of this type may be benign or malignant, and can
cause pain , functional disability, and sometimes pathologic bone fracture.

PAPILLARY FIBROMA - a benign neoplasm of C.T. origin.

LIPOMA - a benign soft tissue tumor derived from ADIPOSE (FAT) tissue (C.T. origin). It is smooth or
lobulated, sessile or pedunculated (foot-shaped), soft, yellowish nodular mass. Vessels are visible over the
surface. Found in the floor of mouth, buccal mucosa, and tongue. YElLOWISH MASS covered by normal
mucosa. A biopsy specimen will FLOAT in the formalin. Easier to diagnose than other tumors because it is
yellowish and soft &smooth. Also will flOAT IN FORMALIN so it is very easy to know if it is a lipoma.

• Microscopic Features: lobules of mature fat separated by delicate C.T. septae.

• Treatment: conservative excision . Recurrence is rare.

RHABDOMYOMA - a RARE benign tumor of SKElETAL MUSCLE. Tongue is most common place in
the head & neck. Sessile non painful covered by normal mucosa

LEIOMYOMA - a benign tumor of SMOOTH MUSCLE (smooth muscle neoplasm). Not painful,
sessile, always benign (covered by normal mucosa). Bundles of spindle shaped smooth muscled cells.

197
 N LYMPHANGIOMA - a benign, yellowish-tan tumor composed of a mass of DILATED LYMPH
VESSElS. The most common site in the oral cavity is the TONGUE, but can appear on the lips & neck.
Derived from endothelial cells, C.T. origin. Clinical Features: painless, nodular, vesicle-like swelling
that equally affects both sexes.

• Superficial lesions are manifested as grayish-red papillary lesions. On the tongue, considerable
enlargement can occur (macroglossia). The papillary lesions may contain fluid, and are often
present at birth or arise early in life, but are less common than Hemangiomas.

• Microscopic Characteristics: can be simple, circumscriptum, or cystic (closely related to cystic

hygroma, containing serous fluid) .

• Treatment: surgery, cryosurgery. May recur due to their lack of encapsulation.

Benign Tumors of Epithelium:

1. Papilloma-a VITAL cualilflower-like, white, verrucuous &pedunculated (foot-shaped) surface.
Must do surgery. Very easy to diagnose. VIRAl. Lesion is not covered by normal mucosa and is a
disease of epithelium. Non-ulcerated, small, and slow growing. Lateral border of tongue a non-
painful area present for months. A benign white lesion on lateral border of tongue, not painful,
verrucous &pedunculated surface looks like cauliflower (abnormal mucosa).
2. Verruca (warts)-similar to a papilloma, but is NOT pedunculated. Viral infection. Do excision &
biopsy. Especially children who have this on their finger and place finger in mouth and spread
the infection to the mouth.

3. Keratoacanthoma-a non-painful crater-formed lesion growing for 2-3 months in the SKIN that
looks like squamous cell or basal cell carcinoma, and can heal by itself, but must still do biopsy.
It is VIRAL and lasts 6 months. It is in the skin and very rarely inside the mouth.

MULTIPLE ENDOCRINE NEOPLASIA SYNDROMES (MEN SYNDROME) - groups of syndromes

characterized by tumors of various endocrine glands that occur in association with a variety of other
pathologic features. The most important aspect of MEN syndrome is medullary carcinoma of the
thyroid due to its ability to metastasize and cause death. Thus, detecting mucosal neuromas may alert
the clinician for early diagnosis and treatment. MEN is classified into 3 groups:
1. Men I Syndrome-tumors or hyperplasias of the pituitary, parathyroids, adrenal cortex, and
pancreatic islets.

2. Men II (Sipple's Syndrome)-characterized by parathyroid hyperplasia or adenoma, but NO tumors

of the pancreas. These patients have pheochromocytomas of the adrenal medulla, and
medullary carcinoma of the thyroid gland.

3. Men III Syndrome-characterized by mucocutaneous neuromas, pheochromocytomas of the

adrenal medulla, and medullary carcinoma of the thyroid gland. The most constant feature
of Men III is the presence of neuromas (especially in the oral cavity), most commonly on the
lips, tongue, and buccal mucosa.

EPULIS GRANULOMATOSUM - most often caused by RETAINED FOREIGN MATERIAL (Le. bone or
tooth fragment) due to an iatrogenic error. Most commonly found in a post-extraction socket, almost
. always within 10 days of the extraction.
• Clinical Features: soft, non-painful, bleeds easily.
• Microscopic Features: granulation tissue within which one may find bone, dentin, cementum, or
foreign material.
• Treatment: curettage.

CONGENITAL EPULIS OF NEWBORNS (CONGENITAL GINGIVAL GRANULAR CELL TUMOR) -

composed of cells identical to cell of a granular cell myoblastoma (granular cell tumor). CE usually
appears on the anterior gingiva of newborns as a non-inflamed, pedunculated or broad-based mass.
Maxillary gingiva involved more than mandibular gingiva, and females are affected more than males.

• Treatment: surgical excision with little possibility of recurrence.

198
GRANULAR CELL MYOBLASTOMA - an uncommon neoplasm of unknown etiology, presenting as
an uninflamed, asymptomatic mass. TONGUE is the most common location in the head & neck region.
It may affect any age group, and females are affected more than males.

Congenital Epulis & Granular Cell Myoblastoma lesions are histologically identical as they both
contain granular cells. However, Congenital Epulis of newborns does not exhibit
pseudo epitheliomatous hyperplasia of the overlaying epithelium, that is often seen in Granular Cell
Myoblastoma.

PYOGENIC GRANULOMA (PREGNANCY TUMOR) - an elevated often ulcerated mass that

bleeds easily, more common in females (pregnant women), and may recur. Caused by minor trauma
that provides a pathway for non-specific organisms & calculus. Most commonly found on the gingiva,
but also lips & buccal mucosa.

• Microscopic Features: exuberant granulation tissue.

• Treatment: surgical excision, but may recur.

PREGNANCY TUMOR - term used for a pyogenic granuloma in a pregnant patient (this is a
pyogenic granuloma), caused possibly secondary to an altered endocrine state (hormone changes)
during pregnancy in the FIRST TRIMESTER. Most common on the GINGIVA, but also lips & buccal
mucosa.

• Microscopic Features: exuberant granulation tissue.

• Treatment: surgical excision, but DO NOT REMOVE UNTIL AFTER PREGNANCY.

IMPORTANT TERMS
ANAPLASIA - a histologic feature of a malignancy. The absence of cell differentiation.

AUTOGRAPH (AUTOLOGOUS GRAPH) - a tissue or organ transferred into a new position within
the body of the same individual.

BIOPSY - the MOST RELIABLE technique to diagnose soft tissue lesions. Scalpel is the instrument of
choice since it cleanly removes tissues without dehydrating them as cautery or the high-frequency
cutting knife may. FORMALIN (1 O%) is the fixative of choice. The rationale for surgical removal and
biopsy of a large periapical lesion suspected to be of inflammatory origin is that a clinical diagnosis can
be confirmed microscopically. Biopsy is the only way to distinguish between a granuloma and a cyst.

EXCISIONAL BIOPSY - involves TOTAL EXCISION of a small lesion for microscopic study. This is
preferred if the lesion size is such that it may be removed along with a margin of normal tissue
and the wound can be closed primarily (i.e. a lcm exophytic mass-a lesion that grows outward
from an epithelial surface on the cheek).

INCISIONAL BIOPSY (DIAGNOSTIC BIOPSY) - removes only a SMALL SECTION of tissue for
examination. This is done when lesions are too large to excise initially without having established a
diagnosis, or are of such a nature that excision would be inadvisable.

CHORISTOMA - a developmental defect characterized by an overgrowth of tissues ABNORMAL to the

organ from which it arises.

199
 DIFFERENTIATION - a measure of a tumor's resemblance to normal tissue.

DYSPLASIA - a type of NON-MALIGNANT cellular growth (not a feature of malignancy), but may
precede neoplastic changes in tissue. Associated with chronic tissue irritation by a chemical agent
(i.e. cigarette smoke), or by chronic inflammatory irritation (i.e. chronic cervitis). The tissue appears
somewhat structureless and disorganized, and may consist of atypical cells without invasion.
Epithelium exhibits acanthosis (abnormal thickening of the prickle cell layer).

HAMARTOMA - a developmental defect characterized by an overgrowth of tissues NORMAL to the

organ from which it arises.

HYPERPLASIA - an increase in the size of a tissue or organ due to an increase in the NUMBER of
component cells.

HYPERTROPHY - an increase in the size of a tissue or organ due to an increase in the SIZE of
component cells.

IATROGENIC - a condition caused by medical personnel or procedures. The term originally applied
to disorders induced in the patient by auto-suggestion based on the physician's examination, manner,
or discussion. Iatrogenic is NOW applied to any adverse condition in a patient occurring as a result of
treatment by a physician, especially to infections acquired during the course of treatment.

IDIOPATHIC - a disease or condition of unknown cause or origin.

METAPLASIA - process where one cell type changes to another cell type in RESPONSE TO
STRESS to assist the host to adapt to stress. The most common type of epithelial metaplasia
involves replacement of columnar cells by stratified squamous epithelium. Metaplasia is NOT a
feature of malignancy.

NOSOCOMIAL- an infection/disease originating in the hospital. An infection not present before

admission to the hospital, but generally occurring 72hrs later. Nosocomial usually refers to patient
disease, but hospital personnel may also acquire a nosocomial infection.

Oncology-the study of neoplasms.

• Neoplasms-a n uncontrolled new growth of tissue.

• Tumor-a localized swelling that mayor may not be a true neoplasm.

• Cancer-a general term for all MALIGNANT neoplasms.

• Carcinoma-a malignant epithelial neoplasm .

• Sarcoma-a malignant mesenchymal (C.T.) neoplasm.

TERATOMA - a benign or malignant neoplasm composed of multiple tissues FOREIGN to the organ in
which it arises

200
NEOPLASMS NOTES
LYMPHOEPITHELIOMA - a poorly differentiated squamous cell carcinoma involving lymphoid
tissue in the tonsils & nasopharynx regions. It has a high frequency in young adults of East Asian
decent. The primary lesion is usually very small (often completely hidden). SWELLING OF THE LYMPH
NODES is the most common presenting symptom, followed by sore throat, nasal obstruction, bloody
nose, &headache.

• This neoplasm is composed of squamous or undifferentiated cells, with a slight-to-moderate amount

of fibrous stroma that contains numerous lymphocytes. Lymphoepithelioma shows METASTASIS AT
AN EARLY STAGE TO THE CERVICAL LYMPH NODES.

• Treatment of choice is x-ray RAOIATON, but the complicating factor is the relative inability to
treat the widespread metastases in the various organs. Prognosis is poor, with a 30%
5-year survival rate.

METASTIC CARCINOMA - the most common malignancy affecting SKELETAL BONES. However,
metastic disease of the mandible and maxilla is unusual (-1 %). Most important, a jaw tumor may be
the first evidence of dissemination of a known tumor from its primary site. Metastases to the jaws
most commonly originates from primary carcinomas of the BREAST, KIDNEY, LUNG, COLON,
PROSTATE, &THYROID. Metastatic carcinoma of the jaws is LEAST likely to originate from the brain. c::>
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• Clinical Features of Metastic Jaw Lesions: may be completely asymptomatic, however there is usually ."
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paresthesia or anesthesia of the lip or chin due to involvement of the mandibular nerve (patient is :z::
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usually aware of slight discomfort or pain). Teeth in the area are loose or extruded (the molar region c::>
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is mainly involved), there can be swelling or expansion of the jaw, and appears as an asymptomatic
radiolucency. Although rare, metastic jaw tumors affect the mandible MUCH more than the maxilla.

Most common OSSEOUS MALIGNANCIES are OSTEOSARCOMAS, followed by Chondrosarcomas,

Fibrosarcomas, & Ewing's Sarcoma.

OSTEOSARCOMA (OSTEOGENIC SARCOMA) - a MALIGNANT bone tumor composed of

anaplastic cells derived from mesechyme. MOST COMMON PRIMARY MALIGNANT TUMOR OF BONE,
arising in LONG BONES which show the greatest longitudinal growth. Joint involvement is rare. Its
PEAK incidence is BEFORE epiphyseal fusion (ages 10-25yrs), but a later peak is associated with
Paget's Disease, Chronic Osteomyelitis, and previous radiotherapy.

• Radiographic Features: most important EARLY radiographic feature of an osteosarcoma of the jaw
is a SYMMETRICALLY WIDENED PDL SPACE around 1 or more teeth. Other radiographic features,
depending on the degree of calcification: sclerotic (excessive bone production producing "SUN-RAY
APPEARANCE"), lytic (irregular radiolucency), & mixed (most osteosarcomas have a mixed
appearance).

• Differential diagnosis for an osteosarcoma of the JAW include:

• Chondrosarcoma, Metastic Carcinoma & Pindborg Tumor.
• Ossifying Subperiosteal Hemangioma & Peripheral Odontogenic Fibroma.
• Scleroderma &Chronic Osteomyelitis.
• Symptoms: tumor or swelling mass, pain, loose teeth, paresthesia, bleeding.

• Histologic classification of an osteosarcoma is based on the dominant type of tissue cell:

1. Osteoblastic-produces osteoid tissue.
2. Chondroblastic-produces cartilage tissue.
3. Fibroblastic-produces fibrous tissue.

• Osteosarcomas can be classified by site of origin into:

1. conventional type that arises within the medullary cavity.
2. juxtacortical tumors that arise from the periosteal surface.
3. extraskeletal osteosarcomas that arise in soft tissue.

201
 ERWING'S SARCOMA - a malignant tumor developing from bone marrow, usually in long bones
or pelvis of adolescent boys (peak ages 10-20yrs). It is an uncommon HIGHLY LETHAL MALIGNAN
NEOPLASM OF BONE of uncertain origin. The pelvis, thigh, and body trunk are the most common sites.

• Intermittent pain and swelling of the involved bone are often the earliest clinical signs/symptoms.
Fever & leukocytosis are also present.

• Histologically, ES is difficult to distinguish from a neuroblastoma or reticulum cell sarcoma, but cells
of Ewing's sarcoma contain GLYCOGEN.

• When the jaws are involved, there is predilection for the RAMUS OF THE MANDIBLE with pain followed
by rap id swelling and loosening of the teeth.

• Radiographically, the most characteristic appearance is MOTH-EATEN destructive radiolucency of

the medulla, with erosion of the cortex with expansion . A variable periosteal "ONION-SKIN"
reaction may also be seen .

MULTIPLE MYElOMA ("PLASMA CElL MYElOMA") - a malignant neoplasm/lesion of bone

marrow & plasma cells and is MOST LIKELY FATAL. Characterized by elevated blood levels of Bence-
Jones Protein & multiple radiolucent areas in the mandible & skull. The tumor consists mainly of
PLASMA CELLS that destroy osseous tissues (there is progressive destruction of bone marrow with
o replacement by neoplastic plasma cells).
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=< • Most patients are older than 40yrs (40-70yrs) affecting males 2x more than females (2: 1). The
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r- vertebrae, ribs, and skull are most often involved. PAIN in the lumbar or thoracic regions of the spine
o
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-< is a common early symptom.

• Jaws are RARELY a primary site, but become involved in 70% of cases. Molar-ramus area is the
most common intra-oral site. Symptoms include swelling, pain, teeth loosening, and paresthesia.

• Radiographic Features: variable; slight demineralization to extensive destruction. Characteristic

finding is multiple, small, discreet "PUNCHED OUT" radiolucencies in involved bones. In a patient
suspected of having multiple myeloma, a LATERAL SKULL RADIOGRAPH best confirms the diagnosis.

• Laboratory Findings: are important to establish a diagnosis. Hypergammaglobulinemia (especially

IgG in 70% of cases). Bence-Jones proteinuria is present in 60-85% of cases.

• Treatment & Prognosis: chemotherapy, radiation. Poor prognosis with median survival time of
2-3 years.

OSTEOCHONDROMA - a BENIGN tumor of bone & cartilage.

ODONTOGENIC MYXOMA - a RARE slow growing, usually asymptomatic JAW TUMOR most often in
the mandible. Patients are usually < 35yrs of age. Eventually causes localized expansion of the jaw.
Treatment: Curettage. Not fatal.

TNM - a method to clinically stage and assess the prognosis and therapy of MALIGNANT
NEOPLASMS (TUMORS) based on the primary tumor's size (T), presence of regional lymph node
involvement (N), and presence of distant metastases (M) . Ex: a carcinoma of the oral cavity may have
a TNM assessment of T2, NI, MO.
• T= SIZE of the primary tumor.
• TX = primary tumor cannot be assessed.
• TO = no evidence of tumor.
• Tis = carcinoma in situ.
• Tl = < 2cm in greatest diameter.
• T2 = 4cm is greatest diameter.
• T3 = > 4cm in greatest diameter.

202
• N= Presence of regional LYMPH NODE involvement.
• NX = regional lymph nodes cannot be assessed.
• NO = no clinically palpable lymph nodes or lymph nodes palpable, but metastases is not suspected.
• N1 = palpable homolateral lymph nodes, not fixed, but metastases is suspected.
• N2 = palpable centralaterallbilaterallymph nodes, not fixed, but metasteses is suspected.
• N3 = palpable lymph nodes and fixed metastases is suspected.

• M= Presence of DISTANT metastasis

• MX = presence of distant metastasis cannot be assessed.
• MO = no distant metastasis.
• M1 = clinical and/or radiographic evidence of metastasis other than regional lymph nodes.

Melanoma exhibits either a "radial" (horizontal) or "vertical" growth phases within the skin:
1. Radial Growth Phase-the INITIAL growth phase of a melanoma just above & below the
dermo-epidermal junction in a horizontal plane. It is clinically macular or only slightly elevated.
2. Vertical Growth Phase-begins when neoplastic cells populate the underlying dermis.
Characterized clinically by an increase in size, change in color, nodularity, & ulceration.
METASTASIS is possible when the melanoma reaches this phase.

MALIGNANT MELANOMA - considered the MOST SEVERE and potentially serious type of SKIN
CANCER mainly due to excessive exposure to UV sun radiation which causes the tanning cells
(melanocytes) in the skin that produce a dark-colored substance (melanin) to undergo uncontrolled o
::a
growth. Melanoma may suddenly appear without warning, but often develops from or near a MOLE :D-
r-
(NEVUS). Common in fair-skin white people, occurring anywhere on the skin. .."
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• SKIN CANCER IS THE MOST COMMON MALIGNANCY IN THE U.S. 1 in 100 people in the U.S. will ....
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develop this cancer in a lifetime. Without treatment, it can widely metastasize and result in death.

• Malignant Melanoma is an uncommon neoplasm of the oral mucosa but exhibits a definite
predilection for the palate & maxillary gingiva/alveolar ridge. Unfortunately, oral mucosa
melanomas have a poor prognosis (5-year survival rate for oral melanoma tumors is -7%) . The most
common intra-oral site for melanoma is the hard palate.

• Linked to excessive SUN EXPOSURE over a lifetime and to PAINFULL SUNBURNS during childhood.

4 Clinical Types of Melanoma:

1. Superficial Spreading Melanoma-the MOST COMMON form of malignant melanoma (65%), &
most common cutaneous melanoma in Caucasians. The lesion is tan, brown, black, or admixed
lesion on sun -exposed skin (especially the back). The cancer begins at one focus in the skin at
the dermo-epidermal junction. It initially grows in a horizontal plane, along and just above &
below the dermo-epidermal junction (this is the "radial" growth phase of melanoma which
predominates), and is clinically macular or only slightly elevated. The "vertical" growth phase
is characterized by an increase in size, change in color, nodularity, and at times ulceration.

2. Nodular Melanoma-much less common and accounts for -13% of cutaneous melanomas. With
Nodular Melanoma, THERE IS NO "RADIAL" GROWTH PHASE (it exists solely in the "vertical"
growth phase which predominates). It presents as a sharply defined nodule with degrees of
pigmentation (may be pink (amelanotic melanoma) or black, and occur more frequently on the
back, head, and neck of men.

3. Lentigo Maligna Melanoma-accounts for -10% of cutaneous melanomas, and is most common
in the ELDERY population. The lesion may grow for years in the "radial" growth phase before
developing into the more aggressive "vertical" growth phase. This radial growth phase is known
as lentigo maligna (melanotic freckle of Hutchinson), while the vertical growth phase is known
as lentigo maligna melanoma .

4. Acrolentiginous Melanoma-occurs on the hands & feet with a reputation for being ignored by
the patient, resulting in the development of metastic disease.

203
 NEVUS - a MOLE (almost all moles are normal). Atypical (Dysplastic) Nevi-unusual moles that are
generally larger than normal moles, and are either flat or have a flat part. They have irregular borders
with variable shades of color (especially brown) . The presence of dysplastic nevi may mark a greater
risk of malignant melanoma developing on apparently normal skin.

BASAL CEll CARCINOMA - a MALIGNANT epithelial cell tumor that characteristically begins as a
papule that enlarges peripherally, forming a central crater that erodes, crusts, & bleeds. Only found
on the skin, and NEVER in the mouth. Primarily caused by EXCESSIVE SUN EXPOSURE (UV radiation)
or to x-rays. Metastasis is rare, but the local invasion by direct extension destroys underlying and
adjacent tissues. Frequently develops on exposed surfaces of the skin, face (nose), & scalp in
middle-aged or elderly people. Treatment: eradicate the lesion by electrodessication or
cryotherapy. IT IS THE MOST COMMON SKIN CANCER, that usually appears as an ulcerated,
crateriform lesion. It may look exactly like squamous cell carcinoma, but RARELY produces
metastasis.

• 0% of intra-oral cancers are basal cell carcinoma .

• Common in adult whites with fair complexions. Produced by sunlight only or in patients with basal
cell syndrome.

• Basal Cell Carcinoma has a much better prognosis than squamous cell carcinoma since it DOES
NOT PRODUCE METASTASIS (it is invasive, so if you do not do surgery, the patient will die, but if
treated, the patient will be cured) . Frontal skin lesion in a 72-year male with 2 years of evolution.
NEVER FOUND INSIDE THE MOUTH.

SQUAMOUS CEll CARCINOMA (EPIDERMOID CARCINOMA) -the MOST COMMON

MALIGNANCY IN THE ORAL CAVITY (90%) & occurs more often in the oral cavity than any other type
of cancer (90% of all malignant oral cavity neoplasms). sec is a malignant EPITHELIAL TUMOR that
is twice as prevalent in males (ages 40-65yrs).

• It is more common on the lower lip than intra-orally. The most common intra-oral site for SCC is
the lateral border &ventral surface of the tongue (from this site, it often metastasizes to cervical
lymph nodes). The dorsal tongue surface is almost never affected . Floor of the mouth is the second
most common intra-oral site, with the worst prognosis.

• Risk Factors: smoking & smokeless tobacco (main risk factor), alcohol, painful & ill-fitting
dentures, and chronic inflammation.

• INVASION is the most reliable histologic criterion for a diagnosis of oral SCC.

• Treatment: surgery &irradiation to remove lymph nodes in neck.

• Squamous Cell Carcinoma can be red, irregular, non-painful lesion. Is also often a white lesion , can
be caused by sun exposure, or be on the floor of mouth due to drinking &smoking. Lasts> 1 month.
• Histology: hyperchromatism , pleomorphism, atypical mitosis, dyskeratosis, alteration of nuclei-
cytoplasm ratio, acanthosis, but NOT sub-epithelial cleft.
• Found mainly in posterior lateral border of tongue, but can be on lip & floor of mouth. NOT
common on dorsum of tongue.
• Found on floor of the mouth and ventral side of tongue. #1 area is the lateral border of the tongue
• Metastic spread occurs via lymphatics. May present as a white lesion, &risk increases with age.

Squamous Cell Carcinoma Occurs in these Head &Neck locations:

1. Nasopharynx: caused by tobacco &alcohol. Represents < 2% of all cancers in U.S. (the least
common squamous cell carcinoma). Affects males ages 30-40yrs. Roof or lateral wall is the
most common site. Signs: cervical mass, earache, sore throat, and nasal obstruction .

2. Palate: uncommon, but caused by tobacco, alcohol, and denture irritation. Represents 10% of
all oral carcinomas (soft palate is more common than the hard palate). Affects men> 60yrs.
Signs: painful ulcer, leukoplakia , exophytic mass.
204
 3. Oropharynx: caused by tobacco & alcohol. Represents 10% of all head & neck cancers, affecting NOTES
men> 50yrs. Signs: sore throat, dysphagia, painful ulcer, cervical mass.

4. Maxillary Sinus: etiology is unknown. Represents 30% of all head &neck cancers. Affects men
> 40yrs. Signs: chronic sinusitis, bulging palate, teeth loosening, paresthesia in the cheek.

5. Tongue: most common site is the LATERAL BORDER, but also occurs on the ventral surface
(under the tongue) (dorsum is the least frequently involved). Tongue cancer causes more deaths
than any other malignant lesion in other regions of the head & neck because the tongue is the
MOST COMMON INTRAORAL SITE OF CANCER that is a highly mobile organ richly endowed with
lymphatics & blood vessels that facilitate metastasis (most commonly metastasizes to the
cervical lymph nodes). It very RARELY gives rise to skeletal metastasis.
• Etiology: tobacco, alcohol, syphilis, Plummer-Vinson Syndrome.

• Mostly effects men >60yrs. on the posterior lateral border and middle third of the tongue.
Presents as a painless ulcer with leukoplakia and erythroplakia .

6. Lips: cancer is more common here than intra-orally (most common site), and 95% are found
on the LOWER LIP (vermillion of the lower lip) of which 90-98% of lower lip cancers occurs in
MALES 60+ due to chronic sun exposure and pipe smoking. This location (lips) is etiologically
related to race, complexion, pipe smoking, sunlight. It is a painless ulcer and keratotic plaque.

7. Floor of Mouth: SECOND MOST COMMON INTRA-ORAL SITE FOR CANCER, occuring most
commonly in the ANTERIOR SEGMENT on either side of the midline near salivary gland orifices.
Caused by tobacco and alcohol. Pre-malignant lesions of squamous epithelium most often occur
here. Prognosis is very poor.
• Typically effects men ages 40-60yrs. Presents as a painless ulcer with leukoplakia
and erythroplakia.

8. Buccal Mucosa: generally occurs along the PLANE OF OCCLUSION, midway anteroposteriorly.
Represents 10% of all oral carcinomas, caused by tobacco, alcohol , and denture irritation.
Presents as a painless ulcer and exophytic mass with leukoplakia .

9. Gingiva & Alveolar Mucosa: more common in the MANDIBLE than maxilla, with posterior sites
affected more often than anterior sites. Represents 10-15% of all oral carcinomas, caused by
tobacco and alcohol. Mainly effects men 60+ years. Common on the mandibular mucosa as a
painless ulcer and plaque-like or exophytic mass.

Squamous Cell Carcinoma is most easily managed when found on the LOWER LIP. SCC is the most
common malignant oral tumor, representing >90% of all oral malignancies. SCC is 9-1 Ox more
common in males than females , and while it is seen in all ages, its highest incidence is after age
40yrs. It is more common on the lips than intra-orally.

• 95% of lip carcinomas occur on the LOWER LIP, and are usually discovered early and only a small
percentage show lymph node metastasis. The prognosis is very good .

• SCC of the tongue is the most common INTRAORAL malignancy. The most common location is the
posterior lateral border, then the posterior 1/3 (tongue base). SCC is uncommon on the dorsum or
tongue tip. These lesions usually metastasize early, and the prognosis is not as good as lip lesions.

• Floor of the mouth is the 2nd most common intraoral location of SCC. It occurs mainly in older men
(especially chronic alcoholics and smokers). These lesions metastasize early and the prognosis is very poor.

• Treatment of choice for ORAL CANCER IS SURGERY.

205
 3 Types of Squamous Cell Carcinoma:
1. Verrucous Carcinoma-a RARE form of squamous cell carcinoma that DOES NOT METASTASIZE,
but occurs in the soft tissues of the oral cavity (mandibular mucobuccal fold, alveolar mucosa,
& palate), or laryngeal cavity due to tobacco chewing, smoking, or snuff dipping. Mostly effects
men 60+ years. The tumor mass has a characteristic whitish, cauliflower or coral-like papillary
appearance. Typically, the lesion develops on the vocal cords of an elderly male who has been
a heavy cigarette smoker. It is known for its slow growth pattern and well-developed
hyperkeratotic epithelial boundaries.

• Pathologically, it is a well-differentiated squamous cell neoplasm that may invade or infiltrate

the borders of adjacent structures, but rarely metastasizes. It can transform into an invasive
form of carcinoma, or coexist with other squamous cell carcinomas. It is often misdiagnosed
histologically as a benign lesion.

• Treatment: Surgery. Prognosis: 60-70% have 5-year survival rate.

• Non-aggressive, very well-differentiated tumor that does not metastasize. Adisease of OLDER
PEOPLE. Can present as a diffuse, WHITE, well-demarcated, painless papillary surface mass
on the UPPER (MAXILLARY) ALVEOLAR RIDGE, measuring 6x4cm, and can be present for 2-3
years before a definitive diagnosis is made. Better prognosis than carcinoma invasive. Can
destroy the bone.
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2. Carcinoma IN SITU: located only intraepithelial (inside epithelium), atypical mitosis,
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::; hyperchromatism, all epithelial layers are affected, but IT DOES NOT INVADE C.T. (basal
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o membrane is intact). Prognosis is better than carcinoma invasive, but must treat. Carcinoma
r-
o in situ is malignant, but CANNOT matastasize due to lack of blood or lymphatic vessels in
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-< epithelium. Located ONLY in the epithelium which does not have blood or lymphatic vessels so it
cannot produce metastasis. Ex: 60-year-old alcoholic female with red FLAT area in the mouth
floor. Area is flat, asymptomatic, present for 4 months, increasing in size, but not painful. Her
medical history is non-contributory.

3. Carcinoma Invasive-Ex: 60-year-old alcoholic female with red area in the mouth floor. Area is
flat, asymptomatic, present for 4 months, increasing in size, but not painful. Her medical history
is non-contributory.

Characteristics of Lesions that may be Malignant:

• Erythroplasia: lesion is totally red or speckled red and white. Ared, non-ulcerated area on a
mucous membrane. The texture can be normal or rough and its size varies (some are so small and
may go undetected, while large areas are conspicuous to casual inspection). There are usually no
symptoms, being neither elevated nor depressed, presenting as Quiet, unpretentious lesions The
border may be sharp, or blend imperceptibly into surrounding normal mucosa. It must constantly be
kept in mind that early carcinoma often appears as an area of erythroplasia. There are certain
areas of the oral mucosa are more prone to malignancy. Additionally, oral cancer is more often seen
in people over age 40yrs. Because of this, an area of erythroplasia in a cancer prone area in a
patient over 40yrs is highly suspicious of malignancy and should be biopsied on the day it is seen
(especially lesions whose duration exceeds 2 weeks).

• Rapid growth

• Ulceration: lesion is ulcerated or is an ulcer.

• Bleeding: bleeds on gentle manipulation.

• Induration: lesion and surrounding tissue is firm to touch. On physical examination, painless
induration of soft tissue suggests an invasive malignant lesion.

• Fixation: feels attached to adjacent structures.

206
ODONTOGENIC ABNORMALITIES
ABRASION - abnormal PATHOLOGIC WEARING AWAY of tooth substance. Pathologic loss of tooth structure.

1. toothbrush abrasion-most often results in V-shaped wedges at the cervical margins in canines
& premolars. Caused by using a hard toothbrush and/or horizontal brushing strokes with a
gritty dentrifice.

2. occlusal abrasion-results in flattened cusps on all posterior teeth & worn incisal edges due
to chewing or biting on hard foods or objects, and chewing tobacco.

ATTRITION - the physiologic wearing away of enamel & dentin due to NORMAL FUNCTION, or most
commonly due to excessive grinding or gritting the teeth together (bruxism). The most noticeable
effects are Polished Facets, flat incisal edges that usually develop on the linguoincisal of maxillary
canines & central incisors, and facioincisal of mandibular canines. Discolored tooth surfaces, and
exposed dentin also occur.

EROSION - chemical oss of tooth structure from NON-MECHANICAL MEANS such as drinking acidic
liquids (soda) or eating acidic foods. Common in bulimics due to regurgitated stomach acids.
Affects smooth and occlusal surfaces.

INTERNAL RESORPTION - an unusual form of tooth resorption that beings centrally within a
tooth's root canal (it looks like a balloon is in the middle of the root canal). Resorption of the dentin
of the pulpal walls may be seen as part of an inflammatory response to pulpal injury, or may be seen in
cases where no apparent cause can be identified. Most cases present no early clinical symptoms. The
first evidence of internal resorption may be the appearance of a pink-hued area on the tooth's
crown that represents the hyperplastic, vascular pulp tissue filling the resorbed areas. If this
condition is discovered before perforation of the crown or root occurs, then RCT can be performed with
a relatively high success rate.

Intrinsic Staining of Teeth can be caused by the following except DIABETES MELLITUS.

• Dentinogenesis imperfecta-causes a translucent or opalescent hue, usually gray to bluish-brown.

• Erythroblastosis fetalis- causes an intrinsic stain that is bluish-black, greenish-blue, tan, or brown.

• Porphyria-causes an intrinsic stain that is red or brownish.

• Fluorosis-causes white opacities, or light brown to brownish-black.

• Pulpal injury-the intrinsic stain starts pink, then usually becomes orange-brown to bluish-black.

• Internal resorption-causes a PINKISH intrinsic stain.

• Tetracyclines-intrinsic stain may vary from light-gray, yellow, or tan to darker shades of gray.

ANKYLOSIS - the fusion of alveolar bone to a tooth. Ankylosis may be initiated by an infection or
trauma to the PDL. The ankylosed tooth has lost its PDL space, and is actually fused to the alveolar
process of bone. There is change in the continuity of the occlusal plane caused by the continued
eruption of non-ankylosed teeth & growth of the alveolar process.

GEMINATION (TWINNING) - a division of a single tooth germ by invagination causing incomplete

formation of two teeth (usually the incisors). Incomplete splitting of a tooth germ.

GOMPHOSIS - a type of fibrous joint where a conical process is inserted into a socket-like
portion (i.e. styloid process in the temporal bone, or the teeth inserted into the dental alveoli).

207
 NOTES FUSION - developmental union/joining of > 2 teeth (germs) in which dentin &another dental tissue
are united (maybe the root).

CONCRESCENCE - a condition where only the cementum of two or more teeth become united. The
joining of teeth by cementum .

TAURODONTISM - enlarged pulp chambers and shortened roots. Usually affects molars.

Dens-in-Dente (Dens Invaginatus) - a "tooth-within-tooth" caused by a deep invagination of

the enamel organ during formation. Most commonly associated with a maxillary lateral incisor.

MESIODENS - the most common SUPERNUMERARY TOOTH (extra tooth like 4th molar) usually
appearing singly or in pairs as a small tooth with a cone-shaped crown and short root visible
between vital permanent maxillary centrals on a radiograph. It may be erupted, impacted , or
inverted. Appears situated in the maxilla near the midline and almost always posterior to normal
central incisors. Thus, many of them are bypassed by the permanent incisors which are permitted to
erupt into their normal position in the arch.

HYPERCEMENTOSIS - excessive formation of cementum around/on the root surface after tooth
eruption (often confined to the apical half of the root, but may involve the entire root). Caused by
trauma, metabolic dysfunction, chronic periapical inflammation, or when a tooth has lost its
antagonist. It is not associated with anyone particular disease, and may be regarded as a dental
anomaly. Hypercementosis is also seen in ACROMEGALY.

• Mainly affects VITAL teeth. Premolars are most often involved, then first &second molars.

• Produces no significant clinical signs or symptoms, but is seen radiographically as a BULBOUS

ENLARGEMENT with a surrounding continuous/unbroken periodontal membrane space and normal
lamina dura.

• There is a form of hypercementosis that is a common feature in Paget's Disease involving the jaws.
Radiographically, there is complete absence of the periodontal membrane space & lamina dura that
surrounds the hyperplastic cementum.

ENAMEl HYPOPLASIA - an enamel developmental defect resulting from INCOMPLETE FORMATION

of the enamel matrix. The enamel is hard in context, but thin &deficient in amount, resulting in
incomplete formation of the enamel matrix with a deficiency in the cementing substance. EH
affects the deciduous (primary) and permanent teeth, and is usually caused by illness or injury during
tooth formation , or due a genetic disorder (genetic forms of EH are considered types of
amelogenesis imperfecta). If only 1 permanent tooth is affected, it is usually caused by physical
damage to the replaced primary tooth.

• Clinical Features: lack of contact between teeth, rapid breakdown of occlusal surfaces, yellowish-
brown stain that appears due to exposed dentin.

ENAMEl HYPOCALCIFICATION - a hereditary dental defect where the enamel is SOFT &
UNDERCALCIFIED, yet normal in quantity due to defective maturation of ameloblasts (a defect in
the mineralization of the formed matrix). Teeth are chalky, surfaces wear down rapidly, and a
yellowish-brown stain appears as underlying dentin is exposed. Affects deciduous &permanent teeth.

AMElOGENESIS IMPERFECTA - an inherited hereditary ECTODERMAL condition/defect

transmitted as a dominant trait that affects both the deciduous & permanent dentition, causing
enamel to be soft, thin, and yellow due to exposed dentin through the thin enamel layer. Teeth are
easily damaged and susceptible to decay. Crowns mayor may not show discoloration. If discoloration
is present, it varies depending on the type of disorder, ranging from yellow to dark brown.

208
• Contact points between teeth are often open, and occlusal surfaces/incisal edges are often
severely abraded.

• Radiographic findings are often distinctive & pathognomonic. When enamel is totally absent, the
radiographic appearance makes the diagnosis obvious. When some enamel is present, thin radiopaque
coverings on the proximal surfaces are visible. When the anatomic crown forms are normal or near
normal, the softness of the defective enamel may not be easily distinguished from dentin.

• In all cases, dentin, pulp, & cementum are NOT affected by AI (unlike dentinogenesis imperfecta).
Exception : AI will only show pulp obliteration if there is advanced abrasion with secondary
dentin formation .

3 types of Amelogenesis Imperfecta where dentin, pulp, &cementum are unaffected by the
AI process:
1. (Type 1) Hypoplastic AI: enamel has not formed to full normal thickness, or may be completely
absent on newly erupted developing teeth due to defective FORMATION of the enamel matrix.

2. (Type 2) Hypomaturation AI: the enamel can be pierced by an explorer tip untler firm pressure
and chipped away from the normal-appearing dentin. Characterized by IMMATURE CRYSTALLITES.

3. (Type 3) Hypocalcified AI: Quantity of enamel is normal, but so soft that it can be removed
during a prophylaxis due to the defective MINERALIZATION of the enamel matrix.

DETINOGENESIS IMPERFECTA (HEREDITARY OPALESCENT DENTIN) - RARE disorder

found in only 1:7,000 children. An inherited/hereditary MESODERMAL defecUdisorder of dentin that
only affects deciduous &permanent teeth.

• Clinical Features: teeth have an amber, gray, or purple opalescence/translucence or discoloration,

pulp chambers may be completely obliterated due to continued deposition of dentin, crowns are
short &bulbous, with narrow roots. Enamel can chip away within 2-4yrs after eruption, exposing
the dentin which is soft and wears away rapidly. Enamel is structurally and chemically normal.

• Clinically, 01 is usually easily detected and identified, as teeth exhibit a translucent or opalescent
appearance. Abnormal constriction at the enamel-cementum junction is another clinical feature
detected by exploration.

• Sometimes linked to Osteogenesis Imperfecta, as the presence of blue sclera or bone fracture
history are signs of osteogenesis imperfecta.

3 Types of Dentinogenesis Imperfecta:

1. Type 1: dentin abnormality occurs in patients with Osteogenesis Imperfecta, characterized by

blue sclera or history of bone fractures.

2. Type 2: the most common, only dentin abnormality exists, with no bone involvement.

3. Type 3 (Brandywine Type): like Type 2, only the dentin abnormally exists. However, there are
clinical & radiographic variations that include multiple pulp exposures in the deciduous
(primary) dentition.

209
 DENTIN DYSPLASIA (ROOTlESS TEETH) - a hereditary disease transmitted as an autosomal
dominant trait. Clinical features include normal enamel, atypical dentin, pulpal obliteration, defective
root formation, tendency toward multiple periapical radiolucencies and early exfoliation of teeth . Not
associated with any systemic C.T. disorder. There are 2 types:

1. Type I (Radicular)-the more common type involving both dentitions. Normal morphology and
color (deciduous & permanent teeth). Mobile teeth , premature exfoliation, short roots (rootless
teeth), obliterated pulp chambers (deciduous), crescent-shaped pulpal remnant (permanent),
periapical radiolucencies, coronal dentin is normal, but root dentin is disoriented. It is pulpal
obliteration by excess dentin "chevron" shaped pulp chambers.

2. Type II (Coronal}-involves both dentitions (but coronal dentin is normal). Deciduous teeth exhibit
bluish-gray opalescent appearance, obliterated pulp chambers, amorphous & atubular dentin in
the radicular portion of the teeth. Permanent teeth exhibit a normal clinical appearance, thistle-
tube pulp chambers & stones, and true denticles. Pulpal obliteration of primary teeth, and pulp
stones in permanent teeth.

ANODONTIA - a developmental abnormality characterized by TOTAL ABSCENSE of teeth.

There are 2 forms:

1. Complete/True Anodontia-a rare condition where ALL TEETH are missing. It may involve the
primary & permanent dentitions, and is usually associated with hereditary ectodermal dysplasia.

2. Partial Anodontia (Congenitally Missing Teeth)-a common condition usually affecting maxillary
&mandibular Jed molars (affects maxillary 3rd more), maxillary laterals, &mandibular 2nd
premolars. General Rule: if only 1 or a few teeth are missing, the absent tooth is the most
distal tooth of any given type (if a molar, then the 3rd molar is missing; if a premolar, then
the 2nd premolar).

OLIGODONTIA - congenital absence of MANY (but not all) teeth.

HYPODONTIA - absence of only a FEW teeth.

WHITE LESIONS
ORAL CANDIDIASIS ("THRUSH" OR "MONILIASIS") - a FUNGAL infection of the oral cavity
or vagina caused by a Candida species (most often Candida albicans) that causes an inflammatory,
pruritic infection with a thick, white discharge. Appears as a diffuse, curly or velvety white mucosal
plaques on the cheeks, palate, and tongue that can be wiped off, leaving a red, raw, or bleeding
surface. The most common symptoms of oral candidiasis are discomfort and burning of the mouth &
throat, and altered sense of taste.

• Candida is a yeast-like fungi that is a normal inhabitant of the oral cavity & vaginal tract, but is
normally held in check by the indigenous bacteria of these areas. Factors that stimulate Candida
growth are extended use of antibiotics (antibiotics prescribed for a dental infection), steroids,
diabetes, pregnancy, or vitamin deficiency (iron, folate, B12, zinc).

• Very common in patients receiving long-term antibiotic therapy or chemotherapy, and

immunosuppressed patients (AIDS).

• Treatment: topical with LOZENGES (trouches) & mouth rinses (Nystatin is most widely used) .

ACUTE PSEUDOMEMBRANOUS CANDIDIASIS - the most common form of oral candidiasis,

usually found on the buccal mucosa, tongue, and soft palate. Oral cytology smears are useful to
diagnose acute pseudomembranous candida by revealing budding organisms with branching
pseudohyphae).

210
ANGULAR CHEILITIS (PERLECHE) - refers to any inflammatory lesion at the level of the labial
commisure (corners of mouth) due to unknown cause. It is generally associated with the loss of
vertical dimension generally observed in elderly patients. Mouth corners become painful, irritated,
red, cracked, and scaly. Candida albicans fungus (Thrush) may grow in the corners of the mouth,
keeping them sore.

• Predisposing Factors: intra-oral Candida albicans infection, loss of inter-maxillary distance

(decreased vertical dimension), trauma to the labial commissure induced by prolonged dental
treatment, & vitamin deficiencies (especially riboflavin or thiamine). Also linked to Candida albicans.

• Treatment: NYSTATIN will eliminate the fungal infection.

ACTINIC CHEILITIS (SOLAR CHEILITIS) - a premalignant condition caused by chronic and

excessive exposure to the UV radiation in sulight. It is the counterpart of actinic keratosis of the
skin, and can also develop into squamous cell carcinoma . There is thickening, whitish discoloration of
the lip at the border of the lip and skin, and loss of the usually sharp demarcation between the red of
the lip and normal skin (vermillion border). Since Actinic Cheilitis is premalignant and may lead to
squamous cell carcinoma, it must be treated accordingly.

WHITE SPONGE NEVUS (FAMILIAL WHITE FOLDED DYSPLASIA) - a BUCCAL MUCOSAL

ABNORMALITY often mistaken for leukoplakia, that follows a hereditary pattern as an autosomal
dominant trait/condition with no sex preference. It is congenital in many instances, but may occur in
childhood or adolescence. The most common location is the buccal mucosa (bilaterally), followed by
the labial mucosa, alveolar ridge, and floor of mouth. The gingival margin &dorsal tongue are almost
never affected.

• Clinical Features: soft, thickened, and corrugated folds of mucous membrane. Mucosa appears
thickened and folded with a soft or spongy texture, and peculiar pearly white or opalescent hue.

• THERE IS NO TREATMENT, but because the condition is benign, the prognosis is excellent. with no
serious clinical complications.

LEUKOPLAKIA - a PREMALIGNANT LESION presenting clinically as a WHITE PATCH or plaque on the

oral mucosa that will not rub off and cannot be assigned as any specific disease. Possible etiologic
factors are tobacco (PIPE SMOKING), alcohol, oral sepsis, and chronic irritation. It is most often due
to tobacco use and chronic irritation. May be present for many months in a heavy pipe smoker. Pipe-
smoking is the most important predisposing etiologic factors for the development of leukoplakia . More
common in elderly men, and does not disappear when stretched. Mouth floor, tongue, and lower lip
are the regions at greatest risk for carcinoma occurring in leukoplakia.

• Leukoplakia is a slow developing change in a mucous membrane characterized by thickened, white,

firmly attached patches that are slightly raised & sharply circumscribed. It is most often caused by
tobacco irritation (pipe smoking), and more common in older men. Lesions on the mouth floor and
base of the tongue are the most aggressive. Most display no dysplasia, but can be premalignant.

• Treatment: BIOPSY. Due to the chance of malignant transformation, ALLlEUKOPLAKIAS MUST BE

BIOPSIED &COMPLETELY EXCISED (if untreated, some of the lesions progress to carcinoma).
Although less common than leukoplakias, erythroplakias have a much greater malignant potential.
Incisional Biopsy-indicated for a 3cm area of leukoplakia of the soft palate. Not indicated for
papillary fibroma, exostosis, Fordyce's granules, or Hemangioma as these are benign.

• Any white or red lesion that does not resolve itself in 2 weeks must be re-evaluated and considered
for BIOPSY to obtain a definitive diagnosis.

• Carcinoma in situ-a term applied to mucosal lesions that resemble leukoplakia in all respects except
that dysplasia is very pronounced and involves almost all epithelial layers. It shows no tendency to
invade or metastasize to other tissues. Exhibits all of the histologic characteristics of malignancy
(pleomorphism, hyperchromatism, abnormal mitoses, anaplasia), but DOES NOT show invasiveness
or extension into adjacent structures.
211
 • Clinical Differential Diagnosis of White Patch: leukoplakia, lupus erythematosus, leukoedema, white
sponge nevus, chemical or thermal burn, candidiasis, lichen planus, & migratory glossitis/stomatitis.

STOMATITIS NICOTINA ("PIPE-SMOKER'S PALATE" OR NICOTINIC STOMATITIS)-

related to pipe smoking, occurs ONLY ON THE PALATE, and mainly affects males. The palate initially
appears red & inflamed, then develops a diffuse, grayish-white, thickened, multinodular popular
appearance with a small red "spot" in the center of each tiny nodule. This "spot" corresponds to the
orifices of palatal salivary gland ducts. Treatment: cessation (stop) smoking. It is usually not a
premalignant lesion.

• Etiology is tobacco (smoking) common in heavy smokers. Found ONLY in the palate (palate is
leathery white and full of keratin (hyperkeratosis with RED DOTS (inflamed minor salivary glands).
The only lesion produced by tobacco that is not cancerous. Usually a white, generalized area
with red dots in the hard palate that is PAINLESS &non-indurated. No treatment except TO STOP
SMOKING and/or give a follow-up appointment. White areas with multiple red dots (inflamed salivary
glands in the palate).

LEUKOEDEMA - a condition that mimics leukoplakia as it appears to be a white patch, but is simply
a variant of normal mucosa. Its appearance varies from a filmy opalescence of the mucosa in the early
stages, to a more definite grayish-white cast with a coarsely wrinkled surface in later stages.
Leukoedema lesion usually occurs bilaterally and are most noticeable along the occlusal line in the
bicuspid and molar region. Diagnostically, one can stretch the tissue and the white disappears
(Important: Leukoplakia does not disappear when stretched). No treatment is necessary, just diagnosis.

• Histologically: epithelium is parakeratotic & acanthotic, with marked intracellular edema of spinous
cells. Leukoedem's white appearance is caused by water within the spinous cells, causing light to
reflect back as whitish.

• Differential Diagnosis: leukoplakia, white sponge nevus, & hereditary benign

intraepithelial dyskeratosis.

LICHEN PLANUS - oral lesion on the BUCCAL MUCOSA appearing as white or grayish-white striae
arranged in a Lace-like pattern (Wickman's Striae) that are often bilaterally & symmetrically
distributed, and usually asymptomatic, but may sometimes cause a burning sensation. Lichen Planus
is a fairly common inflammatory disease, whose cause is unknown, but may be autoimmune. It
usually affects the skin, mouth, or both. Lichen planus of the mouth most commonly affects the
buccal mucous membrane, but may be on the tongue, lips, hard palate, & gingiva.

• Microscopic Features: hyperparakeratosis with thickening of the granular cell layer, development
of a "saw-tooth" appearance of rete pegs, degeneration of the basal cell layer, and infiltration
of inflammatory cells into the sub-epithelial layer of C.T.

• Affects women slightly more than men, and occurs most often in middle-aged adults.

• Treatment: intra-oral lesions respond to topical steroid therapy

• Two forms of lichen Planus (in addition to the usual form):

1. Bullous lichen planus-fluid-filled vesicles project from the surface.

2. Erosive lichen planus-intensely red or raw-appearing lesions, and when they involve
the gingiva, these lesions resemble desquamative gingivitis.

212
HAIRY TONGUE - a condition characterized by HYPERTROPHY of the FILIFORM PAPILLAE. Abenign NOTES
condition of the tongue dorsum which appears furry due to elongated papillae. Color varies from
yellowish-white to brown or black.

4 Types of Papillae on the Tongue: Taste buds are present on only fungiform, circumvallate,
&foliate papillae.

1. Filiform papillae-the most numerous. Small cones arranged in "v" -shaped rows paralleling the
sulcus terminalis, characterized by the absence of taste buds and increased keratinization.

2. Fungiform papillae-scattered among the filiform papaillae. They are flattened, mushroom-
shaped, and found mainly at the tip and lateral margins. Contains taste buds.

3. Circumvallate papillae-the largest but least numerous papillae. Circular-shaped arranged in

an inverted "v" -shaped row toward the back of the tongue. Associated with ducts of Von Ebner's
glands. Contains taste buds.

4. Foliate papillae-found on the lateral margins as 3-4 vertical folds. Contains taste buds.

HAIRY TONGUE - is not Hairy Leukoplakia, but simply discoloration of the DORSUM tongue
surface, elongation &hyperkeratosis of FILIFORM PAPILLAE ON DORSUM SURFACE OF THE TONGUE.

• Can be a white lesion completely covering the tongue dorsum. May be green, BROWN, or black
because filiform papillae are stained/discolored with DEBRIS the patient eats or smokes. Ex: dorsal
surface of tongue of a smoker exhibits elongated, brownish filiform papillae.

• Can present as a bright green, flat area on the tongue dorsum, with very poor dental status & oral
hygiene. The green area is probably DEBRIS.

• Etiology: overgrowth of fungal microorganisms due to smoking or poor oral hygiene (brush tongue).

BENIGN MIGRATORY GLOSSITIS ("GEOGRAPHIC TONGUE OR ERYTHEMA MIGRANS") -

a HARMLESS very common condition where there is desquamation of the filiform papillae.
Characterized by having 1 or more irregular-shaped patches on the tongue. The center area is redder
then the rest of the tongue, and edges of the patch are whitish color. These patches appear and
remain for a short time, heal, then reappear at another site. The patches usually do not respond to
treatment, but disappear spontaneously. Patients may complain of a slight burning of the tongue.
Geographic Tongue often occurs with Fissured Tongue.

FISSURED TONGUE ("SCROTAL TONGUE") - characterized by a deep, usually asymptomatic

(maybe painful if infected with Candida Albicans) MEDIAN FISSURE with laterally radiating grooves
that vary in number, but are usually symmetrically arranged across the DORSUM OF THE TONGUE.
Rare in children, but increases in incidence with age.
Fissured tongue is found in Melkersson-Rosenthal Syndrome (along with Cheilitis Granulomatosum &
Facial Nerve Paralysis) .

FORDYCE'S GRANULES (DISEASE) - ectopic sebaceous glands in the oral mucosa, present in >
75% of adults. Usually appear as yellow or yellow-white submucosal clusters that are normal.

213
 N BLOOD DISEASES
PURPURA - a condition characterized by HEMORRHAGES in the skin &mucous membranes that
cause the appearance of purplish spots or patches. Tooth extractions are contraindicated due to
potential excessive bleeding. Two types:

1. Thrombocytopenic Purpura (Werlhof's Disease)-a bleeding disorder characterized by a

deficiency in the number of platelets, resulting in multiple bruises, petechiae, & hemorrhage
into the tissues. May be caused by heparin (warfarin) therapy. Oral manifestations are
severe/profuse gingival hemorrhage, & palatal petechiae.

2. Thrombotic Thrombocytopenic Purpura (TTP)-a severe and frequently fatal form characterized
by a low platelet count in the blood and thrombosis in the terminal arterioles and capillaries
of many organs.

AGRANULOCYTOSIS - an abnormal condition of blood due to a severe reduction in the number of

granulocytes (neutrophils). It is an acute toxic effecUcondition characterized by pronounced
LEUKOPENIA with a severe reduction in the number of polymorphonuclear leukocytes (PMNs). It is
a toxic effect of certain antithyroid drugs (propylthiouracil, methimazole, carbimazole) .
Agranulocytosis is most commonly caused by ingestion of a drug. The disease can occur at any age,
c::> but is more common in female adults.
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::; • WBe count is < 2,000 with almost complete absence of PMN neutrophils (polymorphonuclear
::c
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c::> leukocytes). Normal WBC count is 4,000-10,000 and neutrophils are usually 50-70% .
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• Agranulocytosis begins with a high fever, chills, and sore throat. The patient suffers from malaise,
weakness, and prostration. Skin appears pale and anemic. The most characteristic feature is the
presence of infection, especially in the oral cavity. Signs and symptoms develop very rapidly (within
a few days), and death may occur soon after.

• Oral lesions (necrotizing ulcerations) are an important phase of the clinical aspects, appearing as
necrotizing ulcerations of the oral mucosa (especially gingiva & hard palate). These lesions are
ragged necrotic ulcers covered by a gray membrane. One important aspect is that there is little or
no apparent inflammatory cell infiltration around the lesions. Histologically, the ulcerated lesions
do not exhibit polymorphonuclear reaction due to the bacteria in the tissues.

• Treatment: find out the causative drug and eliminate it. Administer antibiotics to control the infection
is critical.

• Cyclic Neutropenia-an unusual form of agranulocytosis where patients typically exhibit severe
gingivitis. Severe ulcerations usually seen in agranulocytosis usually do not occur.

SICKLE-CELL ANEMIA (SICKLE-CELL DISEASE) - a chronic, usually fatal inherited form of

anemia marked by crescent-shaped red blood cells, characterized by fever, leg ulcers, jaundice, and
episodic pain in the joints due to the production of abnormal hemoglobin (Hemoglobin S) due to a
genetic defect.

• Found primarily in African-Americans, is more common in females, and usually clinically manifests
before age 30yrs.

• Typical signs of anemia are present (patient is weak, short of breath, easily fatigued, and muscle and
joint pain are common) .

• Dental radiographs are often of diagnostic value as marrow spaces are markedly enlarged
because of loss of many trabeculae. The trabeculae present, are often abnormally prominent.
Occasionally, osteosclerotic areas are noted in the midst of large radiolucent marrow spaces.
However, the lamina dura &teeth are unaffected.

214
LEUKEMIA - is a cancerous condition in which an uncontrolled proliferation of leukocytes leads
to a diffuse and almost total replacement of the red bone marrow with leukemic cells. Leukemia is
classified by the dominant cell type and by duration from onset to death. It can modify the
inflammatory reaction. Its etiology is UNKNOWN, but these agents are believed to be closely
associated with its development:
1. ionizing radiation: increased incidence of leukemia among atomic bomb survivors &
radiologists, usually myelogenous.

2. viruses: shown to cause leukemia in fowl and rodents. Herpes-like viral particles have been
cultured from patients with various types of leukemia and leukemic patients have high
antibody titer to the Epstein-Barr Virus.

3. genetic mutations: Philadelphia chromosome (translocation of chromosome material from

chromosome 22 9) is present in 90% of patients with Chronic Myelogenous leukemia. Also
higher incidence of acute leukemia in patients with Down Syndrome (Mongolism) in which
there is Trisomy 21.

4. Other: chronic exposure to benzol, aniline dyes, and related chemicals has been associated
with leukemia.

Classifications of leukemia: All types of leukemia occur in an acute or chronic form

(but 50% are acute).
1. Myelogenous leukemia-involves granulocytes & megakaryocytes.
• Chronic Myelogenous leukemia is 4 years with death due to hemorrhage or infection.
Philadelphia Chromosome and low levels of leukocyte alkaline phosphatase are common
findings. Massive splenomegaly is characteristic.

2. lymphocytic leukemia-involves Iym phocytes.

• Chronic lymphocytic leukemia runs a variable course (older patients may survive years
even without treatment). lymph node enlargement is the main pathologic finding. May
be complicated by autoimmune hemolytic anemia.

3. Monocytic leukemia-involves monocytes. Oral lesions are most likely observed in MONOCYTIC
lEUKEMIA. Oral lesions may be the initial manifestations of the disease, and include gingivitis,
gingival hemorrhage, generalized gingival hyperplasia, petechiae, ecchymoses, and ulcerations.
Chronic Monocytic leukemia is VERY RARE.

Chronic leukemia (Clinical Features):

• Insidious onset (slow) with weakness and weight loss. Chronic leukemia may be detected during
examination for another condition (i.e. anemia, unexplained hemorrhages, or recurrent intractable
infections).

• Organ involvement similar to acute leukemia: skin is often involved, and may manifest as petechiae
or ecchymoses, recurrent hemorrhages and bacterial infections are common (anemia).

• lab Findings: leukocytosis> 100,000/mm 3 with mature forms (granulocytes & lymphocytes)
predominating.

CHRONIC MYELOGENOUS LEUKEMIA (CMl) - is one of a group of diseases called

myeloproliferative disorders. Other diseases in this class are Polycythemia Vera, Myelofibrosis, &
Essential Thrombocythemia. CML is characterized by uncontrolled proliferation of immature
granulocytes (but is the least malignant leukemia). CML accounts for 20% of all adults leukemias
(typically affects middle-aged individuals). Although uncommon, CML may occur in younger individuals.

• Clinical Signs: spongy bleeding gums, fatigue, fever, weight loss, moderate splenomegaly, joint/bone
pain, and repeated infections.

215
 • leukemic cells in 95% of CMl patients have a Philadelphia Chromosome which is the result of a
reciprocal translocation between chromosomes 9 & 22 which result in a shortened chromosome 22.

• Mean survival time is 4 years with death due to hemorrhage or infection.

POLYCYTHEMIA VERA (PRIMARY ERYTHEMIA) - a chronic myeloproliferative

disorder/condition of TOO MANY ERYTHROCYTES (RBC) produced in the circulation, making blood too
thick to pass easily through small blood vessels in the body. This leads to clot formation and blockage
of the vessels which can lead to a stroke (cerebrovascular accident). Occurs when excess erythrocytes
are produced due to tumorous abnormalities. This occurs in the tissues that produce blood cells.
Usually accompanied by leukocytosis. Splenomegaly, due to vascular congestion, occurs in 75% of
patients. Usually occurs within in ages 20-80yrs., with 60yrs. being the mean age of onset.

• Clinical Features: headache, weakness, weight loss, pruritis, hemorrhage and thrombosis may occur
at any time.

• Oral Manifestations: oral mucous membranes (especially gingiva & tongue) appear deep purplish-
red, gingiva is swollen and bleeds easily, and submucosal petechiae (purplish spots), ecchymoses
(petechiae, but bigger), and hematomas are common .

• Secondary Polycythemia-an increase in the total number of erythrocytes due to another condition
(i.e. chronic tissue hypoxia of advanced pulmonary disease, high altitude (Osker's Disease), or
secretion of erythropoietins by certain tumors.

ACUTE MYElOID/MYElOGENOUS LEUKEMIA (AML) - a malignant disease of bone marrow

where hematopoietic precursors are arrested in an early stage of development (has an abrupt onset).
AML is distinguished from other related blood disorders by the presence of > 30% myeloblasts in the
blood and/or bone marrow. These blasts (myeloblasts) contain AUER RODS in their cytoplasm. It is
the MOST MALIGNANT lEUKEMIA.

ACUTE LEUKEMIA - has an abrupt onset of a few months (not insidious) with fever, weakness,
malaise, severe anemia, and generalized Iympadenopathy. Untreated patients dies within 6 months
(usually due to brain hemorrhage or superimposed bacterial infection). With intensive
chemotherapy, radiation, and marrow transplants, remissions lasting up to 5 years may be obtained.

• Clinical Features: severe anemia, hemorrhages, and slight enlargement of the lymph nodes or
spleen. Primary organs involved are bone marrow, spleen (splenomegaly), & liver (hepatomegaly).
Petechiae & ecchymoses in skin and mucous membranes, hemorrhage from various sites, and
bacterial infections are common.

• lab Findings: leukocytosis 30,000-100,000/mm 3 with immature forms (myeloblasts & Iymphoblasts)
predominating; anemia and thrombocytopenia, prolonged bleeding and coagulation times, tourniquet
test usually positive.

• Acute myelogenous leukemia-is more common in adults.

• Acute lymphocytic (lymphoblastic) leukemia-largely confined to children (it is the most common
leukemia in children. Lymph node enlargement is common. In 75% of cases, the lymphocytes are
neither B nor Tcells, but are called "null" cells. Bone and joint pain are common in children.

ALEUKEMIC LEUKEMIA - a form of leukemia where there are leukemic cells present in bone
marrow, but the circulating WBC are neither immature nor increased in number.

LEUKEMOID REACTION - a marked increase in the number of circulating granulocytes

(neutrophils). This condition is seen in a variety of disorders including chronic infections and
neoplasms.

216
STEM CElL LEUKEMIA - a form of leukemia where abnormal cells are thought to be the NOTES
precursors of Iymphoblasts, myeloblasts, or monoblasts. The cells are too immature to classify.

SUBLEUKEMIC LEUKEMIA - a form of leukemia where leukemic cells appear in the blood, but
there is no significant increase in the number of circulating WBC.

PLUMMER-VINSON SYNDROME - a rare disorder associated with severe and chronic iron-
deficiency anemia that occurs mainly in women ages 30-40yrs. Due to the predisposition to develop
carcinoma of the oral mucous membranes, it is essential to diagnose this early so treatment can be
given ASAP (administer iron, vitamin B complex, and a high protein diet).

• Systemic Symptoms: weakness, pallor, difficulty swallowing (dysphagia) due to esophageal stricture
or web, and difficulty breathing (dyspnea).

• Oral Symptoms: angular stomatitis, smooth, red, painful tongue with atrophy of the papillae.

APLASTIC ANEMIA - a form of anemia where the capacity of the bone marrow to produce RBCs is
defective. It is the most serious and life-threatening blood dyscrasia associated with drug toxicity.

1. Primary Anemia-unknown cause, affects young adults and is usually fatal.

• Systemic symptoms: pallor, weakness, malaise, dyspnea (difficulty breathing),
headache, and vertigo.

• Oral symptoms: spontaneous bleeding, bruising (petechiae), and gingival infections.

2. Secondary Anemia-caused by exposure to toxic agents (i.e. radiation, chemicals, or drugs like
Chloramphenicol). Occurs at any age, with the same symptoms as primary anemia. Prognosis is
good after the cause is removed .

PERNICIOUS ANEMIA - a disease caused by an inability to absorb adequate amounts of vitamin

B12 from the digestive tract. It is a relatively common, chronic, progressive megaloblastic anemia,
caused by the lack of secretion of intrinsic factor in normal gastric juice (intrinsic factor is
necessary for adequate vitamin B12 absorption, which is required for maturation of erythrocytes).
As a result fewer than normal RBC are produced.

• Characterized by a triad of symptoms: generalized weakness, sore painful tongue (atrophic

glossitis), and tingling of the extremities.

THALASSEMIA MAJOR & MINOR - are hemolytic anemias caused by a genetic defect,
characterized by a low level of erythrocytes & abnormal hemoglobin. Oral Manifestations: oral
mucosa may exhibit anemic pallor, flaring of maxillary anterior teeth with malocclusion.

ERYTHROBLASTOSIS FETALIS (HEMOLYTIC DISEASE OF NEWBORN) - a severe hemolytic

disease of the fetus or newborn caused by the production of maternal antibodies for fetal RBC. It
usually involves Rh factor incompatibility between the mother and fetus. Characterized by excessive
destruction of erythrocytes due to an antigen-antibody reaction in the infant's bloodstream
resulting from the placental transmission of maternally formed antibodies against the
incompatible antigens of the fetal blood. In Rh factor incompatibility, the hemolytic reaction only
occurs when the mother is Rh (-) and infant is Rh (+).
• Oral Manifestations: teeth appear to have a green, blue, or brown hue due to the deposition of blood
pigment in enamel and dentin. Enamel hypoplasia may occur, affecting the incisal edges of anterior
teeth and middle portion of the deciduous canine and first molar crown.

ERYTHROCYTE SEDIMENTATION RATE (ESR) - a non-specific test that only monitors the
PROGRESSION OF DISEASE. ESR is the rate at which RBC settle out in a tube of unclotted blood,
expressed in mm/hour. Blood is collected in an anticoagulant and allowed to sediment in a calibrated
glass column. At the end of 1 hour, the lab technician measures the distance the erythrocytes have
fallen in the tube.

217
 • Elevated sedimentation rates are not specific for any disorder, but indicates the presence of
inflammation. Inflammation causing an alteration of the blood proteins that makes RBC aggregate,
becoming heavier than normal. The speed that the RBC fall to the bottom of the tube corresponds to
the degree of inflammation.

• ESR rises during inflammation, tissue degeneration, suppuration, and necrosis. Certain non-
inflammatory conditions (Le. pregnancy) are also categorized by high sedimentation rates.

WISKOTT-ALDRICH SYNDROME - affects only boys and causes eczema, low platelet count, and a
combined deficiency of Band T lymphocytes that lead to repeated infections. Children who survive past
age 10 usually develop cancers (lymphoma and leukemia).

NEUROLOGIC &MUSCLE DISORDERS

Trigeminal Neuralgia (Tic Douloureux) - an excruciating painful illness where the person feels
sudden stab-like pains in the face that usually last only moments, but are among the most severe
pain humans can feel. This pain is provoked by touching a "trigger zone" near the nose or mouth,
caused by degeneration of the trigeminal nerve or by applying pressure to the nerve. Can affect any
of the trigeminal's 3 branches (VI, V2, or V3)' The momentary bursts of pain recur in clusters, lasting
many seconds. Paroxysmal episodes of the pains may last hours.

• Treatment: drug of choice is Carbamazepine (Tegretol) which is an analgesic and

anticonvulsant that usually relieves the pain within 48hrs. Tegretol is also prescribed to treat
certain seizure disorders.

MULTIPLE SCLEROSIS - a chronic, often disabling disease that randomly attacks the CNS
(brain and spinal cord) due to an autoimmune response where the immune system attacks a person's
own tissues. Women are affected 2x more than men, with the onset of symptoms occurring usually
between ages 20-40yrs (tingling, numbness, paralysis, and blindness). Patients with MS may have
facial and jaw weakness, and Bell's Palsy & Trigeminal Neuralgia may develop more frequently in
MS patients.

GLOSSOPHARYNGEAL NEURALGIA - pain similar to trigeminal neuralgia that arises from the
glossopharyngeal nerve (CN 9). It is not as common as trigeminal neuralgia, but the pain may be as
severe. Occurs in both sexes (middle-aged or elderly). It is a sharp, sudden, shooting almost always
unilateral pain in the ear, pharynx, nasopharynx, tonsils, or posterior tongue.

POSTHERPETIC NEURALGIA - a persistent burning, aching, itching, and hyperesthesia along

distribution of a cutaneous nerve after an attack of HERPES ZOSTER. May last a week or many
months. Involves facial nerve (CN 7) & geniculate ganglion which produces Ramsey Hunt Syndrome
(facial paralysis & otalgia/earache).

MYASTHENIA GRAVIS - a chronic condition of EXTREME MUSCLE WEAKNESS due to an

autoimmune disorder in which the body creates antibodies against its own nicotinic ACh
(acetylcholine) receptors in the neuromuscular junctions. The muscles are quickly fatigued with
repetitive use. It is typical for the patient to have a flattened smile and droopy eyes with slow
papillary light responses. Xerostomia and rampant caries may be present because thee acetylcholine
needed for proper transmission of nerve impulses is destroyed, so the salivary glands do not receive
adequate stimulation.

MYASTHENIA GRAVIS - immune system produces autoantibodies that attack Acetylcholine

receptors that lie on the muscle side of the neuromuscular junction causing dysfunction of the
myoneural junction. This decreases the responsiveness of the muscle fibers to acetylcholine released from
motor neuron endings. Difficulty speaking and swallowing, and weakness of the arms and legs are
common. About 10% of people develop a life-threatening weakness of the breathing muscles (a condition
called myasthenic crisis).

218
Myasthenia Gravis Characteristics:
• Occurs more frequently in women and begins between 20-40 years of age.
• Its an autoimmune disease in which the neuromuscular junction function abnormally, resulting in
episodes of muscle weakness.
• most common symptoms are weakness of the eyes (drooping eyelids), double vision (caused by weak
eye muscles), and excessive, specific muscle fatigue after exercise.
• Affects muscles of the face, neck, arms, and legs.
• Drugs that increase the level of acetylcholine (e.g. pyridostigmine or neostigmine) may be given to
for treatment.

EATON-LAMBERT SYNDROME - similar to myasthenia gravis in that it is also an autoimmune

disease that causes weakness. However, Eaton-Lambert syndrome is caused by the inadequate release
of acetylcholine rather than by abnormal antibodies that attack acetylcholine receptors.

MUSCLE SPASM - is the PRIME FACTOR that initiates Myofascial Pain-Dysfunction Syndrome
(MPD). Muscle spasm arises either due to muscular overextension, overcontraction, or fatigue (the
most common cause). MPD is seen mainly in women between ages 20-40yrs. The pain is usually
unilateral, described as a dull ache in the ear or preauricular area that may radiate to the angle of the
mandible, temporal area, or lateral cervical area . The muscle most likely to exhibit tenderness is the
LATERAL PTERYGOID.

• 4 cardinal signs & symptoms of MPD: pain, muscle tenderness, clicking/popping noise in the TMJ, c:::>
:::c
and limitation in jaw motion (especially in the morning). There are no radiographic findings :>
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associated with MPD. =:;
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• Treatment: most cases are self-limiting. Soft diet, limited talking, no gum chewing, moist heat, .",
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NSAlDs & Diazepam (Valium) help relieve the symptoms.

FREY'S SYNDROME (AURICULOTEMPORAL SYNDROME) - an unusual/uncommon

phenomenon that arises due to damage of the auriculotemporal nerve and subsequent
reinnervation of the sweat glands by parasympathetic salivary fibers. Frey's syndrome can occur after
surgery (i.e. removal of a parotid tumor, ramus of the mandible, or infection of the parotid that has
damaged the auriculotemporal nerve (branch of V3). Gustatory sweating is the chief complaint.
Patient exhibits flushing and sweating of the involved side of the face during eating.

BELL'S PALSY - a form of facial paralysis from damage to the FACIAL NERVE. It can occur at any
age, but disproportionately attacks pregnant women, diabetics, and people with influenza, cold, or
other upper respiratory infection.

• Clinical Signs: unilateral paralysis of all facial muscles with loss of eyebrow &forehead wrinkles,
drooping of eyebrows, flattening of the nasiolabial furrow, sagging of the corner of the mouth,
and inability to frown or raise the eyebrows. The upper and lower lips may also be paralyzed on the
affected side. Drooping mouth on one side with a watering eye, loss of taste sensation on the anterior
portion of the tongue may occur.

• After its sudden onset, the paralysis begins to subside in 2-3 weeks, and gradual, complete recovery
occurs in > 85% of patients.

• Important: While giving an inferior alveolar block, if you inject anesthetic solution into the capsule
of the parotid gland, you may cause a Bell's Palsy-like feeling by anesthetizing the facial nerve.

219
 NOTES NON-ODONTOGENIC CYSTS
CONGENITAL CYSTS:
1. Branchiogenic Cyst-arises from the persistence of the second branchial arch cleft. This cyst is
located along the anterior border of the sternocleidomstoid muscle at any level in the neck.
This cyst is lined with ciliated and striated squamous epithelium, and contains a milky or mucoid
fluid . Treatment: complete surgical exicision.

2. Dermoid Cyst-is relatively uncommon in the oral cavity. This cyst often contains hair, sebaceous
and sweat glands, and tooth structures. The most common site is the floor of the mouth.
Treatment: surgical removal of the entire tumor.

3. Thyroglossal Duct Cyst-may arise from any portion of the thyroglossal duct. Thus, is found in a
midline position and is usually dark colored. It may be vascular as to resemble a hemangioma .
Hemorrhage into the mouth is a common and important symptom caused by rupturing of the
overlying veins. Treatment: complete excision of the tract to the base of the tongue (often
including part of the hyoid bone) is needed to cure.

DEVELOPMENTAL CYSTS (Fissural Cysts):

1. Nasopalatine Duct Cyst (Incisive Canal Cyst)-a "heart-shaped" radiolucency in the midline of
the hard palate. It is the most common non-odontogenic/developmentallfissural cyst. Usually
asymptomatic (but patient may complain of tender swelling of the palate) or may produce an
elevation in the anterior part of the palate. Teeth are vital. Treatment: surgical
excision/enucleation. Prognosis is excellent. Occurs within bone (intra osseous).

• Radiographic Features: appears as a circular (round) well-demaracated oval or heart-shaped

radiolucency between and above the maxillary central incisors (rarely just lateral to the midline)
on a radiograph clinically seen as a marked swelling in the region of the palatine papilla,
situated distal to the roots of the central incisors. The pulps of the anterior teeth are vital.
The lesion crosses the midline. Do not confuse with an enlarged palatine foramen.

• Of cysts of the jaw, those cysts that arise from epithelial remnants in the incisive canal are the
most common type of maxillary developmental cyst. Histologically, this cyst walls are lined
with vessels, nerves, and mucous glands (remnants of nasopalatine ducts within bone). They
most often remain limited in size and are asymptomatic. Some however, become infected or
have a tendency to grow extensively. When this occurs, surgical intervention is indicated .

• Palatine Papilla Cyst-the soft tissue (and much less common) variant of the Nasopalatine
Canal Cyst.

2. Nasiolabial Cyst (Nasoalveolar Cyst)-a soft tissue of the upper lip (extraosseous cyst)
superficially located in soft tissue of the upper lip.that histologically develops from epithelial
remnants from the inferior and anterior portion of the nasolacrimal duct. Clinical Characteristics:
swelling below or inside the nostril, may present in the canine region. This cyst is NOT visible
radiographically, but may produce "cupping" of underlying bone. NOT WITHIN BONE
(extraosseous) so cannot be seen on a radiograph. Treatment: enucleation (surgical excision).
Excellent prognosis.

• Microscopic Characteristics: fibrous C.T. forms this cyst's wall. The epithelial lining is
pseudostratified columnar epithelium with numerous goblet cells. .

3. Globulomaxillary Cyst-an inverted "pear-shaped" radiolucency in bone between the roots of

the maxillary lateral &canine (often causes the roots of the involved teeth to diverge) .

• Clinical Features: usually asymptomatic, but occasionally produces swelling with or without
pain. All regional teeth are vital. Occurs within bone (intraosseous) .

• Histologic Features: consists of epithelial remnants at the line of fusion between the globular
& maxillary processes.
220
 • Radiographic Features: inverted pear-shaped radiolucency between the maxillary lateral &
canine roots. Teeth are vital, but roots may be divergent. Do not confuse with a lateral
NOTES
Periodontal Cyst.

• Treatment: enucleation with preservation of teeth . Excellent prognosis.

4. Median Palatal Cyst-rare, but may occur anywhere along the median palatal raphe (usually in
the midline of the hard palate, posterior to the premaxilla. (occurs within bone intraosseous).
May produce swelling on the palate. Clinically, this lesion presents as a firm painless swelling.
Some believe this cyst represents a more posterior presentation of a Nasopalatine Duct Cyst,
rather than a separate cystic degeneration of epithelial rests at the line of fusion of the palatine
shelves.

• Histologic Features: epithelial remnants in line of fusion between the palatine processes.
Appears as a soft fluctuant or crepitant swelling in the midline of the hard palate.

• Radiographic Features: well-demarcated radiolucency in the midline of the hard palate.

• Treatment: enucleation with excellent prognosis.

5. Median Alveolar Cyst-rare, but occurs in the bony alveolus (intraosseous) between the
central incisors. Distinguished from a periapical cyst by the fact that the adjacent teeth
are vital. Treatment: enucleation.

NON-ODONTOGENIC TUMORS
FIBROUS DYSPLASIA - a rare, abnormal condition characterized by the fibrous displacement of
the osseous tissues within the affected bones. The specific cause is unknown. 3 Types of Fibrous
Dysplasia:

1. Monostotic Fibrous Dysplasia-the most common form of fibrous dysplasia (80%) that affects
children &young adults (both sexes equally). This form affects one bone (ribs & femur are
common sites). The jaws are also commonly affected (mainly the maxilla, presenting as a painless
swelling/bulge). A panorex reveals a radiopaque mass/lesion with irregular borders (poorly defined
margins) with "ground/frosted glass" appearance. When several adjacent bones are affected,
it is called "Craniofacial Fibrous Dysplasia".

• The differential diagnosis of fibrous dysplasia of the jaws includes Ossifying Fibroma. However,
radiographically, an ossifying fibroma has a well-circumscribed appearance.

• Craniofacial Fibrous Dysplasia ("Monostotic Fibrous Dysplasia of the Jaw")-often causes

expansion and deformity of the jawbone and tooth displacement. There is radiograph ic
characteristic thickening at the skull base. Radiographically, the lesion is usually radiopaque,
not well-circumscribed, with "ground-glass" appearance. Since documentation supports
the possibility of malignant transformation in patients treated by radiation therapy, treatment
usually consists of surgical removal of the lesion when possible. However, since these lesions
are not usually well-circumscribed, surgical recontouring is often performed to remove the
portion of the lesion causing the facial deformity.

2. Polyostotic Fibrous Dysplasia-usually displays a segmental distribution of the involved bones

(multiple bones) . Occurs during childhood (mainly females who reach puberty prematurely).
Affects long bones, face, clavicles, and pelvic bones. Initial signs may be a limp, pain, or
fracture on the affected side.

221
 3. Albright's Syndrome (McCune-Albright Syndrome)-a disease of unknown cause affecting the
bones (bone disease), skin pigmentation (irregular brown spots/skin pigmentation), and causing
premature sexual development (endocrine problems). The extent of these problems varies
depending on the affected individual. Hallmark sign of Albright's Syndrome is FEMALE
PREMATURE PUBERTY (early sexual development in the male is less common than the female).
Affects young people (males & females equally). Albright's is the most severe form of
polyostotic fibrous dysplasia (involves multiple bones) with endocrine involvement.

• Triad of Symptoms: polyostotic fibrous dysplasia, Cafe-au-Iait brown skin spots, &endocrine
abnormalities (most common is precocious sexual development in females). Also frequent
pathologic bone fractures. Malignant transformation potential of polyostotic (mainly) &
monostotic fibrous dysplasias into osteosarcomas is an additional complication.

• Treatment: No specific treatment. Drugs that inhibit estrogen production (Testolactone) have
been used with some success.

GARDNER'S SYNDROME - a polyposis syndrome inherited in a dominant manner (like Familial

Multiple Polyposis, Peutz-Jeghers Syndrome, & Turcot's Syndrome). The most serious complication of
Gardner's Syndrome is the multiple (thousands) of polyps that affect the large intestine, duodenum,
colon, and stomach. The polyps usually appear around age 15yrs. and eventually undergo malignant
transformation. Thus, the inevitable outcome is COLON CANCER.

• Oral Findings: multiple odontomas, multiple impacted &supernumerary teeth (like in Cleidocranial
Dysostosis), and multiple jaw osteomas that give a "cotton-wool" appearance to the jaws by appearing
as dense, well-circumscribed radiopacities. Associated with bony tumors in the jaw and skull.
• When Gardner's syndrome is suspected based on oral findings, the patient is referred to a
GI for consultation.
• Multiple desmoid tumors (fibromatosis), and epidermoid skin cysts may also occur.

CENTRAL GIANT CELL GRANULOMA - a benign process that occurs almost exclusively within
the JAWBONES caused by trauma (fall, blow, or tooth extraction). Occurs predominantly in children
or young adult ages 0-20yrs (more common in females), and either jaw may be involved (but the
mandible is affected more).

• CGCG lesions are more common in ANTERIOR SEGMENT of the jaws, and not uncommonly, cross
the midline.
• Pain is not a main feature of this lesion. Slight to moderate bulging of the jaw due to expansion of
the cortical plates occurs in the involved area depending on the extent of bone involvement.
• Radiographic Features: multi-locular radiolucency of bone with well-defined margins (similar to
ameloblastoma & odontogenic keratocyst).
• Histologically, the CGCG is made of loose fibrillar C.T. Multi-nucleated giant cells are prominent
throughout the C.T.
• Treatment: curettage or surgical excision. These lesions fill in with new bone after excision.

MANDIBULAR TORI (TORUS MANDBULARIS) - bony exophytic growths that occur along the
lingual surface of the mandible superior to the mylohyoid ridge. Mandibular tori most often appear
on the LINGUAL SURFACE of the mandible, usually in the PREMOLAR REGION.

• Mandibular tori may occur singly, but there is a marked tendency toward bilateral occurrence,
and the lesion is not necessarily confined to the premolar region. Unlike palatal tori, mandibular tori
are more readily demonstrated radiographically.

• Maxillary & mandibular tori are of no pathological significance, and are rarely of clinical significance
while the normal teeth are still present. However, if a complete denture must be made, tori should
be carefully removed.

222
CONDYLAR HYPERPLASIA - a rare, UNILATERAL enlargement of the condyle of unknown cause. NOTES
Many feel it is due to mild, chronic inflammation that stimulates the growth of the condyle or adjacent
tissues. Afflicted patients usually exhibit a unilateral, slowly progressive elongation of the face with
deviation of the chin AWAY from the affected side. The affected TMJ mayor may not be painful, and
there is usually severe malocclusion.

CONDYLAR HYPOPLASIA &APLASIA - can occur unilaterally or bilaterally. If unilateral,

there is obvious facial asymmetry, and both occlusion and mastication may be altered. A shift of
the mandible TOWARD the affected side occurs during opening. In bilateral cases, this shift is
not present.

CENTRAL OSSIFYING FIBROMA - a slow-growing, painless, asymptomatic neoplasm

(tumor}/lesion that may occur in the maxilla or mandible. Because of its slow growth, the cortical
plates of bone and overlying mucosa or skin are almost always invariably intact. It most commonly
involves only one bone (Paget's Disease, however, involves multiple bones).

• May occur at any age, but is far more common in YOUNG ADULTS. It presents an extremely variable
radiographic appearance depending on its stage of development. However, despite the stage of
development, the lesion is always well-circumscribed and demarcated from surrounding bone
(in contrast to fibrous dysplasia). In its early stage, it appears as a radiolucent area, but as it
matures, it becomes a relatively uniform radiopaque mass.

• Early Clinical Feature: displacement of the teeth.

• There is amazing similarity in clinical features between a Central Ossifying Fibroma & Central
Cementifying Fibroma (a tumor of odontogenic origin). These are two separate benign tumors,
identical in nature except for the cell undergoing proliferation (the osteoblast with bone formation
in COF, and cementoblast with cementum formation in the CCF). Treatment: conservative excision.
Recurrence is rare.

HISTIOCYTOSIS X- a group of disorders where abnormal scavenger cells

(histiocytes/macrophages) and another immune system cell (eosinophils) proliferate in the bone and
lungs, causing scars to form . 3 Diseases are grouped under the generic term Histiocytosis and
occur due to metabolic defects in the reticuloendothelial system, and are characterized by the
proliferation of histiocytes (macrophages) of loose C.T.

1. Eosinophillic Granumola-the most benign form of Histiocytosis Xmore common in males ages
20-40yrs. It may be totally asymptomatic, but there may be local pain or swelling. In the mouth,
the mandible is most likely affected with the teeth on the affected side being loose, with signs
of gingivitis.

2. Letterer-Siwe Disease (Acute Disseminated Form}-starts before age 3yrs and is usually FATAL
without treatment. Histiocytes damage the lungs (pneumothorax may occur), skin, lymph glands,
bone, liver, and spleen . Oral lesions are uncommon.

3. Hand-Schuller-Cristian Disease (Chronic Disseminated Form}-usually begins in early childhood

(more common in boys). Triad of Symptoms: exophthalmos, diabetes insipidus, & bone destruction
(skull and jaws). Oral signs: bad breath, sore mouth, loose teeth.

Treatment: people with Hand-Schuller-Christian Disease or Eosinophilic Granuloma may recover

spontaneously. All three disorders may be treated with Corticosteroids &Cyto-toxic drugs (i.e.
Cyclophosphamide). The therapy for bone involvement is radiation. Death usually results from
respiratory or heart failure.

223
 EOSINOPHILLIC GRANULOMA - the most BENIGN form of Histiocytosis Xthat usually affects
the bones & lungs as a result of metabolic defects in the Reticuloendothelial System. It starts
between ages 20-40yrs (young adults). affecting males more than females.

• Clinically, the lesions may present no physical signs or symptoms (may be totally asymptomatic).
However, there may be local pain or swelling, especially if a bone fracture has occurred.

• In the mouth, the mandible is most likely affected, with teeth on the affected side being loose with
signs of gingivitis. When the LUNGS are affected, the symptoms may include coughing, shortness of
breath, & weight loss. Pneumothorax is a common complication.

• Radiographic Features: lesion appear as irregular radiolucent areas involving superficial alveolar
bone. Jaw lesions usually appear as single or multiple radiolucencies that may be so well-
circumscribed as to resemble cysts or periapical granulomas.

• Treatment: bone lesions often resolve spontaneously, and do not require treatment unless they cause
symptoms. Curettage provides diagnostic biopsy material and is curative.

VERRUCIFORM XANTHOMA ("HISTIOCYTOSIS Y") - a benign soft tissue tumor that presents
as a normal or white colored verrucous lesion. It's histogenesis/etiology is UNKNOWN, as it is not
associated with any systemic condition. In adults, the alveolar and palatal mucosa are common sites.
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• Microscopic Features: verrucous, hyperparakeratotic surface with parakeratotic plugging. Large
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-< • Treatment: simple excision; no recurrence .

ODONTOGENIC CYSTS
Nevoid Basal Cell Carcinoma Syndrome ("Basal Cell Nevus-Bifed Rib Syndrome" or
"Gorlin & Goltz Syndrome"): May present the following abnormalities:

1. cutaneous anomalies-includes multiple basal cell carcinomas, other benign dermal cysts &
tumors, palmer pitting, palmer and planter keratosis, and dermal calcinosis.

2. dental & osseous anomalies-includes odontogenic keratocysts (often multiple), mild

mandibular prognathism, rib anomalies (often bifed), and vertebral anomalies.

3. ophthalmologic anomalies-includes hypertelorism with wide nasal bridge and

congenital blindness.

4. neurologic anomalies-includes mental retardation, dural calcification, agenesis of

corpus callosum, and congenital hydrocephalus.

5. sexual anomalies-includes hypogonadism (males). and ovarian tumors (females).

DENTIGEROUS CYST (FOLLICULAR CYST) - an odontogenic cysts always associated with the
crown of an unerupted or developing tooth or dental anomaly (i.e. odontoma). Most commonly
found in relation to a developing 3rd molar. Enlarged dentigerous cysts can cause marked
displacement of teeth due to pressure of accumulated fluid that usually displaces the tooth in an
apical direction. If a tooth with a dentigerous cysts begins to erupt, the bulging the cyst produces on
the ridge is an eruption cyst.

• Clinical Features: found in children & teenagers in mandibular 3'd molar & maxillary canine area
(70% in the mandible). Associated with impacted or unerupted teeth. It's the 2nd most common
odontogenic cyst.

• Radiographic Features: well-defined usually unilocular radiolucency.

224
• Histologic Features: lined by non-keratinized, stratified squamous epithelium, &rete-pegs are NOTES
absent.

• An ameloblastoma is most likely to develop in the wall of a dentigerous cyst.

ERUPTION CYST - a soft-tissue variant of the dentigerous cyst, invariably associated with an
erupting tooth (usually primary, but occasionally permanent teeth). The effects are mostly limited to
the overlying gingival tissues, not bone.

• Clinical Features: lesion usually appears as a smooth-surfaced, reddish-pink or bluish-black,

fluctuant, localized swelling of the ALVEOLAR RIDGE over the crown of an erupting primary or
permanent molar. The intense bluish color (which is often characteristic), is due to an accumulation
of blood. Due to this appearance, it may be mistaken for a hemangioma or hematoma.

• Treatment: in most cases NO treatment is necessary. However, in a few rare cases, incision or
removal of the overlying tissue may be required due to pain or tenderness associated with the lesion.

PRIMORDIAL CYST (FOLLICULAR CYST) - differs from periodontal and dentigerous cysts
because it contains no calcified structures. Located in the mandibular 3'd molar space, and may be
locular, multilocular, or multiple. This cyst is found in place of a tooth rather than directly associated
with a tooth. Equally affects males and females under age 25yrs.

• Radiographic Features: well-defined, oval radiolucent lesion .

• Histologic Features: lined by stratified squamous epithelium with no rete pegs (arises from
epithelium of the enamel organ).

ODONTOGENIC KERATOCYST - follicular &dentigerous cysts that contain keratinizing

material, and differs from other odontogenic cysts due to their microscopic appearance & clinical
behavior. Keratocysts may resemble periodontal, primordial, or follicular cysts, and usually CANNOT be
distinguished radiographically. The most remarkable feature of keratocysts is their great tendency
to reoccur (over 30% reoccur). Usually occurs between ages lO-30yrs. Often associated with an
impacted tooth . 50% are found in the mandibular 3rd molar area.

• Keratocysts increase in size mainly by a process of epithelial cell multiplication.

• Radiographic Features: well-circumscribed radiolucency with smooth margins and thin radiopaque
borders.

• Histologic Features: thin layer of corrugated parakeratin. Uniform thin stratified squamous lining.
Distinct cuboidal to columnar basal layer with varying amounts of keratin debris in the lumen .

• Treatment: excision of the overlying mucosa in the area where the cyst wall is adhered.

TRAUMATIC BONE CYST - may be completely devoid of solid or liquid material (but may contain
blood, fluid, debris, or be completely empty). It is most commonly found in younger people with no sex
predilection, in the mandible between the canine & ramus. Regional teeth are vital. Clinical Case:
large radiolucent area on the mandible apical to the premolars and molars on a panorex. No clinical
symptoms. Teeth are not carious and respond normally to vitality tests. Medical history is
unremarkable. No fluid or tissue is evident.

LATERAL PERIODONTAL CYST - inflammatory in origin, and forms along the lateral surface of the
tooth . If it forms at the root apex, it is a Radicular Cyst. 95% are found in mandibular canine-
premolar area. Apposition with the root of a vital tooth. Usually asymptomatic.

• Radiographic Features: well-defined, round or tear-drop shaped radiolucency with an opaque margin
along the lateral surface of a tooth.

• Histologic Features: thin lining of non-keratinized epithelium.

225
 NOTES DENTAL GRANULOMA - one of the most common of all sequelae of pulpitis, usually found at the
root apex. It can only be distinguished from a radicular cyst histologically.

• Clinical Features: asymptomatic, tooth in non-vital, and may be sensitive to percussion.

• Radiographic Features: circumscribed radiolucency at the tooth apex.

• Histologic Features: fibrous C.T. with macrophages, lymphocytes, cells, and capillaries. Stratified
squamous epithelium is present.

• Treatment: RCT or extraction of the involved tooth.

RADICULAR CYST (APICAL PERIODONTAL CYST OR PERIAPICAL CYST) - MOST COMMON

ODONTOGENIC CYST, usually found at the root apex. It develops within a pre-existing periapical dental
granuloma. Increased osmotic pressure in the cyst lumen is important in its pathogenesis.

• Clinical Features: asymptomatic, tooth is non-vital, tooth may be sensitive to percussion .

• Radiographic Features: circumscribed radiolucency at the tooth apex.

• Histologic Features: exhibits a lumen (true cyst) that is invariably lined by stratified squamous
epithelium. The wall is made of condensed C.T. that contains plasma cells, lymphocytes, and PMN
leukocytes.

• Treatment: RCT with apicoectomy or extraction with curettage of the socket.

RESIDUAL CYST - a situation where a tooth with a radicular (periapical) cyst is extracted, but the
rad icular cyst is left undisturbed and persists within the jaw now as a residual cyst. To prevent a
residual cyst, you must curette the radicular cyst out of the tooth socket after extraction. Equally
affects males and female at any age. Usually asymptomatic, and is found in edentulous areas. It is a
radicular cyst left in the jaw after a tooth extraction.

• Radiographic Features: well-defined radiolucency not associated with a tooth . Usually solitary.

• Histological Features: same as a radicular cyst (apical periodontal cyst) , of stratified squamous
epithelium lin ing the lumen.

FISSURAL CYSTS (DEVELOPMENTAL CYSTS) - are non-dental in origin, and include

nasoalveolar, median palatal, nasopalatine, and globulomaxillary cysts.

GINGIVAL CYST - a rare, circumscribed swelling of the gingiva usually found in the canine &
premolar areas on the mandible. Usually limited to the gingiva, but larger cysts may erode the bone.
Gingival cysts are easily excised .

ODONTOGENIC TUMORS
AMELOBLASTOMA - tumors of odontogenic epithelial origin and MOST COMMON EPITHELIAL
(ECTODERMAL) ODONTOGENIC TUMOR (its occurrence equals the frequency of all other odntogenic
tumors) that consists entirely of odontogenic epithelium that shows the differentiation of the
familiar, histologic layers of the enamel organ at sites. Enlargement of the tumor may expand the
buccal, lingua cortical plates of bone, or palatal bone plates. Resorption of roots of adjacent teeth to
the tumor is common, and in many cases an unerupted mandibular 3rd molar is associated with the
radiolucent defect. Ameloblastomas are slow-growing, locally invasive tumors that usually run a
benign course (do not infiltrate). Often asymptomatic, a painless swelling or expansion of the jaw is
the usual clinical presentation Ameloblastomas occur in 3 different clinical-radiographic situations
with different treatments &prognosis:

226
 1. Multicystic (Solid) Ameloblastoma-represents -86% of all cases, and is the more aggressive
form that requires more extensive treatment (surgical excision). Marginal resection is the most
widely used treatment. En bloc resection is reserved for larger lesions. Most occur in the mandible
(molar-ascending ramus area). 15% occur in the maxilla (posterior regions).

2. Unicystic Ameloblastoma-represents -13% of all intraosseous cases. Most common in younger

patients (50% diagnosed in age 20s). 90% are found in the mandible (posterior area).
Asymptomatic, but large lesions may cause painless swelling of the jaw. These lesions are usually
treated as cysts by enucleation, and should not be over treated. Recurrence is common if
inadequately treated.

3. Peripheral (Extraosseous) Ameloblastoma-uncommon and represents -1 % of all cases. Arises

from rests of dental lamina below the oral mucosa or from basal epithelial cells of surface
epithelium . Painless, non-ulcerated sessile or pedunculated gingival or alveolar mucosal lesion.
Found in patients over wide age range (most are middle-aged in 50s) . Most common in posterior
gingival and alveolar mucosa (more common in mandible).

• Histogenesis: may arise from rests of the dental lamina, epithelial lining of dentigerous cyst, basal
cells of the oral epithelium (mucosa), developing enamel organ, and possibly remnants of Hertwig's
sheath. Consists entirely of odontogenic epithelium that shows the differentiation of the histologic
layers of the enamel organ at sites.

• Clinical Features: most often seen in adolescents in the mandibular (retro) molar area. It is the
most aggressive odontogenic tumor, that is usually benign, but often shows a highly expansive
and locally invasive mode of growth.

• Radiographic Features: multi-locular or uni-Iocular radiolucent lesion on vital teeth with a "soap
bubble" appearance when the radiolucent loculations are large & honeycombed when the loculations
are small. Has irregular-scalloped marginsAppears similar to a Central Giant Cell Granuloma in the
mandible.

• Microscopic Features: various microscopic patterns of the tumor include the follicular (most
common pattern of multiple islands with reverse polarity) & plexiform (also most common pattern
of large anastomosing cords), cystic, acanthomatous (extensive squamous metaplasia, keratin
formation in central portions of epithelial islands), granular cell (cells with prominent granular
cytoplasm), desmoplastic (thin cords), & basal cell (islands of hyperchromatic basaloid cells)
patterns. All are non-encapsulated.

• Treatment: varies depending on the subtype. Recurrence is common (50-90%) if inadequately

treated. Very rarely metastasizes.

ADENOMATOID ODONTOGENIC TUMOR (ADENOAMELOBLASTOMA) - a tumor of ectodermal

origin (purely epithelial) that represents 3-7% of all odontogenic tumors. Limited to younger patients
(l0-19yrs), and uncommon in patients> 30yrs. Not a variant of ameoloblastoma (best classified as a
hamartoma, not a true neoplasm) . Occurs mainly in the anterior maxilla (2x more common in maxilla
than mandible) and females affects 2x more than males. Affects 2nd decade (teenagers).
Asymptomatic or painless swelling.

• Clinical Features: most are small « 3cm diameter). Clinically looks like a gingival fibrous lesion.
Often asymptomatic, circumscribed, unilocular radiolucency associated with the crown of an
unerupted tooth (mostly canines). Radiolucency sometimes extends apically along the root past the
CEJ (helps distinguish it from a dentigerous cyst) . May be completely radiolucent but often contains
fine snowflake calcifications (tiny radiopaque foci).

• Histology: well-defined lesion surrounded by a thick, fibrous capsule. Enamel organ, lining of
dentigerous cyst, reduced enamel epithelium, Rests of Malessez. Derived from ectoderm (epithelial)
enamel organ and remanants of dental lamina.

227
 • Microscopic Features: tumor is composed of spindle-shaped epithelial cells that form sheets,
strands, or whorled masses of cells in a scant fibrous stroma.

• Treatment: completely benign, and its capsule allows it to enucleate easily from bone (enucleation) .
Recurrence is rare, and is not aggressive.

CALCIFYING EPITHELIAL ODONTOGENIC TUMOR ("PINDBORG TUMOR") - an uncommon

lesion/tumor « 1% of all odontogenic tumors) derived purely from ectoderm (epithelial). Found in
patients over wide age range (mainly 30-50yrs), no sex predilection (30% are 4th decade). Uncommon
in children and adolescents. 2/3 of cases occur in mandible (molar-premolar area). Painless, slow-
growing swelling is the most common clinical sign . Rarely extraosseous. Radiolucent-radiopaque
areas associated with an unerupted tooth and amyloid production.

• Radiographic Features: unilocular or more often multi-locular radiolucent defect. Scalloped margin.
Tumor is often associated with an impacted tooth (mandibular 3rd molar). Calcifications within the
tumor are often most prominent around the crown of an impacted tooth.

• Histology: reduced enamel epithelium, has discrete islands, strands, or sheets of polyhedral epithelial
cells in a fibrous stroma.

• Treatment: conservative local resection to include a narrow rim of surrounding bone is the treatment
of choice. 15% recurrence rate (tumors treated by curettage have highest recurrence rate if
inadequately treated). Prognosis is good .

SQUAMOUS ODONTOGENIC TUMOR - a rare benign odontogenic tumor/neoplasm derived purely

from ectoderm (epithelial). Found in patients ages 8-75yrs (average 38yrs). Randomly distributed
throughout the alveolar processes of maxilla and mandible with no site or sex predilection. Most
common complaint is painless or mild painful gingival swelling associated with tooth mobility.

• Clinical Features: may be asymptomatic, painless swelling associated with mobile teeth.

• Radiographic Features: triangular or circumscribed radiolucency lateral to the roots, associated

with an unerupted or erupted tooth. May be ill or well defined area with sclerotic margins. Most are
small lesions that rarely exceed 1.5cm diamteter.

• Histogenesis: Rests of Malassez.

• Treatment: conservative local excision or curettage, and close follow-up . Recurrence is rare.

CEMENTOMA (PERIAPICAL CEMENTAL DYSPLASIA) - odontogenic tumor that occurs most

frequently in the MANDIBLE (anterior/incisor periapical region), and often affects multiple vital
teeth. It represents a reactive process (not a neoplastic process); Cementoma is an unusual response
of the periapical bone to some local factor (i.e. traumatic occlusion or infection). While it appears to
arise from teeth, the lesions arise within bone. Age, gender, location, radiographic appearance, and
tooth vitality are important diagnostic criteria of a cementoma.

• Clinical Features: occurs at the apex of vital anterior teeth, affecting women over age 30yrs
(especially BLACK women) more than men. Asymptomatic, usually multiple, small periapical areas
of radiolucency in the mandibular incisor area. Depending on the stage, a cementoma may appear
radiolucent, mixed radiolucent & radiopaque, or completely radiopaque. 3 Cementoma Stages:

1. osteolytic stage-radiolucency appears on the radiograph .

2. cementoblastic stage-beginning of calcification in the radiolucent area (mixed radiolucent

& radiopaque).

3. mature stage-radiopacity appears on the radiograph surrounded by a thin radiolucent line.

At this stage, the lesion stabilizes and causes no complications, thus no treatment is required .

228
• Radioraphic Features: small sharply circumscribed radiopacity attached to or adjacent to apices of NOTES
teeth. Early lesions are radiolucent, then have a central opacity, and are densely radiopaque when
mature. The opacities are not cementum, but are bone.

• Histogenesis: periodontal ligament (POL)

• A black female with multiple periapical radiolucencies in mandibular incisor area, DO NOT TREAT.

• Treatment: NO TREATMENT IS REQUREO. Simply recognize the condition and periodically observe.

BENIGN CEMENTOBLASTOMA (TRUE CEMENTOMA) - usually affects males < 2Syrs.

Mandibular premolars or molars. Is usually solitary, and may cause expansion of the cortical plates.
Tooth is vital. Histogenesis: POL.

• Radiographic Features: well-demarcated, mottled or densely radiopaque mass with radiolucent

periphery attached to the root, causing the root to resorb.

• Microscopic Features: cementum-like tissue with conspicuous reversal lines, variable amounts of
fibrous C.T. with sheets of uncalcified "cementoid" especially at the periphery.

• Treatment: extraction of the involved tooth.

GIGANTIFORM CEMENTOMA (FAMILIAL MULTIPLE CEMENTOMAS) - affects middle-aged

black women. Multiple, often symmetrical, and may cause jaw expansion.

• Histogenesis: POL.

• Radiographic Features: large, dense often lobulated radiopaqe masses.

• Microscopic Features: large sheets of tissue that resemble secondary cementum.

• Treatment: conservative excision.

CENTIFYING FIBROMA - a well-defined radiolucency with scattered radiopaque foci. Occurs in the
mandible of adults as a painless swelling.

• Histogenesis: POL. Treatment: curettage. Recurrence is rare.

COMPLEX ODONTOMA - an amorphous mass with a thin, radiolucent rim at the junction of
surrounding bone. May prevent eruption of teeth, and more common in the posterior areas of the jaw.
Derived from ectodermal &mesenchymal components of tooth germ . Affects ages 20-30yrs, and found in
the mandibular premolar-molar area. Asymptomatic, but may cause delayed eruption of permanent teeth.

• Radiographic Features: well-defined radiopaque mass surrounded by a narrow radiolucent zone.

Mayor may not be associated with an erupted tooth .

• Microscopic Features: conglomerate mass of dental tissues (dentin, enamel, cementum).

• Treatment: enucleation, and does not recur.

COMPOUND ODONTOMA - derived from ectodermal & mesenchymal components of tooth germ.
Affects ages 20-30yrs, and is common in the maxillary incisor-canine area, but may also appear in the
mandible canine-premolar area (more common in the anterior teeth). May cause delayed eruption of
permanent teeth. May prevent eruption of teeth .

• Radiographic Features: appears as groups of small radiopacities (multiple small tooth-like

structures with thin, radiolucent rim at the junction with surrounding bone.) between the maxillary
premolar and central incisor on a panorex.

229
 • Microscopic Features: multiple, small malformed teeth composed of dentin, enamel, and cementum.

• Treatment: enucleation, and does not recur.

ODONTOGENIC MYXOMA - an aggressive tumor derived from the papilla, dental sac, or PDL.
Occurs in adults 30-40yrs as a painless swelling in the mandible.

• Radiographic Features: poorly defined, multilocular radiolucency that may be associated with an
unerupted or displaced teeth.

• Treatment: curettage with cautery. Has a high rate of recurrence if it is inadequately treated.

ODONTOGENIC FIBROMA - derived from dental papilla dental sac, or PDL. Occurs as a painless
swelling in the mandible of children & young adults.

• Radiographic Features: multilocular or unilocular radiolucency; may be associated with unerupted

or displaced teeth.

• Treatment: enucleation. Recurrence is rare.

Odontogenic Tumors of MIXED origin (Ectodermal-Mesodermal components of tooth germ):

1. Ameloblastic Fibroma-often mistaken for an ameloblastoma. Occurs in ages under 20yrs. Most
common in the mandibular premolar-molar area as a painless swelling (this grows faster than
an ameloblastoma).

• Radiographic Features: well-defined radiolucency often associated with an unerupted tooth.

• Microscopic Features: nests & strands of odontogenic epithelium, and young cellular fibrous
C.T. resembling dental papilla.

• Treatment: conservative excision. Recurrence is rare.

2. Ameloblastic Fibro-Odontoma-affects children under age 20yrs (similar to ameloblastic fibroma),

occurs with equal frequency in the maxilla and mandible. Radiographically and microscopically
appears similar to an ameloblastic fibroma, but may show foci of calcification, and with dentin
and enamel (induction effect). Treatment: conservative excision. Recurrence is rare.

3. Ameloblastic Odontoma-affects children under age, occurs with equal frequency in the maxilla
and mandible (premolar-molar area) as a painless swelling.

• Radiographic Features: well-defined radiolucency with foci of calcification, and mayor may
not be associated with an erupted tooth.

• Microscopic Features: simple ameloblastoma in combination with composite odontoma.

• Treatment: resection of the affected area. May recur if incompletely excised.

PIGMENTED LESIONS OF THE ORAL CAVITY

PEUTZ-JEGHERS SYNDROME (HEREDITARY INTESTINAL POLYPOSIS SYNDROME) - an
inherited disorder transmitted as an autosomal dominant trait, characterized by multiple intestinal
polyps distributed through the entire intestine (especially in the jejunum) and intraoral melanin
pigmentations. Melanin pigmentation of the lips and oral mucosa is usually present at birth
(pigmentation usually appears at an early age, often during the first decade of life, and at this time is
restricted to the oral region.

230
• It is an unusual condition of interest to the dentist due to the associated oral findings. Intraorally,
the pigmentations may be located anywhere on the mucosa, but are most common on the buccal
mucosa, gingiva, and hard palate. The mucosal surface of the lower lip is almost invariably involved.
These spots or macules vary in intensity, and range in shades of brown, blue, and black. The tongue
seldom shows this melanin pigmentation. Although oral pigmentations are harmless, their presence
is important as they indicate a need to investigate the possible presence of multiple polyposis which
may prove harmful. There is a strong tendency for these multiple polyps of the colon to undergo
malignant change.

• During succeeding decades of a patient's life, pigmentations may arise elsewhere on the skin
(especially the extremities). Pigmentations of Peutz-Jeghers Syndrome may occur without
demonstrative evidence of polyps and also multiple polyps may be encountered without
pigmentations.

• When Peutz-Jegher Syndrome is suspected based on oral pigmentations, other conditions to consider
in the differential diagnosis are Addison's Disease & Albright's Syndrome.

AMALGAM TATTOO - a common finding sometimes mistaken for a melanin-pigmented lesion. Most
common locations are the gingiva, buccal mucosa, & alveolar mucosa.

Other Oral Lesions due to CHEMICAL INJURIES:

• Dilantin-an anticonvulsant drug used extensively to control epileptic seizures. An unfortunate side
effect of its use if fibrous hyperplasia of the gingiva (Dilantin Hyperplasia).

• Aspirin Burn-occurs when patients place the tablet against an aching tooth, allowing the cheek or
lip to hold it in position, while it dissolves slowly. Within a few minutes, a burning sensation of the
mucosa is noted, and the surface becomes blanched or white. The caustic action of the drug causes
necrosis of the oral mucosa, with subsequent sloughing of the necrotic epithelium.

• Ingestion of Heavy Metal Bismuth-common to treat certain dermatologic disorders and various other
diseases. Bismuth pigmentation appears as a "bismuth line" (thin, blue-black line in the marginal
gingiva that is sometimes confined to the gingival papilla).

Most pigmented skin tumors are composed of NEVUS cells and are caused by a developmental
anomaly of MELANOCYTES. They are RARE in the oral cavity. The initial flat, raised lesion can become
nodular, with an increase in consistency. Spontaneous involution may occur and malignant
transformation is a rare complication . When found intraorally, pigmented skin tumors most often
occur on the HARD PALATE, but may appear on the gingiva and lips. If a pigmented lesion shows
ulceration, increase in size, color darkening, a biopsy is performed to indicate if malignant
transformation is occurring.

CONGENITAL NEVI (BIRTHMARK) - are usually larger (> lDcm) and as time passes, may change
from flat, pale tan macules into elevated, verrucous, hairy lesions. -15% occur on the head & neck
skin. Have a higher incidence of malignant transformation than acquired nevi. Most common intra-
oral location is the HARD PALATE.

ACQUIRED NEVI (MOLES) - small, usually dark, skin growths that develop from pigment-producing
cells (melanocytes) in skin . Fairly common on the skin and intra-orally (are much more common than
congenital nevi both intra-orally and extra-orally). When present, they are usually on the hard palate, but
may also be on the gingiva & lips. Acquired nevi are microscopically classified into 5 subtypes:

1. intramucosal nevus-most common variety seen in the oral cavity. Nevus cells are located in the
C.T. or lamina propria of the oral mucosa. Under palpation, these nevi appear solid and slightly
raised over the mucosa surface.

2. blue neVUS-2nd most common acquired nevus in the oral cavity. Congenital, painless, color is
based on the deep cutaneous or subcutaneous/submucosal deposits of melanin.

231
 3. compound nevus-rare in the oral cavity. Nevus cells are located at the epithelium-lamina propria
interface deep in the dermis. They are raised and solid.

4. junctional nevus-rare in the oral cavity. Nevus cells are located at the interface between the
epithelium and lamina propria. They are flat and not detected by palpation. Some regard as
premalignant, may undergo transformation into malignant melanoma.

5. intradermal nevus (common mole)-the most common lesion of skin . Nevus cells lie exclusively
within the dermis.

B-K Mole Syndrome &Dysplastic Nevus Syndrome are both characterized by having numerous large,
pigmented atypical nevi with a high risk for developing malignant melanoma.

FOCAL MELANOSIS - may occur at any age and presents as a single or multiple small , flat brown
asymptomatic lesion occurring mostly on the LOWER LIP. Focal melanosis is a term used for two
similar lesions that differ in their location:

1. Labial Melanotic Macule-a lesion that appears on the lips (mostly lower lip), and almost always
occur near the midline. Most lesions measure 5mm or less in diameter.

2. Oral Melanotic Macule-a lesion that appears intra-orally on the gingiva, buccal mucosa, and
o palate. Most lesions are under lcm in diameter.
::c
;0,.
r-
-0
:.:::c Treatment: melanotic macules with a relatively short history are excised to establish a definitive
o
r-
diagnosis and to rule out the possibility of malignant melanoma. Lesions present> 5 years without a
o change in size or color, are followed unless the patient requests removal.
CD
-<

Conditions that Demonstrate Pigmentation of Intra-Oral Mucous Membranes:

1. Addison's Disease ("Chronic Adrenocortical Insufficiency" or "Hypocorticolism)-results from

hypofunction of the adrenal cortex, characterized by BRONZING of the entire skin. It is a rare
endocrine disorder that occurs when the adrenal glands do not produce enough cortisol
(glucocorticoid) due to either a disorder of the adrenal glands (primary adrenal insufficiency), or
inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency). Cortisol's
most important function is to help the body respond to STRESS. Occurs in all age groups, affecting
men and women equally. The main concern when performing dental procedures on a patient
with Addison's disease is the adrenal cortex has no capacity to produce extra cortisol in
response to stress, and may lead to Addison's Crisis.

• Clinical Signs: usually begin gradually and include weight loss, loss of appetite, muscle
weakness, low BP, darkening (hyperpigmentation) of the skin in both exposed & unexposed
parts of the body (most visible on scars, skin folds, pressure points like elbows, knees,
knuckles, toes, and oral mucous membranes). Also nausea, vomiting, diarrhea.

• Oral Signs: diffuse pigmentation of gingiva, tongue, hard palate, &buccal mucosa. Although
cutaneous pigmentation will most likely disappear, after therapy, pigmentation of the oral
tissues tends to persist.

• Lab Tests: show low blood concentrations of Na+ and glucose, increased serum K+, and
decreased urinary output of certain steroids.

2. Albright's Syndrome (McCune-Albright Syndrome)-a severe form of polyostotic fibrous

dysplasia that causes lesions of nearly al bones in the skeleton, brown patches of cutaneous
pigmentation (cafe-au-Iait spots), and endocrine dysfunction (especially precocious puberty
in girls) . There is an increased incidence of osteosarcoma seen with polyostotic fibrous dysplasia .

232
 3. Peutz-Jeghers Syndrome (Hereditary Intestinal Polyposis Syndrome)-an inherited disorder
transmitted as an autosomal dominant trait, characterized by multiple intestinal polyps
distributed through the entire intestine (especially in the jejunum) and intraoral melanin
pigmentations that usually appear during the first decade of life, and at this time is restricted
to the oral region. They may be located anywhere on the mucosa, but are most common on the
buccal mucosa, gingival, and hard palate. The mucosal surface of the lower lip is almost
invariably involved .

PSEUDOCYSTS ("NOT TRUE CYSTS")

NO EPITHELIAL LINING
TRAUMATIC BONE CYSTS (PSEUDOCYSTS) - non-cysts found in the mandible (between
canine &ramus) of mainly TEENAGERS, assumed to be caused by trauma. It manifests as a painless,
well-defined radiolucency that frequently extends between the teeth with a scalloped appearance.
Although sometimes asymptomatic, it may produce jaw enlargement. Pain is rarely associated with the
lesion, and regional teeth are vital.

• AKA: simple bone cyst, hemorrhagic bone cyst, unicameral bone cyst, extravasation bone cyst,
idiopathic bone cyst, and solitary bone cyst.

• Treatment: consists of opening the lesion, curettage, and closure. It may contain blood,
serosanguineous fluid, debris composed mainly of a blood clot, or may be completely devoid of solid
material.

ANEURYSMAL BONE CYST - a benign lesion of bone generally regarded as a "reactive

process" (not a neoplastic or cystic process). It is an uncommon expansile osteolytic bone lesion
consisting of a proliferation of vascular tissue that forms a lining around blood-filled cystic
lesions. Most occur equally in males and females under age 20yrs, and is uncommon after age 30yrs.

• Commonly involves the proximal humerus, femur, tibia, &pelvis (uncommon in the jaws, but if it
appears, it is usually in the mandible). Lesions are usually tender or painful, especially on motion
of the affected bone. Upon entering the lesion surgically, excessive bleeding is encountered and the
tissue often resembles a "blood-soaked" sponge.

• Histology: has no epithelial lining (thus is a "pseudocyst"). It consists of fibrous C.T. stroma
containing many cavernous or sinusoidal blood-filled spaces. Fibroblasts & macrophages
(histiocytes) line the sinusoids. Multi-nucleated giant cells (similar to cells of a giant cell granuloma)
are dispersed throughout.

• Radiographic Features: distinctive lesion as the bone is expanded and appears cystic with a
"honeycomb" or "soap-bubble" appearance.

• Treatment: surgical curettage or excision, with little change of recurrence.

Other Pseudocysts:
1. Latent bone cyst-
2. lingual Mandibular Concavity-

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 RED-BLUE LESIONS
MEDIAN RHOMBOID GLOSSITIS - frequently affects MIDDLE-AGED ADULTS. It was once thought
to be a congenita l abnormality related to the persistence of the tuberculum impar, but is now believed
to be a permanent end result of a chronic Candida Albicans infection. Diabetics, immunosuppressed
patients, and patients on long-term antibiotic therapy are most susceptible.
• Clinical Features: smooth, denuded, BEEFY, red lesion devoid of filiform papillae. Most common
location is the MIDLINE of the DORSUM OF TONGUE, just anterior to circumvallate papillae. Generally
asymptomatic, and no treatment is usually necessary.

PYOGENIC GRANULOMA - a benign lesion whose MOST common site is the INTERDENTAL
GINGIVA, but may also occur on the lower lip, tongue, & buccal mucosa. They rarely occur on other
areas of the oral mucous membrane. It is believed it arises due to minor tissue trauma (i.e.
cementation of a crown or calculus) that provides a pathway for the invasion of non-specific types of
microorganisms. Pregnant patients are prone to these lesions (called a "Pregnancy Tumor" in a
pregnant patient).

• Clinical Features: soft, pedunculated broad-based growths with a smooth red surface due to the
presence of hyperplastic granulation tissue that contains many capillaries. They are often ulcerated,
bleed easily, and may have a raspberry-like appearance.

• Treatment: Excision. May occasionally recur.

ERYTHROPLAKIA - a persistent, velvity red patch that cannot be characterized clinically as any
other condition. Like "leukoplakia", it has no histologic connotation, but most erythroplakias are
histologically diagnosed as severe epithelial dysplasia, carcinoma in situ , or invasive squamous cell
carcinoma. May be located anywhere in the mouth , but are MOST likely found in the mandibular
mucobuccal fold, oropharynx, and floor of the mouth. Equally affects males and females, especially
over 60yrs (are most commonly affected).

RENDU-OSLER-WEBER DISEASE (HEREDITARY HEMORRHAGIC TElANGIECTASIA)-

congenital hereditary form of hemangioma, characterized by numerous SPIDER-LIKE telangiectases
on the face, neck, chest, lips, gingiva, buccal mucosa, and tongue. Epistaxis (nosebleeds) is on the
earliest signs of this disease.

ENCEPHALOTRIGEMINAL ANGIOMATOSIS ("STURGE-WEBER DISEASE") - uncommon

congenital syndrome of unknown etiology (sometimes classified as a variant of hemangioma). It
consists of a unilateral facial lesion (port-wine stain) distributed over the trigeminal nerve,
accompanied by a similar vascular disorder of underlying meninges & cerebral cortex. Usually occurs
unilaterally.

JUVENILE NASOPHARYNGEAL ANGIOFIBROMA - a rare, benign neoplasm that nearly always

affects ADOLSCENT MALES. It characteristically produces a NASOPHARYNX MASS that leads to
obstruction or epistaxis. Treatment is surgery, and recurrences are common.

BURNING TONGUE SYNDROME - patients usually do not exhibit clinically detectable lesions,
but symptoms of intense pain and burning. BTS is frustrating for the patient and clinician because
there is usually no clear-cut cause and no uniformly successful treatment. Typically affects MIDDLE-
AGED FEMALES (it affects men too, but usually at an older age). Rare in children & teenagers.

• Possible Etiologic Factors: anemias (pernicious anemia & iron deficiency anemia), diabetes
mellitus, gastric disturbances (i .e. hyperacidity or hypoacidity), psychogenic factors (emotional
conflict, cancerophobia), trigeminal neuralgia, microorganisms (especially Candida Albicans &
Streptococci), xerostomia (dry mouth) associated with Sjogrens Syndrome, anxiety, & drugs. Local
irritation (tobacco, spices), and vitamin deficiency (especially Bcomplex).

234
PERIPHERAL GIANT CELL GRANULOMA - relatively uncommon, pedunculated broad-based NOTES
growths with a smooth surface (usually). Always occurs on the GINGIVA (between 1't permanent molar
&incisors) or ALVEOLAR PROCESS. Mandibular gingiva is affected more than the maxillary gingiva. It
represents an unusual hyperplastic C.T. response to injury of gingival tissues. They are reddish-blue in
color, sometimes lobulated, and bleed easily. Most patients are older than age 20yrs (Central Giant Cell
Granuloma occurs mainly before age 20yrs) . Affects females 2x more than males.

• Radiographs are usually negative. Clinically, it may resemble a fibroma or pyogenic granuloma.

• Histologic sections are DIAGNOSTIC and are histologically identical to Central Giant Cell Granuloma.
It consists of a non-encapsulated tissue mass composed of a del icate reticular &fibrillar C.T. stroma
with multi-nucleated giant cells.

• Treatment: complete surgical excision .

HEMANGIOMA - benign tumor consisting of a mass of blood vessels. It can range from being a small
mass, to very large sacs of unsightly red, purple, or blue blood vessels (they can enlarge to very alarming
sizes). Present at birth, childhood, or arise later in life (enlarges as the child grows). In certain locations,
large hemangiomas can interfere with proper organ development and function.

• Clinical Features: a common tumor characterized by PROLIFERATION OF BLOOD VESSELS, affecting

females 2x more than males (2: 1). It is a soft, smooth, blue, red, purple, or purplish-red mass that
most commonly affects the tongue, buccal mucosa , lips, and pa late.

• Histogenesis (Etiology): Endothelial cells, C.T. origin.

• Microscopic Features: 3 types (capillary, cavernous, & hemangioendothelioma).

Hemangioendothelioma has stratified squamous epithelium covering of loose, fibrous C.T. that
contains many thin-walled engorged vascular spaces.

• Treatment: laser therapy or surgery. May regress spontaneously. Incisional biopsy is contraindicated.

SALIVARY GLAND TUMORS

BENIGN SALIVARY GLAND TUMORS CLINICAL FEATURES - normal mucosa, painless,
nodular, localized , movable, firm , slow-growing, well-differentiated , and encapsulated/well-
circumscribed.

• Radiographically, a benign neoplasm in bone may be distinguished from a malignant neoplasm in

that in a benign lesion, the cortex remains in tact, but may be thinned and the part involved may
be expanded. Also, the margins are usually defined and demarcated from surrounding bone.

Benign Salivary Gland Tumors:

• Pleomorphic Adenoma (Mixed Tumor}-the MOST COMMON BENIGN salivary gland tumor.

• Monomorphic Adenomas: Basa l Cell , Canalicular, Myoepithelioma, Sebaceous, Papillary

Cystadenoma Lymphomatosum (Warthin's Tumor), Onocytoma (oxyphilic/ac idophilic adenoma).

• Most common site of intra-oral MINOR salivary gland neoplasms/tumors is the PALATE. Most
common site of intra-oral MAJOR salivary gland neoplasms is the PAROTID GLAND.

NECROTIZING SIALOMETAPLASIA - a lesion of the MINOR salivary glands, characterized by

necrosis of the glandular parenchyma with associated squamous metaplasia & hyperplasia of the
ductal epithelium. Its etiology is unknown , but may be related to vascular insufficiency and infarction
of the glands. HARD PALATE is the most common site.

235
 • The lesion shows no racial or sex predilection, with most patients> 40yrs of age. Clinically, it presents
as a tender deep ulcer with sharply demarcated margins. Histologically, there is lobular necrosis of
the glandular parenchyma, with squamous metaplasia & hyperplasia of the ductal epithelium.
Clinically and histologically, the lesion may stimulate a malignancy. In the past, the condition was
misdiagnosed as a squamous cell or mucoepidermoid carcinoma.

• After performing a biopsy and establishing a diagnosis, additional treatment is usually not
recommended since healing usually occurs within 6-12 weeks.

MUMPS - most common VIRAL DISEASE of the salivary glands caused by an RNA-Paramyxovirus.
Clinically, 90% of cases occur before age 14yrs. A major sign is sudden salivary gland swelling
without purulent discharge from the duct. Parotid gland is involved 90% of the time, and is
bilaterally involved in 2/3 of the cases. Patient presents with mild fever, malaise, and anorexia. Most
cases are self-limiting.

• Complications: orchitis (inflammation of the testis) and epididymitis can occur in post-pubertal
males, and may cause sterility. CNS disturbances causing meningitis & encephalitis. Deafness,
myocarditis, pancreatitis, oophoritis, and pyelonephritis.

• Serum amylase may be elevated during the acute phase. Prevent by administering a live attenuated
vaccine which is 95% effective for a least 5 years. However, in non-inoculated patients, it can still
cause acute non-suppurative salivary adenitis.

RNA Paramyxoviruses-causes MEASELES (RUBEOLA) & MUMPS:

1. Rubeola is characterized by the formation of KOPLIK SPOTS in the oral cavity. Koplik spots are
small bluish-white lesions surrounded by a red ring. These lesions cannot be wiped off and occur
opposite the molars.

2. Mumps-causes enlargement of the parotid glands, and serious complications include deafness
in children and orchitis (inflammation of the testis) in males past puberty.

DEVELOPMENTAL SALIVARY GLAND DEFECTS - are relatively rare, asymptomatic, nearly

impossible to be manually palpated, and are discovered only during radiographic examination of the
area. The radiographic image is a ROUND or OVOID RADIOLUCENCY ranging from 1-3cm in
diameter. It generally develops below the mandibular canal, just anterior to the angle of the
mandible, and below and just behind the mandibular 3'd molar.

MUCOCELES (MUCOUS RETENTION CYST) - most frequently occur on the LOWER LIP (rarely
on the upper lip) usually due to trauma. It involves the MINOR salivary glands and their ducts (i.e.
trauma to the salivary duct by lip biting or pinching). Mucoceles is a COMMON LESION that may also
appear on the palate, cheek, tongue, and floor of mouth. Treatment: Excision .

• Clinical Features: may lie fairly deep in the tissue, or be exceptionally superficial. Depending on its
location, its clinical appearance varies:

• superficial mucocele-appears as a raised, circumscribed vesicle, several millimeters to lcm in

diameter with a bluish translucent cast.

• deeper mucocele-appears as a fluctuant swelling also, but the tissue is normal in color.

RANULA ("TRUE RETENTION CYST") - a fluctuant & painless lesion that presents as a
translucent, bluish, well-rounded, smooth-surfaced bulge that protrudes from one side of the
mouth floor. It characteristically occurs UNILATERALLY in the floor of the mouth. Arises in association
with secretory ducts of the SUBMANDIBULAR or SUBLINGUAL GLANDS, and is usually caused by an
obstruction due to a salivary stone or soft organic substance.

236
• A history of increased size just before or during a meal, and decrease in size between meals is NOTES
of diagnostic significance.

• Treatment: surgical by com plete excision or by removing the roof of the cyst. If it persists, excision
of the gland may be needed.

MIKULlCZ'S DISEASE ("BENIGN LYMPHOEPITHELIAL LESION") - rare salivary gland lesion,

closely related to Sjogren's Syndrome, manifested as a progressive, asymptomatic enlargement of
the PAROTID & SUBMANDIBULAR glands. It is initially unilateral, but over time becomes bilateral. Its
etiology is unknown, but there is increasing evidence that both Mikulicz's & Sjogren's syndrome are
actually autoimmune diseases where the patient's own salivary gland tissue becomes
antigenic.Occurs most often in MIDDLE-AGED WOMEN.

• Histologic Features: replacement of gland parenchyma by lymphocytic infiltrate that contains

scattered epimyoepithelial islands within (this is the histologic cornerstone for the diagnosis).

• Most lesions are BENIGN, but malignant transformation of the epimyoepithelial islands may occur.

Clinical Features of MALIGNANT Salivary Gland Tumors: painful, ulcerated mucosa, nodular, firm ,
fixed, rapid growth, invasion, immovable, metastasis, and not well-differentiated (anaplastic) .
Metastasis is the most important characteristic that distinguishes a malignant tumor form a benign
tumor. Paresthesia is suggestive of metasatic disease.

• Histologic Features of Malignancy: anaplasia, abnormal mitosis, pleomorphism, hyperchromatism,

increased nuclear-cytoplasmic ratio.

• Host response to a malignancy is best reflected by lymphocytic infiltration at the edge of a tumor.
The most characteristic feature of a malignancy ratherthan an inflammatory lesion, is the malignancy
will grow after the causative agent is removed. The most important characteristic of malignant
neoplasms that distinguishes them from benign neoplasms, is the malignancy's ABILITY TO
METASTASIZE.

• Histologic Grading of Malignant Neoplasms: attempts to estimate the aggressiveness of degree of

malignancy of a malignant neoplasm based on the degree of differentiation of the component cells
and number of mitoses. This grading is mainly applicable to squamous cell carcinomas, and is of
limited clinical use. Most pathologist use 3 grades, and prefer to designate squamous cell
carcinomas as well-differentiated, moderately well-differentiated, or poorly differentiated.
1. Grade 1 = well-differentiated.
2. Grade 2 = moderately well-differentiated.
3. Grade 3 = poorly undifferentiated.
4. Grade 4 = undifferentiated.

Malignant Salivary Gland Tumors:

1. Adenocarcinoma (NOS not otherwise specified)-affects major salivary glands (50%) & minor
glands (50%). Its frequency is 25% minor glands, 5% submandibular glands, and 3% of parotid
tumors. Usually presents as an asymptomatic mass. There is an 80% survival rate for low-grade
carcinoma, and 40% survival rate for high-grade carcinoma.

2. Adenoid Cystic Carcinoma-a malignant salivary gland tumor that most often affects minor
salivary glands of the palate (70%), parotid gland (15%), and submandibular gland (14%).
Represents 31 % of minor salivary gland tumors, 14% of submandibular gland tumors, and 2%
of parotid gland tumors. Patient presents with pain and/or nerve dysfunction in 25%-33% of
patients. Facial weakness or paralysis is common. Often slow, but relentless in progression of
disease, with a 20% twenty year survival rate.

3. Acinic Cell Carcinoma-a malignant salivary gland tumor most likely associated with the
parotid gland (96%), submandibular gland (2-3%), and minor salivary glands of the palate (1-
2%).2-4% of parotid tumors are acinic cell carcinoma. Patient presents with swelling, pain, or
tenderness, and may have facial weakness or paralysis. 90% cure rate.

237
r - ... _--- ------------- .- -----------------------~

4. Mucoepidermoid Carcinoma-usually occurs in the parotid gland (SO%), palate (13%), &
submandibular gland (6%). Represents 10% of minor salivary gland tumors, 6% of parotid
tumors, and 5% of submandibular tumors. Patient usually has asymptomatic swelling, with a
peak incidence in the Jed decade of life (30s). Patient may have facial weakness or paralysis.
Low-grade carcinomas have an 85-100% 5-year cure rate, while high-grade carcinomas have a
20-45% 5-year cure rate .

Metabolic Conditions Associated with Chronic Salivary Gland Enlargement: diabetes mellitus,
chronic alcoholism, malnutrition (anorexia & bulimia) , obesity, hypertension, & hyperlipidema. Not
hypothyroidism. PAROTID GLAND is most frequently enlarged (either unilaterally or bilaterally).
Other conditions associated with parotid gland enlargement:
1. Sjogren's Syndrome & Sarcoidosis
2. Warthin's tumor (Papillary Cystadenoma Lymphomatosum).
3. Infections (mumps, actinomycosis, tuberculosis).
4. Benign Lymphoepithelial Lesion (Mikulicz's Disease) .
5. Acute Epidemic Parotitis.
S. Ma Inutrition.

SJOGREN'S SYNDROME - a salivary gland disorder of unknown cause, but is autoimmune in

nature. Marked mainly by chronic inflammation of the salivary and lacrimal glands, that usually
progresses to fibrosis and atrophy of these glands. Most commonly affects post-menopausal
c:> women who present with dry eyes, dry mouth, with -50% of cases, having BILATERAL enlargement of
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r- the parotid & submandibular glands.
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• Symptoms: rheumatoid arthritis, xerostomia (dry mouth), & keratoconjunctiva sicca (dryness of
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the eyes). However, al13 symptoms rarely occur in one patient. The decrease in salivation may cause
rampant caries reminiscent of radiation caries.

• Histologic Features: the histological features of the salivary gland lesions in Sjogren's Syndrome &
Benign Lymphoepithelial Lesion (Mikulicz's Disease) are identical.

• Treatment: treatment is mainly symptomatic. The keratoconjunctivitis is treated with ocular

lubricants, and xerostomia is treated with saliva substitutes (artificial saliva). Biopsy of the labial
or palatal salivary glands, sialograms, salivary flow rate tests, and blood work may help to establish
a diagnosis. However, radiation, surgical excision, and chemotherapy is NOT used as treatment.

• Malignant lymphomas &"Pseudolymphomas" ("Atypical Benign Lympohiod Hyperplasia") develop

in some patients diagnosed with Sjogren's Syndrome. Thus, the requires close follow-up of patients.

XEROSTOMIA (DRY MOUTH) - is not a disease, but is a symptom of certain diseases. Xerostomia
is caused by sialadenitis (an insidious inflammatory disease of the major salivary glands), Sjogren's
syndrome, medications (i.e. anticholinergic drugs (Atropine & Scopolamine) & antipsychotics
(Phenothiazines: Chlorpromazine & Prochlorperazine), cancer therapy, nerve damage, and conditions
like Alzheimer's, stroke, bone marrow transplants, endocrine disorders, stress, anxiety,
depression, and nutritional deficiencies. Xerostomia is often caused by failure of the salivary glands
to function normally, but it may also occur in people with normal salivary glands. Xerostomia can
cause health problems by affecting nutrition, and psychological health. Extreme cases can cause
rampant tooth decay and periodontal disease.

OCCLUSAL RADIOGRAPHS - are useful for locating SIALOITHS (salivary calculus or salivary
stones) in WHARTON'S DUCT (SUBMANDIBULAR DUCT). The deposition of calculus in the salivary ducts
and glands becomes more common as we reach middle-age. The most common symptoms of an
obstruction is an increase and decrease in swelling of the gland (especially at mealtime) . The swelling
mayor may not be painful, and may occur in children too. Transillumination of the soft tissue is useful
to detect sialolithiasis in children.

• Rate of occurrence in the SUBMANDIBULAR GLAND &DUCT is much higher than in the parotid or
sublingual glands due to the submandibular saliva's tenacity, and long, irregular shape of the duct.

238
• Treatment of choice is surgical extirpation of the sialolith. Salivary stones located in the glandular
parenchyma also usually require removal of the gland .

• Occlusal radiographs are not useful for locating Sialoliths in Stensen's duct, identifing the mental
foramen or hyoid bone.

ONCOCYTOMAS ("OXYPHILIC/ACIDOPHILIC ADENOMA") - a small, benign RARE glandular

tumor composed of large cells with a granular &eosinophilic cytoplasm due to the presence of
many mitochondria. Can occur in the kidney, salivary glands, & endocrine glands. Its development
may be related to the AGING PROCESS.

• Clinical Features: most commonly seen in the parotid glands of patients over age 50 (slightly more
common in women). Their growth is slow, and they rarely reach any significant size.

• Histologic Features: the tumor is an encapsulated mass composed of relatively large cells with
BRIGHT PINK CYTOPLASM and small, round nuclei. The cells may be arranged in sheets or cords, or
form tubular or acinar structures.

• Treatment: surgical excision; recurrence is rare.

• Sialoscintigraphy-a simple, non-invasive procedure that can usually separate benign entities like
Warthin's tumor & Oncocytoma of the salivary glands from malignant tumors, and greatly affects
the course of treatment.

WARTHIN'S TUMOR ("PAPILLARY CYSTADENOMA LYMPHOMATOSUM") - neoplasm almost

exclusively found in the PAROTIO GLAND, arising from heterotopic ductal epithelium within lymph
nodes or near the parotid gland .

• Clinical Features: most patients are over age 50 (5: 1 male predominance). -5% of the tumors are
bilateral (95% unilateral). The tumor most often arises in the lower pole of the parotid as a non-
tender, slowly enlarging, firm-to-fluctuant nodule over the ANGLE or RAMUS OF THE MANDIBLE.

• Histologic Features: tumor is encapsulated and composed of cystic spaces containing an

eosinophilic coagulum into which extend papillary projections of the lining epithelium . The
epithelium consists of a double row of cells with eosinophilic, granular cytoplasm, a luminal layer of
tall columnar cells, and a basal layer of round, cuboidal, or polygonal cells. Interspersed among the
cystic spaces are aggregates of lymphoid tissue (some with germinal centers).

• Treatment: surgery; recurrence is uncommon. Malignant variants of the tumor have been reported,
but are rare.

PLEOMORPHIC ADENOMA ("BENIGN MIXED TUMOR") - the MOST COMMON tumor of the
major &minor salivary glands. The term "mixed tumor" is used because the neoplasm is believed to
be of both ectodermal &mesenchymal origin.

• Clinical Features: MOST COMMON SALIVARY GLAND NEOPLASM. Affects more women than men (most
patients between 40-60yrs) . -93% arise in MAJOR salivary glands (these are almost exclusively
PAROTID neoplasms (84%). Present as painless lumps below and anterior to the ear. -7% arise
in the oral cavity with the palate being by far the most common intra-oral site where they appear as
firm, painless swellings, and in most cases, do not cause ulceration of the overlying mucosa.

• Histologic Features: the epithelial component consists of round, polyhedral, elongated, or stellate
cells that are relatively small and stain uniformly. The mesenchymal component varies from areas
of myxomatoid tissue, to areas of dense, hyalinized C.l, pseudocartilage, or bone.

• Treatment: Pleomorphic Adenomas are invariably encapsulated or well-demarcated, and surgical

excision with a generous margin of normal tissue is the treatment of choice. Inadequate initial
removal of the mixed tumor in major salivary glands may cause recurrence. -25% of benign mixed
tumors undergo malignant transformation if the lesions are untreated for an extended period of time.
239
 ULCERATIVE CONDITIONS
STEVENS-JOHNSON SYNDROME - a severe bullous form of Erythema Multiforme where
systemic symptoms are severe, and lesions are extensive, involving multiple body areas (especially
mucous membranes). SJS is characterized by the acute onset of fever, and eruptive, ulcerative lesion
on the skin, oral mucosa, and eyes. Frequently, the genitalia, lungs, and joints are affected , and it can
be fatal. Blindness can occur due to a secondary infection.

• Clinical Features: typical "BULL'S-EYE-SHAPED" LESIONS with the classical triad of eye lesions,
genital lesions, & stomatitis. The lesions are severe and often vesicular or bullous, with hemorrhage
after denudation.

• Treatment: IV fluids, systemic steroids, palliative rinses and antibiotics.

ERYTHEMA MULTIFORME - a type of allergic hypersensitivity reaction in response to

medications, infections, or illness. Medications associated with erythema multiforme include
sulfonamides, penicillins, barbiturates, & phenytoin. Associated infections include herpes simplex &
mycoplasma infections. The exact cause is unknown, but is believed to involve damaged blood vessels
of the skin with subsequent damage to shin tissues. It occurs mainly in children and young adults, and
its diagnosis is primarily based on the classic TARGET OR "BULL'S-EYE-SHAPED" SKIN LESION that
appears as a central lesion surrounded by concentric rings of pallor and redness over the dorsal
aspect of the hands and forearms.

• A low-grade fever, general malaise, and headache usually precede the appearance of the lesions by
4-7 days.

• Oral lesions appear as red macules, papules, or vesicles that may become eroded and painful.
These lesions are covered by a yellowish-white membrane after rupturing.

• Treatment: topical palliative rinses and sometimes low-dose systemic steroids.

RECURRENT APHTHOUS/ULCERATIVE STOMATITIS ("RECURRENT APHTHOUS ULCERS"

OR "CANKER SORES") - appear to be associated with STRESS such as a bacterial infection,
trauma (self-inflicted, oral surgery procedures, routine dental procedures), endocrine conditions
(menstrual cycle) , allergic factors (certain foods or drugs), immunologic abnormalities, iron, vitamin
B, or folic acid deficiencies. Cause is unknown, but they may be caused by an autoimmune reaction.

1. Recurrent aphthous minor-most common form of the disease, referred by the lay public as a
"canker sore". The lesion occurs somewhat more frequently in women than men, beginning as a
single or multiple superficial erosion covered by a gray membrane (1-5 lesions). The lesion is
usually VERY PAINFUL, and varies from 2-3mm, to over 10mm in diameter. The lesions generally
persist for 7-10 days, and heal gradually with little or no evidence of scarring.

2. Recurrent aphthous major-characterized by the occurrence of large, 1-10 painful ulcers that
occur at frequent intervals and many patients with this disease are seldom free from the presence
of at least one ulcer. Unlike the minor aphthous ulcer, these lesions persist for up to 6 weeks and
leave a SCAR upon healing.

3. Recurrent herpetiform-characterized by crops of multiple, small, shallow ulcers, often up to 100

in number, and may occur in any area of the oral cavity. These lesions are present almost
continuously for 1-3 years, with relatively short remissions.

Important: vesicular lesions (vesicles) DO NOT PRECEDE the formation of these ulcers. This is a
distinctive diagnostic feature . In healing of an ulcer, the epithelium that will eventually cover the
defect is derived from intact epithelium at the ulcer margin .

GRANULOMATOUS INFLAMMATION - a subtype of chronic inflammation cha racterized

morphologically by granulomas.
240
• Granulomas-nodules of epithelioid cells that are modified macrophages with abundant eosinophilic NOTES
cytoplasm, usually < 2mm in diameter, surrounded by lymphocytes, plasma cells, and fibroblasts.

• Granulomatous infections include:

• Mycobacterial Diseases (Tuberculosis & Leprosy).
• Fungal Diseases (Histoplasmosis, Blastomycosis, &Coccidioidomycosis).
• Parasitic Diseases (Schistosomiasis).
• Syphilis (primary, secondary, or tertiary) & Cat-Scratch Disease.
• Silicosis &Berylliosis-granulomatous lung diseases produced by the occupational
exposure to dusts.
• Sarcoidosis-a chronic disorder of unknown etiology characterized by the formation of tubercles of
non-necrotizing epithelioid tissue.

ACUTE INflAMMATION - is involved with PNEUMONIA where there is purulent exudates in

response to a bacterial infection.

ACTINOMYCOSIS - a subacute-to-chronic bacteria infection with Actinomyces (usually A. israelii)

which are gram (+) filamentous bacteria that are normal inhabitants of the oral cavity and GI tract,
characterized by contiguous spread, suppurative &granulomatous inflammatory reaction, and
formation of multiple abscesses and sinus tracts that discharge SULFUR GRANULES. This infection is
the infection most likely to result in CHRONIC SUPPURATIVE LESION about the jaws. The most common
clinical forms are cervicofacial (i.e. lumpy jaw), thoracic, and abdominal actinomycosis.

CERVICOFACIAL ACTINOMYCOSIS (''lUMPY JAW") - the most common manifestation of

Actinomycosis. Infection typically occurs in patients with poor dental hygiene or after surgery. In the
initial stages, there is soft tissue swelling of the perimandibular area . Direct extension into the adjacent
tissues occurs over time, along with the development of fistulas that discharge purulent material
containing yellow sulfur granules (these granules are actually colonies of infecting organisms).

HISTOPLASMOSIS - disease caused by the fungus Histoplasma Capsula tum. Its symptoms vary
greatly, but this disease primary affects the lungs. Occassionally, other organs are affected (this form
is Disseminated Histoplasmosis). The infection is usually asymptomatic, but may produce a benign,
mild pulmonary illness (the primary form of the disease).

• Oral Manifestations: nodular, ulcerative, or vegetative lesions on the buccal mucosa, gingiva, tongue,
palate, or lips usually covered by a non-specific gray membrane and are indurated.

MUCORMYCOSIS ("PHYCOMYCOSIS/ZYGOMYCOSIS") - infection caused by a water mold

fungus (Mucorales).

• Rhinocerebral Mucormycosis-mucormycosis of the nose & brain that is a severe and usually fatal
infection, seen mainly in patients with chronic debilitating diseases (especially Diabetes Mellitus).
Symptoms: pain, fever, an eye socket infection (Orbital Cellulitis) with a bulging of the affected eye
(Proptosis). The nasal septum, palate, or sinuses may be destroyed. A brain infection may cause
convulsions, inability to speak properly, and partial paralysis.

• Treatment: administration of Amphotericin B given IV or injected directly into the spinal fluid.

SYPHILIS - a sexually transmitted disease caused by a spirochete Treponema Pallidum that occurs
in 3 stages (primary, secondary, &tertiary). Syphilis is usually treated with Penicillin administered
via an injection.

1. Primary Syphilis-the first symptom of primary syphilis is a non-painful ulcer ("chancre") that
appears 2-6 weeks after exposure/infection. It is usually found on the part of the body exposed
to the partner's ulcer (i.e. penis, vulva, or vagina). It can also develop on the cervix, tongue, lips,
or other parts of the body. The chancre disappears within a few weeks, even if the person is not
treated. If not treated during the primary stage, -33% of people will progress to chronic stages.

241
 2. Secondary Syphilis-a highly infectious stage that occurs 6 weeks after non-treatment of primary
syphilis. It is often marked by a skin rash characterized by brown "penny-sized" sores. Widely
disseminated spirochetes cause mucous membranes to exhibit a reddish-brown maculopapular
cutaneous rash and ulcers covered with a mucoid exudates (mucous patches). Condylomata lata
(elevated broad-based plaques) are also seen on the skin and mucosal surfaces.

3. Tertiary Syphilis-occurs in infected people many years after non-treatment of secondary syphilis.
A GUMMA (a focal nodular mass) typifies this stage. Most commonly occurs on the PALATE &
TONGUE. Bacteria damages the heart, eyes, brain, nervous system, bones, joints, or almost any
other part of the body. In this late stage, untreated syphilis, although not contagious, can cause
serious heart abnormalities, mental disorders, blindness, other neurologic problems, and
death. Headache, stiff neck, and fever are symptoms of neurosyphilis.

CONGENITAL SYPHILIS - caused by an infection by the spirochete Treponema Pallidum during

the fetal period. Expectant mothers with syphilis can transmit the disease through the placenta to the
unborn infant. Nearly 50% of all infants infected during gestation die shortly before or after birth. The
severity of congenital syphilis depends on the time that the organisms pass the placental barrier
(protected up to the 16 th week), the mother's stage of syphilis, and the fetus's immunologic response.
If treated by the 4th or 5th month, 95% show no manifestations. However, if untreated, fetal sepsis
may result in stillbirth or visceral & mucocutaneous manifestations.

c::> • Newborn Symptoms: irritability, blood discharge from nose, early rash (small blisters or flat or bumpy
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:!:i and soles), saddle nose, frontal bossing, short and high maxilla .
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." • Older InfantIYoung Child Symptoms: bone pain, joint swelling, abnormal teeth (Hutchinson's incisors)
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permanent incisors that are usually peg-shaped, widely spaced, and notched at the end with a centrally
placed crescent-shaped deformity. Also gray, mucous-like patches on the anus and vulva (Condyloma
lata), saber shins (bone abnormality of the lower leg), visual loss, CN VIII nerve deafness & intestinal
keratitis, and scarring of the skin around earlier lesions of the mouth, genitalia, and anus ("rhagades").

• Sequela of congenital syphilis: Big frontal bone, Saddle nose, Hutchinson's teeth (very wide incisor
crowns), & mulberry molars-looks like a mulberry. Not all people with mulberry molars have
syphilis. There is NO chancre in congenital syphilis.

VESICULO-BULLOUS DISEASES
HERPES SIMPLEX VIRUS - always a vesicle (small virus full of fluid) that when it breaks, the
crust forms due to dried fibrin. Herpes simplex is related to viruses that cause Mononucleosis,
Chickenpox, and Shingles (not Mumps). HSV is one of the most common viral diseases affecting man.

HERPES SIMPLEX VIRUS TYPE 1 - oral herpes (affects outside of lips, face, skin, & oral
mucosa) TRANSMITTEO BY DIRECT CONTACT. HSV 1 includes herpetic gingivostomatitis (primary &
secondary, and herepes labialis). It is labial & intra-oral herpes that are groups of small ulcerations in
the hard palate, outside of lips, gingiva, or hands and fingers. HSV-l causes these different types of
oral or para-oral presentations:

• HSV Treatment: is primarily "SUPPORTIVE" and is focused on relieving the acute symptoms so that
fluid and nutritional intake can be maintained. Treatment involves analgesics, topical anesthetics
prior to eating, maintain electrolyte balance, and antiviral agents. Corticosteroids are
contraindicated in patients with HSV infections.

242
 1. Primary Herpetic Gingivostomatitis (Acute Herpetic Gingivomatitis)-the primary herpes
infection generally affects young children (under age 5), but may also affect young adults
(15-25yrs). It usually occurs in a child who has not had any contact with the Type 1 HSV, and
who thus has no neutralizing antibodies. Nearly all primary infections are of the subclinical
type that may only have flu-like symptoms, with 1 or 2 mild sores in the mouth that
go unnoticed by parents. In other children, the primary infection may be manifested by
acute symptoms (known as acute herpetic gingivostomatitis) these prodromal symptoms include
(fever, malaise, irritability, headache, dysphagia, vomiting, cervicallympadenopathy) 1-2 days
prior to local lesions. Then, fiery red gingival tissues and small yellowish vesicles form that
rupture quickly, causing painful shallow, round, discrete ulcers with an erythematous (red) halo
on the FREE & ATTACHED MUCOSA. Thus, the primary infection of HSV1 can range from
subclinical (asymptomatic) to severe systemic infections. Dehydration is the most serous
potential problem that can occur due to the child not wanting to eat or drink because of the pain.
Ageneralized marginal gingivitis may precede the ulcers.

• Primary Herpes is most common in CHILDREN &YOUNG ADULTS. These patients develop
fever, irritability, regional lymphadenopathy, and headache. Within days, the gingiva becomes
intensely inflamed. Any part of the oral mucosa and lips may become involved. Vesicles then
form and rupture shortly later to leave shallow VERY PAINFUL ulcers covered with a GRAY
MEMBRANE and surrounded by a RED HALO. The ulcers heal on their own in 7-14 days.

• Treatment: fluid intake, good oral hygiene, and gentle debridement of the mouth. In healthy
individuals, the lesions heal spontaneously in 7-14 days (usually runs a course of 12-20 days)
and the ulcers heal without scarring.

• After recovery from primary HSV infection, the virus is not cleared from the body, but lies
dormant in a non-replicating state in the sensory nervous system (trigeminal ganglion).
Periodically, latency reactivates and allows the virus to return to the skin or mucous
membranes, where it causes a recurrent infection .

• Primary herpes occurs only in YOUNG PATIENTS (baby, children, adolescents). Fever, malaise,
pain, or could be CHICKENPOX (varicella zoster virus) in a 6yr old child. Multiple vesicles,
sick for 1 week.

AFTER the initial primary attack during the early childhood, herpes simplex virus remains inactive
(inactive form) most commonly in the CN VTRIGEMINAL GANGLION (sensory nerve ganglia), but
often reappears later as the familiar "cold sore" on the OUTSIDE of the lips ("Recurrent Herpes
Labialis"). Emotional stress, trauma, and excessive sun exposure are factors that cause recurrent
herpetic lip lesions. Acyclovir 5% ointment (Zovirax) can successfully reduce the duration and
severity of these lip sores.

2. Secondary (Recurrent) Herpetic Stomatitis-generally occurs in ADULTS, triggered by trauma,

fatigue, URI, stress, allergy, or UV exposure that causes the release/reactivation of the latent
HSV-1 virus. This reactivation causes a recurrent infection (i.e. cold sores) on the lips (that is
bound to periosteum), hard palate, attached gingiva, and alveolar ridge. Site-specificity is a
characteristic manifestation.

• Recurrent Herpes Simplex Virus-cold sores are the most common manifestation of infection
and usually occur on the lips. Some factors often associated with a recurrent outbreak are
sunburn, fatigue, emotional upset, trauma, upper respiratory tract infection, or menstruation.
Often 1 day before the formation of vesicles, a tingling or itching of the skin or mucosa occurs.
Vesicles ulcerate and resolve just like in primary herpes.

• Recurrent Herpes remains LOCALIZED. Most common in lower lip or inside mouth. Lasts -2
weeks then heals by itself, but recurrent herpes virus always lays dormant in the trigeminal
nerve ganglion. Mayor may not have fever, malaise. Vesicles in hard palate .

• Ayoung boy has a very sore mouth, general malaise, and an oral temperature of 102°F, the
most probable diagnosis is Herpetic Stomatitis.

243
 NOTES 3. Herpes Labialis (Fever Blisters or Cold Sores}-an extremely common disease caused by Herpes
Simplex Virus Type l. Characterized by an eruption of small, usually painful blisters on the skin
of the lips, mouth, gingiva, or skin around the mouth. The reason most patients suffering from
Recurrent Herpes Labialis rarely give a history of having had acute herpetic gingivostomatitis is
that the primary infection was subclinical. Herpes Type 1 lesions (cold sores) are found more
forward in the mouth (tongue, gingiva, buccal mucosa) appearing as vesicles (small, clear,
ulcerated, and crusty blisters) around the mouth and on the lips.

• Histologically, the cytopathic effect (CPE) takes the form of BAllOONING DEGENERATION of
the epithelial cells with loss of cohesion to adjacent cells. The nuclei are often multiple,
with margination of the chromatin around the intra-nuclear inclusions called Lipschultz
Bodies. These changes are seen in Tzanck smear scrapings taken from an unroofed vesicle.

HERPES SIMPLEX VIRUS TYPE 2 ("HERPES GENITALlS" OR "GENITAL HERPES")-

transmitted via SEXUAL CONTACT, and affects the mucosa of the genitalia and anal regions, but may
also occur in mouth. Not as common as HSVl. "Genital Herpes" may have serious consequences in
pregnant women because the virus can be transmitted to the infant during vaginal delivery, and can
damage the infant's CNS and/or eyes.

HERPES SIMPLEX VIRUS TYPE 3 - caused by Herpes varh:ella-zoster virus (Does not cross the
midline and is very painful). Produces recurrent herpes (adult shingles/herpes zoster), &
chickenpox (primary herpes). Occurs after activation of varicella virus, the affected skin shows
redicule vesicles, and the lesion follows the path of the trigeminal nerve. NOT on both sides of the
face as it only goes to the midline. May occur in an elderly patient with history of leukemia
(compromised immune system). Presents with area of ulcerations and very painful crusts.

VARICELLA VIRUS - can cause Herpes Zoster lesions along sensory nerve roots in later life. It is
a member of the herpes virus group that causes chickenpox (varicella) &shingles (herpes zoster).
Varicella virus is highly contagious and may be spread by direct contact or droplets. The histology of
chickenpox and shingles shows the same cytopathic effect as herpes simplex.

1. Chickenpox-primarily a disease of childhood that peaks at school-age in winter and spring,

characterized by the appearance on the skin and mucous membranes of successive crops of
typical pruritic vesicular lesions that break easily and scab. It is usually accompanied by mild
constitutional symptoms (fever, malaise), and is most contagious 1 day before the rash's onset
and until all of the vesicles have crusted. It is relatively benign in children, but adult infection
may be complicated by pneumonia and encephalitis. ZIG (Zoster Immune Globulin) reaches
morbidity in high-risk children.

2. Shingles (Herpes Zoster}-caused by the reactivation of a LATENT varicella-zoster virus that

may have remained in the body from a childhood chickenpox. The virus reaches sensory ganglia
of the spinal and cranial nerves, producing an inflammatory response. Characterized by painful
vesicles on the skin or mucosal surfaces along the distribution of the sensory nerve.
• Herpes Zoster (Shingles}-16-yr old male with fever &malaise, DOES NOT CROSS THE MIDLINE,
and is very painful. Can also be in a 65-year old male with a history of leukemia (weak immune
system) who had chickenpox as a child. The affected skin shows vesicles and lesions follow the
path of the nerve due to activation of varicella virus.

HERPES SIMPLEX VIRUS TYPE 4 - caused by Epstein-Barr Virus (EBV) a member of the herpes
virus group that causes Infectious Mononucleosis (kissing disease), Hairy leukoplakia, & Chronic
fatigue syndrome, and two forms of cancer (Burkitt's Lymphoma & Nasopharyngeal Carcinoma).

1. Hairy Leukoplakia-this is NOT hairy tongue. Appears 99% of time in HIV+ patients. ALWAYS
white furry lingual lesions on LATERAL tongue borders (bilateral) caused by EPSTEIN-BARR
VIRUS. Can do a biopsy, but can usually diagnose without biopsy. Anti-viral medication removes
the lesion, but it reappears when patients stops taking medications. So only treat if the patient
requests. Presents as a WHITE extensive area in the LATERAL border of the tongue, present for 4
months, asymptomatic. The surface lesion is irregular, bluish areas on the gingiva, candida, and
recurrent herpes infection may coexist. 99% occurs in HIV+ patients, so patient should get
244 an HIV test.
 2. Infectious Mononucleosis-has no specific oral manifestations, but secondary lesions occur and NOTES
neck swellings. Neck swellings are also characteristic of Hodgkin's Disease and Tuberculosis.

3. BURKITT'S LYMPHOMA-a high-grade Non-Hodgkin's Lymphoma (cancer)/neoplasm with a viral

etiology that is endemic in Africa, but occurs only sporadically in North America. There are
significant differences between the African &Non-African forms, but BOTH are histologically
identical. One is manifested most often as a large osteolytic jaw lesion (African Form), the other
as an abdominal mass (Non-African Form). EPSTEIN-BARR VIRUS is implicated in this cancer.

• African Burkitt's Lymphoma (African Jaw Lymphoma)-patients are younger (age 3-8yrs)
than the non-African form. Affects male more than females (2:1), & typically involves the
jaws mandible, maxilla, &abdomen. Extranodal involvement of the retroperitoneum, kidneys,
liver, ovaries, and endocrine glands may be affected .

• Jaw lesions usually present as expanding intraoral masses with mobility of the involved
teeth. Radiographically, there is a "MOTH-EATEN", poorly marginated destruction of bone.

• Non-African Burkitt's Lymphoma-patients are generally older (ages 9-12yrs), with no

gender/sex predilection. It presents most often as an ABDOMINAL MASS involving
mesenteric lymph nodes or Peyer Patches in the ileocecal region, often with intestinal
obstruction. Involvement of the gonads, retroperitoneum, and other viscera are less common.

Burkitt's lymphoma is the FIRST HUMAN CANCER WITH STRONG EVIDENCE OF VIRAL ETIOLOGY.
Epstein-Barr virus (herpes-type virus) has been isolated from cultures of tumor cells and patients
with Burkitt's lymphoma have high titers of antibodies against EBV. Also, an antibody against a
surface antigen on the tumor cells has been shown. Important: Epstein-Barr Virus is also associated
with infectious mononucleosis, & orally hairy leukoplakia.

HERPES SIMPLEX VIRUS TYPE 5 - cytomegalovirus affects salivary glands.

HERPES SIMPLEX VIRUS TYPE 8 - associated with Kaposi's sarcoma-AIDS/HIV. Kaposi

Sarcoma: 34-year old male with AIDS, common on palate. Can have Kaposi Sarcoma without AIDS,
but in U.S. it is usually with AIDS. It is a superifical cancer on the skin, multiple, made of blood
vessels, &is NEGATIVE to pressure test (so do not confuse with Hemangioma which is + to
pressure test). Palate is a very common place for Kaposi's sarcoma. Mostly associated with HIV, but
can have Kaposi's sarcoma even without AIDS. (-) to pressure test. Red lesions on hard palate.

KAPOSI'S SARCOMA - an oral manifestation most commonly associated with AIDS. It is a

MALIGNANT NEOPLASM originating in the skin, characterized by abnormal vascular proliferation
(its cancer of the lining of the blood vessels). It occurs on multiple sites, especially lower extremities.
The initial lesions are small, red papules that enlarge and fuse to form purple-to-brown spongy
nodules. It spreads to lymph nodes and internal organs.

• Intraorally, the HARD PALATE is the most common location, followed by the gingiva &
buccal mucosa.

• Important: AIDS is caused by the RNA retrovirus (HIV = HTLV-III) acquired by sexual contact
(homosexual & heterosexual), or from contaminated blood products.

Tests To Diagnose Herpetic Lesions:

1. Tzanck Smear-a cytologic examination of fluid harvested from an unopened vesicle stained with
giemsa, and viewed by the light microscope. The pathologist looks for epithelial cells with
intranuclear inclusions called Lipshultz Bodies).

2. Fluorescent Staining-cells show (+) fluorescence when stained with fluorescent labeled HSV
immune serum and globulin. This procedure is used to distinguish between herpes loster &
herpes simplex.

3. Isolation in Tissue Culture

245
 NOTES 4. Antibody Titers (Anti-HSV Ab Titers)-a test for complement fixing or neutralizing antibody in acute
and convalescent sera, and on tissue sections (this begins in 1 week, and peaks in 3 weeks).

5. Biopsied Material-shows an intra-epithelial cleft covered by an exudates of fibrin &PMN

leukocyte. The epithelium exhibits degenerative cells that include bizarre giant cells, and cells
with displaced chromatin with perinuclear halos and inclusions. *An Arthrogram is NOT a
diagnostic test to diagnose herpetic lesions.

HERPANGINA - an acute infectious disease that affects YOUNG CHILDREN caused by a Group A
Coxsackie Virus. It is a stomatitis (inflammation of the mouth) caused by a strain of Coxsackie virus.
It is differentiated in clinical practice from Type 1 Herpes (cold sore virus) since herpangina oral
ulcerations usually occur in the back of the throat around the tonsils and rear portion (posterior) of the
palate. The oral lesions/vesicles may also appear on the tongue.

• Clinical Features: are mild and of short duration compared to Type 1 Herpes. Herpangina begins
with a sore throat, fever, headache, and sometimes vomiting & abdominal pain. Papules or vesicles
soon form in the pharynx, and evolve into shallow ulcers that heal spontaneously. Herpangina usually
runs its course in less than 1 week. Treatment: palliative.

HAND, FOOT & MOUTH DISEASE - a VIRAL INFECTION that produces red-erythematous
lesions/macules/vesicles areas in the mouth, foot, &hands, but usually goes undiagnosed. Oral
lesions/vesicles appearing on buccal mucosa, tongue, gingiva, &lips.

• Patient has fever & malaise (may be confused with a cold). HFMD is self-limiting, disappears by itself
in < 15 days, & will not return. Erythematous macules that develop central vesicles. HFMD can occur
in ch ildren. Patient will have the antibodies. It is a very mild disease that not many people notice
because it is often not diagnosed.

BENIGN MUCOUS MEMBRANE PEMPIGOID (BMMP) - is a chronic self-limiting

mucocutaneous autoimmune disease, usually limited to oral and ocular mucous membranes
(conjunctival involvement may cause blindness). Usually effects women over age 50yrs. It is more
common in the oral cavity, but causes much less morbidity and mortality (has a better prognosis) than
Pemphigus. It occurs more often than realized due to improper diagnosis.

• Avesiculobullous disease where auto-antibodies act against basement membrane components

(BELOW the epithelium = subepithelial vesicle), between epithelium &C.T. so destruction is below
the epithelium. Usually shows nice epithelium since the epithelium is complete & C.T. is separated
(not seen in Pemphigus).

• Oral lesions usually present as a "desquamative gingivitis" in which vesicles form, rupture, and
leave gingival erosions. Found in all mucous membranes, but is less severe than Pemphigus.

• Treatment: biopsy and systemic STEROID therapy. Painful ulcers in mouth.

Important: MAJOR histological difference between BMMP &Pemphigus Vulgaris is BMMP vesicles
are subepidermal with no acantholysis. However, in Pemphigus Vulgaris, there is acantholysis &a
supra basilar vesicle.

PEMPHIGUS VULGARIS - a chronic RARE skin disease characterized by the formation of

vesicles &bullae produced by dyhesion (acantholysis) of epidermal cells due to an autoimmune
mechanism where antibodies attack the intracellular junction of epithelium . It rarely occurs before age
30yrs (usually ages 30-50yrs), and occurs more frequently in JEWISH people.

• Oral lesions are often the FIRST MANIFESTATION. Intact bullae are rarely seen in the oral cavity,
rather, large areas of ulceration and erosions are often seen covered by a white or blood-tinged
exudates. Sometimes, areas of epithelium will slide off simply by rubbing of an apparently unaffected
area (Nikolsky's Sign-an indication of Pemphigus vulgaris that may also be found in BMMP. This
sign occurs when apparently normal epithelium may be separated at the basal layer and rubbed
off when pressed with a sliding motion). Pemphigus is often fatal without treatment, which includes
246 high-dose systemic steroids or chemotherapy (Le. Methotrexate).
• Histologic Features: vesicles and bullae are formed entirely intraepithelially, just above the basal NOTES
layer of cells (supra basilar vesicles) . There is intercellular edema &loss of intercellular bridges
with loss of cohesiveness (acantholysis or dyhesion). Clumps of cells are often found floating free
in the vesicle space (Tzanck cells) .

• Pemphigus Vulgaris is the most common form, and is more severe than Pemphigoid (BMMP). With
Pemphigus, the patient has auto-antibodies produced against epidermal cell surface glycoprotein
(a component of desmosomes that attaches epithelial cel ls together) causing painful ulcers in the
mouth. More common in older females (> 50yrs). Intraepithel ial vesicle. Avery bad disease whose
only treatment is steroids. Patient has vesicles on skin , GINGIVA is red , inflamed and is the most
common location in mouth.

• Due biopsy, need 2 small portions of tissue (1 in a vile, the other goes into a vile of Michel solution
(the fixative to do the immunofluorsence). If bullae is intraepithelial then its Pemphigus Vulgaris.
If bullae are between epithelial &C.T. it is Pemphigoid. Produce Ab against desmosomes (attach
one epithelial cell to another), so desmosomes are destroyed and the epithelium is broken causing
gingival ulcerations. Must do BIOPSY to diagnose. Tissue in "Michel solution" yellowish fluorescence
areas show where antibodies against desmosomes.

3 Other types of Pemphigus: Pemphigus Vegetans, Pemphigus Follaceus,

&Pemphigus Erythematosus.

RUBELLA VIRUS - causes German Measles (Rubella) that presents with a characteristic rash (flat,
pink spots on the face that spreads to other body parts). Oral manifestations may include swollen and
congested tonsils, and red macules.

HEPATITIS A("VIRAL OR INFECTIOUS HEPATITIS") - the form of hepatitis caused by an RNA

Enterovirus that is usually transmitted by the FECAL-ORAL ROUTE. It is an infectious disease of the
LIVER that most often occurs in young adults and is prevalent in areas with inadequate sewerage.
SHELLFISH from contaminated waters is also a prime source. Initial symptoms (fever, abdominal
pain , nausea, then jaundice) appear after an incubation period of 3-6 weeks.

• Damage to liver cells causes increased serum levels of enzymes like transaminases, normally
active in liver cells. The detection of the increased serum levels of transam inases is used to diagnose
the disease. In most cases of Hepatitis A, the infection is self-limiting, and recovery occurs within
4 months.

HEPATITIS B ("SERUM HEPATITIS") - an infectious LIVER DISEASE caused by a DNA virus that
produces liver inflammation and necrosis. Main method of transmission is exposure to contaminated
blood or serum (but can also be transmitted sexually or via blood transfusions). There is a high rate
of transmission among drug addicts who often use contaminated needles.

• Signs &Symptoms: are similar to Hepatitis A (fever, abdominal pain, nausea), but it has a longer
incubation period of 2-3 months. Symptoms develop slower, but last a longer duration. Most
patients fully recover, but some develop chronic liver disease.

• Hepatitis B transmission is a MAJOR CONCERN to the dental profession, which have at least 3x
higher risk than the general population to acquire this virus. Thus, ALWAYS USE UNIVERSAL
PRECAUTIONS. Hepatitis D is found ONLY in patients with acute or chronic episodes of Hepatitis B.

• HB vaccine is recommended for all health care personnel. Aseries of 3 doses is required
(the 2nd and 3'd doses are given at 1 &6 months after the 1't dose. The injection is given 1M
(in the deltoid muscle).

The presence of SURFACE ANTIGEN (A or B) in a patient's serum indicates the patient is potentially
infected with Hepatitis ("carrier state")' These Hepatitis viruses are VERY HEAT RESISTANT (even
more than the AIDS virus). However, autoclaving properly will kill them.

247
 VERRUCAL PAPILLARY LESIONS
VERRUCA VUGLARIS (SQUAMOUS PAPILLOMA) -the common WART of VIRAL etiology
(caused by Papilloma virus) that is a common skin tumor analogous to the oral papilloma. It has an
incubation period of 6 weeks to 1 year. Although it is a primary lesion of the skin, it may occur in the
oral cavity (especially lips & palate). Clinically, it is a sessile, soft, CAULIFLOWER-LIKE LESION.

• Microscopically: is a papillomatous lesion in which the epithelium is thrown into folds. The lesion
shows alternating hyperkeratosis, parakeratosis, and long epithelial ridges. If excised, they usually
do not recur, but autoinoculation is possible. Intraorally, that is how most cases develop.

PAPILLOMA - the most common benign neoplasm of EPITHELIAL TISSUE ORIGIN. It appears as a
pedunculated (foot-shaped), or sessile whitish cauliflower-like mass on the tongue (posterior
border), lips, gingiva, or soft palate. Papillomas are soft in the oral cavity, but on exposed areas of
the lips, are usually rough & scaly.

• Microscopic Features: finger-like projections of stratified squamous epithelium supported by thin

cores of vascular fibrous C.T. Epithelium may show hyperkeratosis or parakeratosis. Histogenesis:
squamous epithelium.

• Treatment: conservative excision; recurrence is rare.

INFLAMMATORY FIBROUS HYPERPLASIA ("EPULIS FISSURATUM") - is found at the

area of the denture borders, more commonly in the maxilla than mandible caused by ill-fitting
prosthesis (dentures).

• Clinical Features: rolls of tissue in muco-Iabial fold , pink, elongated, firm, ulceration, soft lesion.

• Treatment: surgical excision and re-evaluate the prosthesis or remake or reline the dentures.

INFLAMMATORY PAPILLARY HYPERPLASIA ("PALATAL PAPILLOMATOSIS") - found on

the hard palate (vault), caused by poor oral hygiene and ill-fitting dentures (prosthesis) .

• Clinical Features: numerous red papillary projections, a soft lesion.

• Treatment: surgical excision and correct the prosthesis (reline or remake the denture).

248
$HAPTER $

249
 PEDIATRIC DRUGS
INHALATION (NITROUS OXIDE) - the most frequently utilized route of administration for seda-
tion in pediatric patients.
• Nitrous oxide is a slightly sweet smelling, colorless, inert gas that must always be coupled with at
LEAST 20% oxygen. N20 is quickly absorbed from the lungs and is physically dissolved in the blood.
• When one turns on the N20, the initial concentration is 20%. Initially, some start with
100% oxygen.
• Maximum concentration of N20 should not exceed 50% (some say 40%).
• When one starts conscious sedation, the flow rate is about 6 liters/minute. The correct total
liter flow of nitrous oxide-oxygen is determined by the amount necessary to keep the reservoir bag
113-2/3 full.
• The earliest symptoms of conscious sedation is LIGHT HEAOEONESS. Laughing or crying,
paresthesia of arms, legs, and oral cavity, and feeling of floating are seen in the second stage.
• After sedating a child, always keep an eye on the status of the child.

• There is no biotransformation, and the gas is rapidly excreted by the lungs when the concentration
gradient is reversed. It is recom mended that the patient be maintained on 100% oxygen for 3-5
minutes after the sedation period.

• N20 creates an altered state of awareness with impaired motor function. It is a CNS depressant,
but produces little analgesia. The combined volume of gases being delivered (oxygen and nitrous)
should be at least 3-S liters/min. The operator should encourage the patient to breathe through their
nose with the mouth closed. The feeling of floating or giddiness with tingling of the digits is the
proper response to nitrous oxide.

• For restorative dentistry, N20 and local anesthesia is usually all that is needed to treat a child who
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-< C"> SEDATIVE-HYPNOTICS - their principal effect is sedation and sleepiness.
1. Chloral Hydrate-a drug widely used for pediatric sedation by acting on the CNS to induce
sleep. At normal doses, the sleep induction does not affect breathing, BP, or reflexes. It may be
used before some surgeries or procedures to help relieve anxiety and induce sleep. When used
with analgesics, it can help manage pain after surgery. Its onset of action is lS-30 min when
given orally. Children often enter a period of excitement and irritability before becoming
sedated. As with barbiturates, pain may cause paradoxical reactions.

2. Short-Acting Barbiturates: Secobarbital (Seconal) &Pentobarbital (Nembutal) are sedative

drugs sometimes used for pediatric conscious sedation by oral administration, but are of very
limited value. They are non-analgesic and may cause hyper-excitability rather than sedation in
some children.

Child Antibiotic Prophylactic Regimens for Dental Procedures

Situation Antibiotic Regimen
Standard general prophylaxis Amoxicillin SOmg/kg orally 1hr before procedure
Unable to take oral medications Ampicillin SOmg/kg 1M or IV within 30min
before procedure
Allergic to Penicillin Clindamycin 20mg/kg orally 1hr before procedure
Cephalexin or Cephadroxil SOmg/kg orally 1hr before procedure
Azithromycin or Clarithromycin lSmg/kg orally 1hr before procedure
Allergic to Penicillin and cannot Clindamycin 20mg/kg IV within 30min
take oral medications Cefazolin of proced ure
2Smg/kg 1M or IV 30min of procedure
*Remember lib = .4S3kg

250
PULP TREATMENT
PULPECTOMY (RCT) - the suggested treatment when an II-year old child traumatized a perma-
nent maxillary central incisor and the tooth becomes painful, with swelling, and a periapical radi-
ograph discloses a pathosis associated with the apex.

• This is treated the same way that you would treat the adult patient. At age 11, the root of a maxillary
central incisor should be completely formed, thus an apexification procedure is NOT indicated.
If the root were not fully formed, then an apexification process should be started. This involves the
placement of calcium hydroxide paste into the canal to stimulate continued apical closure.

• PUlpectomy is the treatment of choice when the primary mandibular 2nd molar in a 4-year old has a
large carious lesion with pulpal involvement. Radiographically there is periapical pathology on the
distal root. There is also furcation involvement and slight mobility. Pulpectomy is the treatment of
choice when there is periapical pathology. If there were no periapical pathology, a formocresol
pulpotomy is indicated . If the child were older and there was a periapica l radiolucency but successful
pUlpectomy could not be accomplished, the treatment of choice is extraction and placement of a
space maintainer to prevent damage to surrounding bone and the developing permanent tooth.

• When performing a pulpectomy on primary teeth, the canals are filled with ZOE paste because it
causes only a minimal tissue reaction and it resorbs when the primary tooth begins its normal
resorption process.

• Chronic pulpal infection in primary molars is usually first noted radiographically as a change in the
bony furcation.

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no tooth mobility, but the dentist notes a sma", draining sinus tract adjacent to the tooth. Treatment ,..., ,...,
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PULPOTOMY - preserves radicular VITAL pulp tissue when the entire coronal pulp is amputated, and
allows resorption &exfoliation of the primary tooth, but preserves its role as a natural space main-
tainer. The reason to perform a pUlpotomy using either of the following two techniques is that the coronal
pulp shows evidence of inflammation and degenerative change due to microorganisms located there.
1. Calcium Hydroxide Pulpotomy Technique-treats permanent teeth when there is a pathological
change in the pulp at the carious exposure site. CHT is especially indicated for permanent teeth
with immature root development and with healthy pulp tissue in the root canals. The success
of a pulpotomy in this case would be indicated when the root apex (if incompletely formed)
completes its full development in time (apexogenesis). This technique is completed in one
appointment. Only those teeth free of symptoms of painful pulpitis (severe toothache, lingering
pain) are considered. Adentin bridge will form at a level below the level of amputation of the
coronal pulp. Histologically, you would see a necrotic layer immediately under the
calcium hydroxide.
2. Formocresol Pulpotomy Technique-treats primary teeth with a carious exposure. Teeth
selection is the same as for the CaOH technique, and is performed in one appointment. After the
coronal pulp is removed (amputated), a cotton pellet moistened with formocresol is placed in
contact with the pulp stumps and remains for 5 minutes. The pellet is then removed and the pulp
chamber dried. Athick paste of ZOE is placed over the chamber and the tooth is restored. The
success of formocresol pUlpotomy for a primary tooth depends primarily on a vital root tip.
Formocresol (formalin and cresol) causes surface fixation of the pulpal tissue and
odontoblast degeneration.
• Indications: tooth sensitive to sweets, pulp exposure during caries excavation, and
radiographic evidence of deep caries approximating the coronal pulp .
• Contraindications: radiographic evidence of internal resorption is a contraindication for a
formocresol pulpotomy on a primary molar. Also, a tooth that is painful with swelling is a
contraindication to a pulpotomy. You need healthy ROOT pulp tissue for pulpotomy success .
• The success of a pUlpotomy for a primary molar depends primarily upon a VITAL ROOT PULP.

251
 DIRECT PULP CAPPING ~ primarily used on permanent teeth (not widely used on primary teeth
because of eaOH's alkaline pH) . To perform a direct pulp cap on a primary tooth, the tooth MUST be
asymptomatic and must be a small exposure with little or no hemorrhaging. eaOH can effect (irritate)
the pulp mildly or most often severely:

• With a mild irritation, there is a mild inflammatory reaction that resolves itself and regroups as
reparative dentin.

• With severe irritation, internal resorption can occur. In primary teeth, severe irritation often results
in internal resorption. However, in permanent teeth, this rarely occurs because the severe
inflammatory response causes reparative dentin formation.

• Contra indications of performing a direct pulp cap on primary teeth:

• Spontaneous pain from the tooth (symptomatic).
• A large exposure (only used for pinpoint/small exposures) .
• Excessive hemorrhaging (bleeding).
• Radiographic evidence of internal resorption .

INDIRECT PULP CAPPING ~ its primary goals are to preserve pulp vitality, prevent pulp exposure,
save tooth structure, arrest caries, and promote reparative dentin formation.

• Indications: mostly for permanent teeth with rampant caries and large carious lesions close to the
pulp that are not chronically painful.

• Contraindications: do not use in cases where there is spontaneous pain, furcation involvement, or
pulpal involvement. Most pediatric dentists feel indirect pulp capping is contraindicated in the
primary dentition .
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caries then placing calcium hydroxide and an interim restoration like IRM (reinforced ZOE).

• The greatest problem in pulpal diagnosis is predicting the amount or extent of inflammation.
Successful management of deep caries and pulpally involved teeth in children depends on the extent
of pulpal inflammation.

Emergency Treatment of Fractures of Permanent Teeth with Immature Apices:

1. Class I: smooth enamel edges, restore the tooth .
2. Class II: apply calcium hydroxide to exposed dentin and restore the tooth with a
permanent restoration.
3. Class III: immediately after injury, apply calcium hydroxide over exposure and place a temporary
restoration. If the exposure is large or the injury was several hours or days ago, perform a calcium
hydroxide pulpotomy. Once the apex closes, do a pUlpectomy.
4. Class IV: do a calcium hydroxide pulpotomy. Once the apex closes, do a pulpectomy.

In an older child with a fully formed apex, if there is a pinpoint exposure and it has been a while
(day) since the fracture, conventional ReT with gutta percha is the treatment of choice. If the child is
seen immediately, then a direct pulp cap with calcium hydroxide is indicated, followed by a permanent
restorat io n.

252
PEDIATRIC DISEASES &CONDITIONS
Cleft Palate & Cleft Lip are the MOST COMMON craniofacial malformations, accounting for 50% of
all defects. They can be unilateral or bilateral.
1. Cleft Lip-a separation of the two sides of the lip that occurs during the 5th _6 th week of embryonic
life due to failure of the maxillary & frontonasal processes to merge. Cleft lips are more
common in MALES, and more common on the left side than right side.
• 4 CLASSES OF CLEFT LIP:
1. Class I: a unilateral notching of the vermillion NOT extending into the lip.
2. Class II: unilateral notching of the vermillion, but the cleft extends into the lip,
but NOT to the nose floor.
3. Class III: a unilateral notching of the vermillion, but the cleft extends into the lip and
floor of the nose.
4. Class IV: any bilateral clefting of the lip whether incomplete notching or complete clefting.
• Cleft lip deformity occurs during 4-6 weeks of pregnancy. Cleft lip occurs following the failure
of the permanent union between the maxillary process & frontonasal process.
2. Cleft Palate-an open ing in the roof of the mouth where two sides of the palate did not unite. It
occurs in 6th _8 th week of embryonic life. Isolated clefts of the palate are more common in females.
It is characterized by a fissure in the midline of the palate due to the fai lure of the two sides to
fuse during embryonic development.
• The most severe handicap imposed by cleft palate is an impaired mechanism preventing
normal speech and swallowing. The child almost always needs orthodontic treatment once the
palate is surgically repaired . Speech therapy is also required since these patients have
problems related to the inability of the soft palate to close airflow into the nasopharynx.
Orthognathic surgery may be needed to correct the concave appearance of the face due to
deficient maxillary growth.
• 4 CLASSES OF CLEFT PALATE:
1. Class I: involves only the soft palate. ,..., ,...,
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4. Class IV: involves the soft palate and continues through the alveolus on both sides of
the premaxilla.
• Cleft palate deformity occurs/develops during the 1st trimester of pregnancy (6-9wks) .

Speech problems associated with cleft lip & palate are usually the result of the inability of the soft
palate to close air flow into the nasal area.

ACUTE NECROTIZING ULCERATIVE GINGIVITIS (ANUG, VINCENT'S ANGINA OR

"TRENCH MOUTH") - an acute gingival disease characterized by painful hyperemic gingiva,
punched-out erosions of interproximal papilla, covered by a GRAY pseudomembrane with an accom-
panying fetid/foul odor.
• ANUG is an acute fusospirochetal infection of the gingiva caused by fusiform/fusobacterium,
spirochetes, & Prevotella intermedia. ANUG is a progressively painful infection with ulceration,
swelling, and sloughing off of dead tissue from the mouth and throat due to the spread of infection
from the gums.
• ANUG is usually associated with poor oral hygiene, and is most common in conditions where there
is crowding and malnutrition. Emotional stress and smoking are also risk factors.
• Debridement helps clear up the infection and antibiotics reduce acute symptoms.
• Rarely occurs in pre-school children and has a slow onset.
• ANUG usually affects YOUNG ADULTS ages 15-35 years old. It is rare in preschool children, and is
easily diagnosed due to involvement of interproximal papillae and presence of a pseudomembranous
necrotic covering of the marginal tissues.
• Clinical Manifestations: inflamed, painful, bleeding gingival tissues, poor appetite, fever, general
malaise, and fetid odor. ANUG is necrotic, foul-smelling ulcers of the gums and throat.
• Treatment: debridement, H202 mouth rinses, and antibiotic therapy.

253
 PRIMARY (ACUTE) HERPETIC GINGIVOSTOMATITIS - a viral infection characterized by in-
tensely inflamed gingiva, sore throat, fever, malaise, lymphadenopathy, and small fluid-filled vesicles
on the mucosa of the lips, tongue, and gingival (round ulcers with red areolae on the cheeks are
characteristic). This disease is self-limiting, and the acute ph ase generally lasts 7-10 days. Oral flu-
ids are very important in children to prevent dehydration.
• Debridement does not clear up the infection and antibiotics do not help this viral infection.
• Common in PRE-SCHOOL children with a rapid onset.

ATROPHIC GINGIVITIS - characterized by gingival recession without a corresponding rate of alve-

olar bone loss. Minor marginal and papillary gingival inflammation is found. RECESSION is the main
clinical finding.

ACUTE LYMPHOCYTIC/LYMPHOBLASTIC LEUKEMIA (ALl) - the most common PEDIATRIC

CANCER (peaks around age 4) that is a life-threatening disease where cells that normally develop into
lymphocytes (lymphoblasts) become cancerous and rapidly replace normal cells in bone marrow. ALL is
the form of acute leukemia most responsive to therapy.

• Early signs in a child are fatigue, pallor, weight loss, and easy bruising. This progresses to fever,
hemorrhages, extreme weakness, bone/joint pain, and repeated infections.

• The most common type of leukemia in children is lymphoblastic leukemia .

• Oral Features: gingival oozing, petechiae, hematoma, ecchymosis, oral ulceration, pharyngitis,
gingival infection that is unresponsive to conventional therapy, and submandibular lymphadenopathy.

• Children with leukemia are very susceptible to Candida fungal infections, thus, nystatin rinses or
popsicles are effective treatments.
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APERT SYNDROME - a genetic defect that falls under the broad classification of cranial-limb
anomalies, primary characterized by specific malformations of the skull, midface, hands, and feet.
Blindness is NOT a clinical feature .

• Dental Considerations: often associated with supernumerary teeth (disrupt eruption of other
teeth), severe crowding, and Class III malocclusion.

• Major Features: prematurely fused cranial sutures, retruded midface (often corrected with Lefort III
surgery), fused fingers and toes.

AUTISM - a complex developmental disability that typically appears in the first 3 years of life due to
a neurological disorder that affects brain functioning (4x more prevalent in boys than girls). Dental
management depends on the degree of mental retardation and the child's language development.
Sedative drugs and reducing the sound level of the high-speed handpiece are beneficial when treating
autistic children.
• It is difficult to treat an autistic patient because of impaired communication (inability to
communicate with the child).

ATTENTION DEFICIT DISORDER (ADD) - a condition characterized by an attention span that is

less than expected for the age of the child, hyperactivity, and impulsive behavior. These children
are easily distracted, have difficulty paying attention, and may be unable to focus more than a few
moments on mental tasks. They may be physically active and behave impulsive. The cause is un-
known, and is lOx more common in males than in females.

• Typically affected children, whether intellectually handicapped or not, perform poorly in school
because of the inability to attend to tasks or sit still during school.

• If there are any questions concerning the child's ability to handle dental treatment, contact the
child 's physician . In most cases, the child does not require special treatment.
254
• Methylphenidate (Ritalin)-a mild CNS stimulant often used in ADD children (children over age 6) . NOTES
Among the more serious adverse reactions are nervousness, insomnia , and anorexia.

• Amphetamines (Le. Dextroamphetamine) also treat ADD.

ACHONDROPLASIA - the most common form of short-limb dwarfism that occurs in all races,
equally affected males and females. Many of these children die before age 1. Deficient growth in the
cran ial base is evident in many children who survive.
• Clinical Features: disproportionate short stature (head is large, and arms/legs are short compared
to the trunk length). Prominent forehead, depressed bridge of the nose, small maxilla causing
overcrowding of teeth, and Class III malocclusion.

GIGANTISM - oral manifestations are an enlarged tongue causing the teeth to be tipped either to the
buccal or lingual. Mandibular prognathism and roots may be longer than normal are other oral features.

PITUITARY DWARF - the eruption rate and shedding of the teeth are delayed . Clinical crowns and
roots appear smaller, the dental arch is smaller causing malocclusion , and the mandible is underde-
veloped.

CElLULITIS - an acute spreading infection of the dermis and subcutaneous tissues causing
pain/tenderness, erythema , edema , and warmth of the affected area (hallmarks of cellulitis). Cellulitis
is a common infection that may progress to a serious illness by uncontrolled spread contiguously or via
the lymphatic or circulatory systems. Group AStreptococci &Staphylococcus Aureus are the most
common causative organisms.

• Cellulitis may be caused by a necrotic primary or permanent tooth , resulting in considerable swelling
of the face or neck, and the tissue appears discolored . It is a very serious infection that can be life-
threatening. The child appears acutely ill and may have a very high temperature with malaise and
lethargy.

• Cellulitis in a child is harder to treat because dehydration occurs more frequently, rapidly, and
severely in children.

• Treatment includes bringing the child to the hospital if the signs and symptoms warrant it.

LUDWIG'S ANGINA - cellulitis that affects the submandibular, sublingual, & submental spaces,
and causes elevation of the tongue and mouth floor resulting in obstruction of the patient's airway
and makes swallowing impossible. The patient MUST be taken to the hospital immediately.

CRETINISM (CHILD HYPOTHYROIDISM) - a deficiency disease caused by the congenital ab-

sence of THYROXINE (hormone secreted by the thyroid gland). Cretin ism is severe hypothyroidism in
a child, characterized by defective mental and physical development.

• Cretins have dwarfed bodies with curvature of the spine and a pendulous abdomen.

• Limbs are distorted , their features are coa rse, and their hair harsh and scanty.

• Severe mental retardation is caused by the improper development of the CNS. If cretinism is
recognized early, it can be markedly improved with the use of thyroid hormones.

• Dental Findings: underdeveloped mandible, overdeveloped maxilla , enlarged tongue causing

malocclusion like anterior open bite and flared anterior teeth, delayed tooth eruption, and longer
retention of the deciduous teeth.

255
 CYSTIC FIBROSIS - an inherited disease of exocrine glands, affecting -30,000 children and
adults in the U.S. Cystic fibrosis causes the body to produce an abnormally thick, sticky mucus due to
a faulty transport of Na+ and CI within cells lining organs like the lungs and pancreas. The glands
most affected are in the pancreas, respiratory system, and sweat glands.

• Cystic fibrosis has various symptoms. The most common are very salty tasting skin, persistent
coughing, wheezing, or pneumonia, excessive appetite, but poor weight gain, and bulky stools.

• An individual must inherit a defective copy of the CF gene (one from each parent) to get the disease.
In CF cells, salt does not move properly because the protein product of the CF gene is defective and
makes a faulty channel for the chloride to exit.

• Cystic fibrosis is usually recognized in infancy or early childhood, occurring mainly in Caucasians.
Early signs are a chronic cough, frequent foul-smelling stools (steatorrhea), and persistent upper
respiratory infections. The most reliable diagnostic tool is the SWEAT TEST (shows elevated levels of
Na+ and CI).

• A high percentage of children with cystic fibrosis have dark-colored teeth.

• Cystic fibrosis is a combination of steatorrhea, chronic respiratory infections, and functional

disturbances in secretory mechanisms of various glands.

CLEIODOCRANIAL DYSPLASIA (DYSOSTOSIS) - an inherited disorder of bony development

characterized by absent or incompletely formed clavicles, characteristic facial appearance, and dental
abnormalities. Occurs equally in M& F, with the presence of supernumerary teeth being one of the
most distinguishing features.
• Other dental findings: delayed permanent teeth eruption, peg-shaped teeth, and congenitally
.., ..,
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opment of the skin &associated structures (hair, nails, teeth, sweat glands). Severa I types of ecto-
dermal dysplasia exist, but the x-linked anhidrotic ectodermal dysplasia is the most common.

• Teeth develop abnormally with possible complete failure of the teeth to develop (anodontia) or
oligodontia (partial anodontia) . Conical-shaped anterior teeth characteristic of oligodontia and
associated with ectodermal dysplasia.

• Atrophic skin, defective hair, partial anodontia, &hypoplastic sweat glands.

• Anhidrotic Ectodermal Dysplasia-a condition that only affects males, characterized by lack of
perspiration caused by partial or complete absence of sweat glands.

Retained primary teeth are an outstanding oral manifestation of Ectodermal &Cleidocranial dys-
plasias. This prolonged retention of the primary teeth may cause a change in the path of eruption of
the succeeding teeth.

DIABETES - a disease where the body cannot properly use and store glucose. Glucose backs up in
the bloodstream causing blood glucose levels to rise too high. The classic triad of symptoms is always
present (polydipsia/extreme thirst, polyphagia/extreme hunger, &polyuria/frequent urination).
Weight loss, poor wound healing, or extreme unexplained fatigue are other symptoms.
1. Type I Diabetes (Insulin-Dependent Diabetes or Juvenile-Onset): diabetes affecting young adults
where the body completely stops producing insulin. Type I diabetics are totally insulin deficient,
thus must take daily insulin injections to survive. Juvenile diabetics tend to be unstable, brittle,
and prone to ketoacidosis. Blindness is a serious complication that may develop.

• Oral Complications: xerostomia , infection, poor healing, increased incidence and severity of
periodontal disease, and burning mouth syndrome.

256
DIPHTHERIA - an acute, contagious disease caused by the bacterium Corynebacterium diphthe- NOTES
ria, characterized by the production of a systemic toxin which is very damaging to tissues of the heart
and eNS. Immunization is available to all U.S. children.

DOWN SYNDROME (TRISOMY 21) - congenital defect caused by a chromosomal abnormality.

Clinical features are fairly recognizable and include:
• Low caries rate/susceptibility, but a high prevalence of periodontal disease.
• Delayed tooth eruption (primary teeth may be retained until age 14-15) and a high prevalence of
ma locclusion.
• Enamel dysplasia
• Delayed physical and mental development.
• Short, stocky build with a broad, flat face with slanting eyes, short nose, and small, low set ears.
• Prominent, thickened tongue
• Heart defects are common , so SBE prophylaxis is required for dental treatment.
• Reduced resistance to infections (a consideration in dental management of a Down Syndrome child).
• Down Syndrome child is affectionate, fearful of quick movements, but capable of learning dental
procedures. They need a comprehensive preventive program, and often have difficulty accepting
dental care, but cooperation is improved by using gradual exposure to the dental office.

GINGIVOSTOMATITIS - a disorder involving sores on the mouth &gingiva caused by herpes virus
(HSV-1) , characterized by inflammation of the gingiva and mucosa , and multiple mucosal ulcerations.
It is common especially among children.

ACUTE (PRIMARY) HERPETIC GINGIVOSTOMATITIS - generally affects children under age 3

with prodromal symptoms (fever, malaise, irritability, headache, dysphagia, vomiting, & lym-
phadenopathy) that occurs 1-2 days prior to the local lesions (ulcers) in the oral cavity.
• Treatment in children is directed toward relieving the acute symptoms so that fluid and nutritional
intake can be maintained. Applying a mild topical anesthetic (i.e. Dyclone) before mealtime ,..,
c::I ,..,
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temporarily relieves the pain and allows the child to eat a soft diet. Bed rcst and isolation from other ..... -
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children are recommended. This condition usually subsides after 7-10 days. '" .....
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• Primary herpetic gingivostomatitis is MOST likely to occur in children ages 1-5 years.
• The virus that causes acute herpetic gingivostomatitis is closely related to the herpes virus that
causes chickenpox (varicella loster).

Common Sequelae of Acute Herpetic Gingivostomatitis:

• Recurrent herpes labialis (cold sores on lips). Exposure to sunlight may cause the appearance of
cold sores on the lips. Acyclovir 5% ointment (Zovirax) may be applied topically as the first symptom
of the lesion (tingling sensation).
• Clinically AHG can result in spherical discrete vesicles.
• Child will have circulating anti-herpes antibodies (HSV-1 antibodies) .

HERPANGINA - a viral infection (strain of coxsackie Avirus) usually of young children, character-
ized by oral ulcers, but a high fever, sore throat, and headache may precede the appearance of the le-
sions (ulcers with a white to whitish-gray base and red border usually on the roof of the mouth and in
the throat). The ulcers can be very painful, and there only usually only a few lesions. The disease usu-
ally runs its course in < 1 week. Treatment is palliative.

Hemangioma - the most common benign tumor of INFANTS. Hemangiomas are vascular birth-
marks where the proliferation of blood vessels leads to a mass that resembles a neoplasm. Heman-
giomas differ from other vascular birthmarks because they are biologically active (their growth is
independent from the child's growth). Most hemangiomas appear within a week or two after birth , and
are 5x more common in girls.
• Hemangiomas are common on the lips, tongue, and buccal mucosa, appearing as flat or raised
lesions, usually deep red or bluish-red and rarely well-circumscribed. Hemangiomas are removed
surgically, while other do not require treatment.
• Asymptomatic, soft, bluish lesion on the tongue, present for 5 years and has had a minimal increase
in size.

257
r

LYMPHANGIOMA - a fairly well-circumscribed nodule or mass of lymphatic vessels that occur

most often in the neck and axilla. These are compressible and spongy red-to-blue translucent enlarge-
ments/lesions Treatment: excisional biopsy.

NEUROFIBROMA - a moderately firm, encapsulated tumor caused by the proliferation of Schwann

cells. Found on the tongue, buccal mucosa, vestibule, & palate. Neurofibromas appear as solitary or
multiple sub-mucosal enlargements, and may become malignant (5-15%). Multiple lesions are asso-
ciated with Neurofibromatosis (Von Recklinghausen's Disease).

NURSING-BOTTlE CARIES (BABY BOTTLE TOOTH DECAY OR BOTTLE MOUTH

SYNDROME) - a widespread carious destruction of the deciduous (primary) teeth most com-
monly affecting the MAXillARY INCISORS. Inappropriate feeding of children may cause a typical
nursing pattern decay. There is early carious involvement of the maxillary anterior teeth, followed by
maxillary & mandibular 1st molars, and mandibular canines. Mandibular incisors are less affected
since the tongue covers them.

• AKA: Early childhood caries, Nursing caries, Bottle caries, or Infant caries.

• Nursing bottle caries is RAMPANT DECAY due to sleep time bottle-feeding combined with
Streptococcus mutans activity. The stagnation of milk around the necks of anterior teeth and
fermentation of the disaccharide lactose (a sugar found in milk), also contributes to this caries process.

Preventive Measures:
• Infants should not be put to sleep with a bottle containing a liquid other than water.
• Infants should be encouraged to drink from a cup prior to their first birthday, and should be weaned
from the bottle at 12-14 months of age.
• Infants should start to supplement their diet with non-liquids at age 4-6 months.
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-< C"> • Within 6 months of eruption of the first tooth (no later than the first birthday) it is time for the first
dental visit.

PIERRE ROBIN SYNDROME - a hereditary disorder that presents micrognathia (smallness of the
jaws), glossoptosis (downward displacement or retraction of the tongue), & a high-arched or cleft
palate. Most children require orthodontics.

PORPHYRIA - a group of inherited disorders involving abnormalities in the production of heme pig-
ments, myoglobin, & cytochromas. It can result in discoloration of teeth. Porphyrias are character-
ized by 3 major findings:
1. Photodermatitis (light sensitivity causing rashes).
2. Neuropsychiatric complaints.
3. Visceral complaints (abdominal pain, cramping).

Diagnosis of Porphyria: a child present with red urine, purplish-brown teeth, sensitivity to sunlight,
and develops blisters and swelling on the face and hands when exposed to sunlight.

Causes of Tooth Discoloration:

1. Porphyria-a condition that results in discoloration of teeth.
2. Cystic Fibrosis: these children have teeth dark in color (ranging from yellowish-gray to dark
brown), and may be related to the usual high doses of tetracycline given to these children.
3. Erythroblastosis Fetalis: characterized by an excessive destruction of erythrocytes. Primary teeth
may have a blue-green color.
4. Tetracycline Therapy: can cause tooth crowns to become discolored from yellow-to-brown, and
gray-to-black. The drug stains permanent teeth that have not completed enamel formation at the
time the drug is given (i.e. if a 5-year old child receives tetracycline therapy, the teeth affected
will be the canines, premolars, and 2nd molars. Important: incisors and lsI molars have already
completed enamel formation.

258
RIEGER'S SYNDROME - characterized by delayed sexual development, hypothyroidism, and dental
features like hypodontia, underdeveloped premaxilla, cleft palate, and a protruding lower lip.

RECURRENT APHTHOUS ULCERS (CANKER SORES) - the cause is UNKNOWN, but they can be
triggered by stress, dietary deficiencies (iron, folic acid, vitamin B12), menstrual periods, hormonal
changes, food allergies, etc.

• Appear as painful white or yellow ulcers surrounded by a bright red area on non-keratinized oral
mucosa and inner surface of the cheeks, lips, tongue, soft palate, and base of gingiva.

• Usually begin with a tingling or burning sensation, followed by a red spot or bump that ulcerates.
Pain spontaneously decreases in 7-10 days, with complete healing in 1-3 weeks.

• Recurrent aphthous ulcers & intra-oral herpes lesions are distinguished largely on their location.
Recurrent aphthous ulcers occur mainly on mobile mucosa, while intra-oral herpes lesions occur on
tissue bound to periosteum.

• Occur more in women than men. May occur at any age, but usually first appear between ages
10-40yrs.

3 Classes of Recurrent Aphthous Ulcers:

1. Recurrent aphthous minor- < lcm in diameter, are common, last over 2 weeks, and heal
without scarring.
2. Recurrent aphthous major- > lcm in diameter, are much less common, last over 2 weeks,
and heal with scarring.
3. Recurrent herpetiform-consists of clusters and ulcers. Patients with frequent recurrences
should be screened for diabetes mellitus or Bechet's Syndrome.
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Topical Steroids are suggested to relieve aphthous ulcer symptoms: Triamcinolone (Kenalog) in :z:
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Ora base 0.1 %, Disp: 5gm tube, Sig: coat the lesion with a thin film after each meal and at bedtime. c:;;~
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GRAND MAL EPILEPSY - the most common seizure disorder (present in 90% of epileptics).
-60% of epileptics have this form alone, while 30% have other seizure types in addition to grand mal.
Grand mal epilepsy can occur in any age. This tonic-clonic type seizure is produced by neurological
disorders, or develops in a neurologically sound brain secondary to a systemic metabolic or toxic dis-
turbance. Grand mal seizures usually last 2-5 minutes.
• Ayoung epileptic who has a grand mal seizure in the dental office generally recover if restrained
from self-injury and oxygen is maintained.
• Treatment for tonic-clonic seizures (grand mal) position the patient in the supine position,
preventing injury to the convulsing patient, initiating basic life support (head tilt). If cyanosis occurs,
oxygen is administered.

PETn MAL EPILEPSY (ABSENCE SEIZURES) - almost always develops in childhood usually in
children under age 16. Clinically, this seizure consists of a brief lapse of consciousness, normally
lasting 5-10 seconds, and rarely lasts beyond 30 seconds. The patient makes no movement during the
episode, and termination of the episode is equally abrupt. Management of petit mal and partial
seizures is of a protective nature. The doctor merely prevents any injury to the victim. There is little
or no danger to the victim, so that even without assistance from staff members, morbidity seldom oc-
curs. However, if this seizure should last a significant length of time, medical assistance is required.

MEASLES (RUBEOLA) - a highly contagious viral illness characterized by fever, cough, and spread-
ing rash due to PARAMYXOVIRUS. The incubation period is 1-2 weeks before symptoms usually appear.
• Koplik's Spots-1-2mm yellowish-white oral lesions pathognomonic of measles, appearing usually
as necrotic ulcers surrounded by a bright red margin on the buccal mucosa.
• Before immunization, measles were common during childhood, as 90% of the population was infected
by age 20.

259
 N GERMAN MEASLES (RUBELLA) - a fairly benign viral disease, with symptoms of a red, bumpy
rash, swollen lymph nodes (around the ears and neck), and a mild fever. Some people feel achy. The
virus can manifest in the oral cavity as small petechiae-like spots on the soft palate. The defects of
congenital infection from an infected mother are more severe (enamel defects, hypoplasia, pitting,
and abnormal tooth morphology).
• Hypoplastic primary incisors is a dental anomaly resulting from maternal rubella in the first trimester
of pregnancy.

MUMPS - an acute contagious viral infection characterized mainly by unilateral or bilateral swelling
of the salivary glands (usually the PAROTID =PAROTITIS). Mumps is usually a childhood disease, but
may also affect adults. The papilla on the opening of the parotid duct on the buccal mucosa is often
puffy and reddened.

SMALLPOX (VARIOLA) - an acute viral disease that manifest clinically by a high fever, nausea,
vomiting, chills, and headache. The skin lesions begin as small macules and papules that first appear
on the face, but rapidly spread to cover much of the body. Oral manifestations: ulceration of the oral
mucosa and pharynx. Sometimes, the tongue is swollen and painful, making swallowing difficult.

SCARLET FEVER - an exotoxin-mediated disease arising from group A-beta-hemolytic streptococ-

cal infection that peaks in children 4-8 years old. Symptoms include strep throat, sudden onset of
fever, sore throat, headache, nausea, vomiting, abdominal pain, muscle pain, fatigue, and STRAW-
BERRY TONGUE.

• Enlargement of fungiform papillae extending above the level of the white desquamating filiform
papillae gives the appearance of an "unripe strawberry". During the course of scarlet fever, the
coating disappears and the enlarged red papillae extend above a smooth denuded surface, giving
the appearance of a red strawberry or raspberry.
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• Penicillin is the drug of choice for treatment. Early diagnosis and treatment are important to prevent
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ODONTOGENIC ABNORMALITIES
AMELOGENESIS IMPERFECTA - an inherited condition in which teeth are covered with thin, mal-
formed enamel. This genetic condition is transmitted as a dominant trait and causes SOFT, THIN
ENAMEL. Teeth appear yellow due to dentin visible through the thin enamel. Teeth are easily damaged
and susceptible to decay. The pulpal outline and root morphology appears normal.
• Treatment: depends on its severity and demands of esthetic improvement. Since the dentin is normal,
the teeth can be prepared for full crowns.

DENTINOGENESIS IMPERFECTA - an inherited condition and dental anomaly transmitted as a

dominant trait that causes undermineralized dentin . It can affect the primary & permanent dentition.
Crowns are bulbous with short roots, and teeth may appear gray or brown with opalescent dentin that
overgrows and obliterates the pulp cavity. Teeth wear rapidly. 3 types of DI exist:
1. Type I: often associated with osteogenesis imperfecta. Child may also have blue sclera,
fragile bones, and hearing loss.
2. Type II: the most common type of dentinogenesis imperfecta .
3. Type III (Brandywine Type): characterized by multiple pulpal exposures in the deciduous dentition.

DENS-IN-DENTE (DENS INVAGINATUS) - a "tooth within a tooth" caused by an invagination of

all enamel organ layers into the dental papilla. It most frequently involves the MAXILLARY LATERAL
INCISOR. The pulp is usually exposed, thus is necrotic or inflamed and the pulp canals should be
cleaned and filled (RCT). This invagination can range in severity from an accentuated lingual pit to a
"dens-in-dente" .

260
ENAMEL HYPOCALCIFICATION - a hereditary dental defect affecting the enamel of primary and NOTES
permanent teeth. The enamel is soft and undercalcified in context, but normal in quantity due to the
defective maturation of ameloblasts (defect in mineralization of the formed matrix). The teeth are
chalky, the surfaces wear down rapidly, and a yellow-to-brown stain appears as the underlying dentin
is exposed .

ENAMEL HYPOPLASIA - a developmental defect in which the enamel is hard in context, but thin
and deficient in amount due to defective enamel matrix formation with a deficiency in the cementing
substance. There is a lack of contact between teeth, rapid breakdown of occlusal surfaces, and a yellow-
ish-brown stain that appears where dentin is exposed. This condition affects both primary and permanent
teeth, and can be transmitted genetically, or caused by environmental factors (i.e. vitamin deficiency, flu-
orosis, or metabolic disturbances during the prenatal period). It is a common dental sequelae in a child
with a history of generalized growth failure in the first 6-months of life. Hypoplastic areas on teeth are
seen if a child has illnesses in early childhood. Hypoplastic enamel is also a dental manifestation of hy-
poparathyroidism, preventable by early treatment with vitamin D.

CONCRESENCE - the state of teeth joined together only by cementum. Atype of fusion that occurs
after root formation is complete, possibly due to a traumatic injury.

GEMINATION - a process where a single tooth germ splits or shows an attempt to splitting to form
two completely or partially separated crowns, resulting in incomplete formation of two teeth. Most
commonly occurs in the incisor region.

FUSION - a condition produced when two tooth buds are joined together during development and ap-
pear as a macrodent (single large crown). Fusion usually occurs in the incisor area. The single crown
may have two roots or a grooved root, but there are usually two root canals. It is often difficult to dis-
tinguish between gemination and fusion.
• Fusion or gemination of teeth occurs during the initiation and proliferation stages of tooth ,...,
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ANODONTIA - a developmental abnormality characterized by the TOTAL ABSENCE OF TEETH.
1. Complete True Anodontia-a rare condition in which all of the teeth are missing. It may involve
both primary and permanent dentitions; usually associated with hereditary ectodermal dysplasia.
2. Partial Anodontia (Congenitally Missing Teeth)-rather common and usually affects maxillary 3rd
molars, maxillary lateral incisors, &mandibular 2nd premolars. As a rule, if only one or a few
teeth are missing, the absent tooth is the most distal tooth of any given type (if molar, then it
would be the 3'dmolar) .

OLIGODONTIA - congenital absence of MANY, but not all teeth.

HYPODONTIA - absence of only a few teeth.

Conditions that cause DELAYED exfoliation of primary teeth and DELAYED eruption of permanent teeth:
• Systemic conditions: Cleidocranial dysostosis, Down syndrome, Ectodermal dysplasia, Gardner's
syndrome, Osteogenesis imperfecta, rickets, severe congenital heart disease, and mental retardation.
• localized pathologic conditions: abscess of a primary tooth, or ankylosis of a primary or
permanent tooth .
• Hypothyroidism, Hypopituitarism, Hypoparathyroidism, and heredity/genetics.

HEREDITY is most frequently responsible for the congenital absence of teeth. The roots of the primary
tooth will resorb slower than normal without the presence of the permanent tooth. As a general rule, if
only 1 tooth or a few teeth are missing, the absent tooth is the MOST DISTAL TOOTH of any given type
(i.e. if a molar is congenitally missing, it is almost always the 3rd molar; if an incisor is missing, it is
nearly always the lateral, if a premolar is missing, it is almost always the 2nd premolar). Rarely is a ca-
nine the only missing tooth.

In the case of a congenitally missing 2nd premolar, you want to maintain the primary 2nd molar as
long as possible. If it is still present, it may be ankylosed . Cessation of eruption is most diagnostic of
an ankylosed primary molar.
261
 N Over-retained primary teeth in the mixed dentition may prevent the normal eruption of permanent
teeth, may be caused by the abnormal root resorption of the primary teeth, and are often treated
by extraction.
• Used caution when extracting over-retained primary teeth as the succedaneous tooth bud may
be in close proximity. This is especially true when placing the beaks of forceps into bifurcations of
primary molars in older children. The most common cause of fracture of root tips in extracting a
primary molar is root resorption between the apex and bifurcation.
• If a permanent tooth bud is accidentally extracted while removing a primary molar, the best
treatment is to immediately orient the tooth bud, replant the bud using digital pressure, and suture.
The best way to extract a primary molar that has the permanent tooth bud close to it is to section the
tooth and remove the parts individually.

Child Periodontium vs. Adult Periodontium:

• Child periodontium has greater blood and lymph supply.
• Alveolar crest is flatter, and alveolar bone is thinner (especially in the lamina dura area) since
there are fewer trabeculae in the alveolar bone of the pediatric patient.
• Gingival pocket depths are larger and the attached gingiva is narrower.
• Gingival tissues are redder because the child's gingiva is more vascular, thinner, and less
keratinized .
• There is lack of stippling because the C.T. of the lamina propria is shorter and flatter.
• Child has rounded and rolled gingival margins due to normal eruption patterns.
• Cementum is thinner and less dense than the adults, as cementum increases with age.
• POL fibers run parallel to the teeth. In adults, POL fibers are more horizontal against the tooth. The
child's POL is also wider (this is why you may see more tooth mobility and decreased resistance to
forces) . POL fiber bundles increase with age.

c....,
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-< ..,- Primary teeth begin to form at 6 weeks in utero &begin to calcify at 4 months in utero. Permanent
teeth begin to develop at 4 months in utero.

Stages in the Tooth's Development (life Cycle):

1. Initiation (Bud Stage)-the initial interaction between oral epithelium & mesenchyme
(ectomesenchyme) formation of dental lamina. Fused or geminated teeth occur during this stage.
2. Proliferation (Cap Stage)-the tooth's shape is evident and the enamel organ is formed . Fused
or geminated teeth occur during this stage. Fusion or gemination of teeth occurs during
initiation & proliferation stages of tooth development.
3. Differentiation (Bell Stage or Histodifferentiation)-final shaping of the tooth, cells differentiate
into specific tissue-forming cells (ameloblasts, odontoblasts, cementoblasts, and fibroblasts)
in the enamel organ.
• Dentinogenesis imperfecta &Amelogenesis imperfecta occur during the Bell Stage.
4. Apposition-cells that were differentiated into specific tissue-forming cells begin to deposit the
specific dental tissues (enamel, dentin, cementum, & pulp). The majority of cells of the dental
pulp are fibroblasts. "
5. Calcification (Mineralization)-primary teeth begin to calcify/mineralize during the 2nd
trimester of pregnancy (14 weeks or 4 months in utero).
• In a 2 year-old child, 40 teeth have calcified.
• At birth, 20 deciduous and 41'1 molars have commenced mineralization (24 teeth) .
• Maxillary and mandibular 1'1 molars begin to calcify at birth and are the first to
begin calcification .
• Mandibular 3,d molars are the last teeth to begin calcifying at age 8-10 years.
• The cariostatic effect of fluoride is manifested during the calcification stage of
tooth development.
• Tetracycline stain is incorporated and discoloration occurs during calcification.
• Calcification of the roots is completed by age 3-4.
6. Eruption-the emergence of tooth structure through the gingiva.
7. Attrition-loss of tooth structure.

262
Tooth development is initiated by mesenchyme's inductive influence on the overlying ectoderm.
Enamel is derived from ectoderm of the oral cavity. Ectodermal cells determine crown root and shape.
All other tooth tissues differentiate from the associated mesenchyme (mesoderm). Tooth development
depends on a series of sequential cellular interactions between epithelial & mesenchymal components
of the tooth germ. Once the ectomesenchyme influences the oral epithelium to grow down into the ec-
tomesenchyme and become a tooth germ, the following events occur:

Stages of Tooth Histogenesis (the formation and development of tooth tissues):

1. Elongation of the inner enamel epithelial cells of the enamel organ. This influences
mesenchymal cells on the periphery of the dental papilla to differentiate into odontoblasts.
2. Differentiation of odontoblasts.
3. Deposition of the 1sl layer of dentin.
4. Deposition of the 1'1 layer of enamel.
5. Deposition of root dentin & cementum.

KORFF'S FIBERS - a rope-like grouping of fibers in the pulp periphery that are involved with forma-
tion of the dentin matrix.

HERTWIG'S EPITHELIAL ROOT SHEATH (HERS) - an epithelial diaphragm formed/derived from

the joining of the inner + outer enamel epithelium of the enamel organ. After crown formation, the
root sheath grows down and shapes the tooth root and induces root dentin formation. Uniform growth
of HERS results in formation of a single-rooted tooth, while medial outgrowths or evaginations of the
sheath produce multi-rooted teeth.

When a tooth clinically erupts in the mouth, 2/3 of the root structure has developed. For primary teeth,
the root is completely formed by 18 months (for permanent teeth, it takes 3 years).

LOBES - primary centers of ossification always separated by developmental grooves that are very ,..,
c:::::r ,..,
-c
prominent in posterior teeth and form specific patterns. The minimum number of lobes from which :z: c:::::r
..... -
-~
en .....
any tooth may develop is 4. ..... :;g
:;g -
-< C")

• Alobe is one of the primary sections of formation in the development of the tooth's crown (it represents
a cusp on posterior teeth, and mamelons & cingula on anterior teeth).

• Anterior teeth lobes are much less noticeable and are separated by developmental depressions. All
anterior teeth have 4 lobes (3 labial, 1 lingual = cingulum).

• Premolars have 3 buccal + 1 lingual lobe (except mandibular 2nd premolar which has 3 buccal + 2
lingual lobes).

• 1'1 Molars have 5 lobes (5 cusps); one lobe for each cusp. The average age when the mineralization
of permanent 1st molar crown is completed is 4-5years.

• 2nd Molars have 4 lobes (4 cusps); 1 for each cusp.

• 3rd Molars have at least 4 lobes (4 cusps) 1 for each cusp, but variation are seen. Maxillary 3'd molars
usually have only 3 cusps.

• Mamelons-rounded or conical prominences on the incisal ridge of newly erupted incisors that represent
the 3 lobes from which the incisors developed from . Mamelons are usually worn off after the tooth
comes into functional position. The presence of mamelons in a teenager or adult is evidence of
malocclusion (usually an anterior open bite relationship where the incisors do not touch).

263
 NOTES
Primary Tooth Eruption
Age in Months Teeth Erupted Teeth
7 4 4 mandibular central incisors
11 8 4 maxillary lateral incisors
15 12 4 first molars
19 16 4 canines
23 20 4 second molars
*At age 15 months, 12 teeth have erupted (4 centrals, 4 laterals, and 4 molars).
*At age 19 months, 16 teeth have erupted (4 centrals, 4 laterals, 4 molars, & 4 canines).
*In the eruption sequence of a primary dentition, the first molar erupts before the canine.
*There are no premolars (bicuspids) in the primary (deciduous) dentition.

"Rule of Four" enables you to determine the number of teeth present at any given time and implies
the eruption of 4 teeth every 4 months beginning with 4 teeth at age 7 months.

Deciduous dental formula of man: I 2/2 + C 111 + M2/2 = 10 x 2 = 20 (5 per quadrant =

10 per arch = 20)

Permanent dental formula of man: I 212 + C 111 + B 2/2 + M 3/3 = 16 x 2 =32 (8 per quadrant =
16 per arch =32)

Closure of the apices of deciduous teeth occurs 18 months AFTER eruption.

3 Cardinal Rules of Tooth Eruption:

..,
C-c .., 1. girls teeth eru pt before boys.
:z:
.....
-:Do -
C 2. mandibular teeth before maxillary.
(I> .....
..... :::a
:::a-
3. slender teeth before stocky.
-< C")

MIXED DENTITION - a dentition phase during which some teeth present in the oral cavity are per-
manent, and some are deciduous (primary). The earliest indication of a mixed dentition consists of the
primary dentition &permanent mandibular 1't molars. 3 periods of dentition in man:
1. Primary dentition (6 months to 6 years)
2. Mixed dentition (6 to 12 years)
3. Permanent dentition (12+ years)

After the permanent teeth have reached full occlusion, small tooth movements occur to compensate for
wear at the contact areas (by mesial drift) and occlusal surfaces (by deposition of cementum at the
root apex).

Primary Dentition Eruption Schedule

Eruption Date (Months) Primary Maxillary Tooth Primary Mandibular Tooth
6 Central Incisor
7 Lateral Incisor
7-1/2 Central Incisor
9 Lateral Incisor
12 1st Molar
14 1st Molar
16 Canine
18 Canine
20 2nd Molar
24 2nd Molar
Active eruption of teeth occurs after Y2 the root IS formed.
264
 NOTES
Primary Dentition Calcification Schedule
Maxillary Tooth Hard Tissue Formation Begins
Central 3.5 months in utero
Lateral & 1st Molar 4.0 months in utero
Canine & 2nd Molar 4.5 months in utero
Mandibular Tooth Hard Tissue Formation Begins
Central 3.5 months in utero
Lateral & 1st Molar 4.0 months in utero
Canine & 2nd Molar 4.5 months in utero

Usual Exfoliation (Fall-out) Age of Deciduous Teeth:

• Primary central incisors are exfoliated between ages 6-8.
• Primary lateral incisors are exfoliated between ages 7-9.
• Primary canines are exfoliated between ages 9-12.
• Primary 1't & 2nd molars are exfoliated between ages 10-12.

Primary Teeth VS. Permanent Teeth:

• Primary teeth are lighter in color than permanent teeth.
• Pulp cavities are proportionately larger in primary teeth.
• Crowns of primary teeth are more bulbous and constricted than permanent teeth.
• Crown surfaces of all primary teeth are much smoother than permanent teeth (less pits &grooves
in primary teeth).
• Crowns of primary anterior teeth are wider M-D and shorter incisocervically than permanent
anterior teeth.
• Crowns of primary molars are shorter and narrower M-D at the cervical third than permanent molars. ..., ...,
C> ...,

..... -
:z: C>

• Roots of primary anterior teeth taper more rapidly than permanent anterior roots. cn==
..... ::c
• Roots of primary molars are longer and more slender than permanent molar roots. ::c
-< -C")
• Enamel ends abruptly at the cervical line on primary teeth, rather than becoming thinner as on
permanent teeth.
• Buccal and lingual surfaces of primary molars are flatter above the crest of contour than on
permanent molars.

Primary Molars VS. Permanent Molars:

• Primary crowns are shorter with pronounced B &L cervical ridges and a constricted cervical area .
• Primary occlusal table is narrow F-L.
• Anatomy is shallower (i.e. cusps are short, ridges are not as pronounced, and fossae are not as deep).
• A prominent mesial cervical ridge (makes it easy to distinguish rights from lefts).
• Roots are longer and more slender than the roots of permanent molars. The roots are extremely narrow
M-D and very broad lingually.
• Roots are very divergent and less curved. There is little or no root trunk.
• The sum of the M-D widths of primary molars in anyone quadrant is 2-5mm greater than
the permanent teeth that succeed them (premolars). Also, the enamel on the occlusal surfaces
of primary molars is of uniform thickness and is -1mm thick, compared to permanent molars
(2.5mm) thick.

265
 N PRIMARY DENTITION
SUCCEDANEOUS TEETH - in each quadrant, 5 permanent teeth (incisor, canine, & premolars) suc-
ceed/replace the 5 primary teeth. Permanent molars do not replace primary teeth, thus are not suc-
cedaneous teeth.
• The last primary tooth to be replaced by a permanent tooth is usually the maxillary canine (the
permanent maxillary canine usually erupts between age 11-12). Permanent mandibular canine
usually erupts between 9-10yrs.

NON-SUCCEDANEOUS TEETH - do not succeed/replace deciduous teeth (permanent maxillary &

mandibular 1'\ 2nd , & 3'd molars).

A6-year old should have all 20 primary teeth and 4 first molars (6-year molars) clinically visible in
the mouth.
• Permanent mandibular centrals erupt between ages 6-7.
• Permanent maxillary centrals erupt between ages 7-8.

A7-year old should have 18 primary teeth (except the two mandibular centrals) and 6 permanent
teeth (all 4 first molars &2 mandibular central incisors) clinically visible.

MANDIBULAR CENTRAL INCISOR -the first deciduous (primary) tooth to erupt.

MAXILLARY CENTRAL INCISOR - the first succedaneous tooth to erupt.

• The crown of the primary maxillary central incisor is larger M-D than the permanent maxillary
central incisor.
• Primary maxillary central incisor has a shorter crown length inciso-cervically than the
...,
C"tJ
:z:
..., permanent maxillary central incisor.
...... -C • primary maxillary central incisor's incisal edge is straighter than the permanent maxillary
c;;~
...... :::<:I
:::<:1- central's incisal edge .
-< ..,
• No mamelons are present on the primary maxillary central incisor, only on permanent
maxillary central incisors.
• Labial and lingual cervical ridges are prominent on all primary incisors.

When extracting primary incisors where the roots have been partially resorbed due to pressure from the
developing permanent teeth, the facial part of the remaining primary root is usually the longest and
most securely attached to the gingiva .

PRIMARY MAXILLARY LATERAL INCISOR - the most common congenitally missing primary
tooth (although this is rare). This tooth is most often atypical in size (i.e. peg-shaped).
• A patient who has permanent central incisors, permanent canines, and primary canines anterior to
the premolars most likely has congenitally missing permanent lateral incisors.
• Most common congenitally missing permanent tooth is the 3rd }11olar, then the mandibular 2nd
premolar, then the maxillary lateral incisor.

PRIMARY MAXILLARY CANINE - the teeth most likely to be crowded out of the arch.
Mesial cusp ridge is longer than the distal cusp ridge, and its cusp is much longer &sharper than the
permanent maxillary canine. This is the opposite on all other canines. It also is very wide and short.

PERMANENT MANDIBULAR 2ND PREMOLARS - the tooth most likely malposed in cases of
mandibular arch space discrepancy.

266
PRIMARY MANDIBULAR pT MOLAR -this tooth does not resemble any other primary or
permanent tooth.
• It has an oval occlusal surface that is wider M-D than B-L.
• From an occlusal view, the MB angle is acute and prominent due to the mesial cervical ridge on
the buccal surface. The DB angle is obtuse.
• Occlusal table is rhomboid-shaped, and is the chewing surface inside the cusp ridges and
marginal tables.
• Has a prominent transverse ridge that unites the MB + ML cusps, and separates the mesial
portion from the rest of the occlusal surface.
• MB cusp is always the largest and longest cusp, occupying nearly 2/3 of the buccal surface.
• ML cusp is larger, longer, and sharper than the DL cusp.
• Crown is wider M-D than cervico-occlusally.
• Mesial marginal ridge is very well developed and resembles a cusp. It has a prominent MB
cervical ridge.
• Class II cavity preparations are difficult due to its morphology, and it has NO central fossa.
• Mandibular 1st Molar-the first permanent tooth to erupt and first to begin calcifying.
• Maxillary 1't Molar-the second permanent tooth to erupt.
• Maxillary and mandibular 151 molars are NOT succedaneous teeth.
• Primary 151 molars are the teeth with the most noticeable morphologic deviations from
permanent teeth.

PRIMARY MANDIBULAR 2ND MOLAR:

• Its morphology and amalgam preparation outline closely resembles the permanent mandibular
151 molar.

• Relative size of the distal cusp. The MB, DB, and distal cusps are nearly equal in size. However, the
distal cusp of the permanent molar is smaller than the MB and DB cusps.
• From the buccal aspect, it is has a narrow M-D dimension at the cervical portion of the crown
compared to the dimension M-D on the crown at the contact level. The mandibular permanent 151
,...,
<::I -g
,...,
molar is wider at the cervical portion. :z:
..... -<::I
-:too
• Groove patterns are different on the occlusal surface. en .....
..... ;::c
;::c-
• Primary molar has more divergent roots to allow eruption of the 2nd premolar. -< C")

• Primary molar has a more prominent facial crest of contour.

• Primary 2nd molar has the greatest F-L diameter of all primary teeth.

PRIMARY MAXILLARY 1ST MOLAR - this is the most atypical tooth of all the molars (primary
and permanent). It is intermediate in form and development between a premolar and molar.
• It is the smallest molar in all dimensions EXCEPT the labiolingual diameter.
• The crown of this tooth is bicuspid (two cusped). It has a wide MB (the longest cusp) and narrow ML
cusp (second longest and sharpest). The indistinct cusps are the DB & DL.
• Its cervical line is higher mesially than distally.
• The cervical ridge stands out very distinctly on the MB portion of the tooth.
• H-shaped occlusal pit-groove pattern.
• Primary maxillary 1st molar has THREE ROOTS and its root form closely resemble the permanent
maxillary 151 molar.

PRIMARY MAXILLARY 2ND MOLAR - while smaller, this tooth morphologically resembles the
permanent maxillary 1't molar.
• The crown's F-L measurement is greater than its M-D measurement.
• May have a 5th cusp of Carabelli.
• Has a prominent MB cervical ridge and an oblique ridge.
• MB cusp is almost equal in size or slightly larger than the ML cusp.
• The MB pulp horn is the largest and longest.
• Primary 2nd molars are larger than primary 151 molars and resemble the form of permanent 151 molars.

267
 N
Permanent Dentition Eruption Schedule

Eruption Date (Years) Age Range (Years) Maxillary Mandibular

6 6-7 1st molar 1st molar (erupts first)
6 6-7 Central incisor
7 7-8 Central incisor
7 7-8 Lateral incisor
8 8-9 Lateral incisor
10 9-10 Canine
10 10-12 1st premolar 1st premolar
11 10-12 2nd premolar 2nd premolar
11 11-12 Canine
12 11-13 2nd molar
12 12-13 2nd molar
20 17-21 3rd molar 3rd molar

% of root formation is complete at the time of eruption. Root apex is fully developed
2-3 years after eruption.
A normal 6 year old has all 20 primary teeth and 4 permanent first molars.

Permanent Dentition Calcification Schedule

Maxillary Tooth Hard Tissue Formation Begins
,..., ,...,
c ....
:z: c
--t - Central 3-4 months
u;~
--t ::a
::a
-< -C"> Lateral 10-12 months
Canine 4-5 months
1st Premolar 1.5-1.75 years
2nd Premolar 2-2.5 years
1st Molar Birth
2nd Molar 2.5-3 years
3rd Molar 7-9 years
Mandibular Tooth Hard Tissue Formation Begins
Centra I & Latera I 3-4 months
Canine 4-5 months
1st Premolar
2nd Premolar
.1.75-2 years
2.25-2.5 years
1st Molar Birth
2nd Molar 2.5-3 years
3rd Molar 8-10 years

*Permanent 1st Molars begin to calcify AT BIRTH. Tooth buds initiated after birth are premolars
and 2nd & 3rd molars.

268
 Important Human Development Facts:
• At age 6, a child 's head is 90% of its adult size. This is typical of all neural tissues in the body. At
birth, the cranial vault is very near the size it will eventually attain in adulthood (compared to the
cranial base, mandible, mid-face, etc.). The brain and cranial base are fully developed by age 6.
• At birth the jaw is large enough to accommodate all primary teeth if they were to erupt simultaneously.
• At birth, the width of the face has reached its greatest percentage of its adult size (as opposed to
height and depth).
• At birth , the palate is flat. In adults, it is vault-shaped (this occurs by deposition of alveolar
crestal bone).
• In early life, tonsils function to filter bacteria and program the production of antibodies.
• At birth, a newborn cannot differentiate between sour, salt, or bitter tastes.
• From ages 6-12, the body's lymph tissue is 200% of its normal adult mass. Consequently, enlarged
tonsils in a 6-year old are at age 12, most likely smaller because lymphoid tissue in the nasopharynx
decreases at puberty, while at the same time, the genital tissue is developing.

FLUORIDE &SEALANTS
Fluoride is the most effective caries prevention agent available. It is com pletely safe when used
properly. However, ingestion of high fluoride concentrations can cause nausea, vomiting, dental fluoro-
sis (mottling), or in extreme cases, death (especially in children) .
• Preventive dentistry for Adolescents: frequent dental visits, fluoride rinses at home, fluoride tray
applications, brushing and flossing, sealants, and fluoride tablets.
• Topical fluoride (with occlusal sealants) is the primary preventive agent during adolescence (past
age 12) because the entire dentition (except 3rd molars), normally erupts by age 13. Thus, fluoride
tablets may not be as beneficial. Fissure sealants succeed by altering host susceptibility.
• Caries activity is directly proportional to the consistency, frequency, & oral retention of
fermentable carbohydrates ingested. ..........
c.."
:z c
• To prevent dental caries, the Centers for Disease Control &Prevention recommends at least ..... -
cn~
0.7ppm of fluoride be present in drinking water. The maximum fluoride amount is 1.2ppm. .....
""-
-< ..,
""
• The optimal concentration of fluoride for community water depends on AIR TEMPERATURE.

A 15-year old female has lived in a non-fluoridated area her entire life. When she moves to a commu-
nity where the drinking water naturally contains 6ppm of fluoride, she will experience an increase in
the amount of fluoride stored in her bones.
• Moderate fluorosis will not occur, because by age 15 her entire dentition has undergone complete
" enamel calcification (except possibly the Jd molars). A 50% reduction in dental caries is not
probable because her entire dentition has already undergone complete enamel calcification.
• Water fluoridation and diet supplementation may affect tooth morphology, while self and
professionally applied topical treatments will not.
• Fluorides often added to water supplies are sodium fluoride, sodium silicofluoride, &
hydrofluosilicic acid.
• Deposition of fluoride occurs on the smooth surfaces of teeth .

Fluoride's main effect occurs AFTER the tooth has erupted above the gingiva ("post-eruptive").
This topical effect happens when small amounts of fluoride are maintained in the mouth in saliva and
dental plaque. Fluoride works by stopping or even reversing the decay process. It keeps enamel strong
and solid by preventing the loss of and enhancing the re-attachment of important minerals from tooth
enamel. Fluoridation of community water is credited for reducing tooth decay by 50-60% in the
U.S. since WWII. Recent estimates show decay reduction at 18-40%, which reflects that even in
communities that are not optimally fluoridated, people are receiving some benefits from other
sources (i.e. bottled beverages, toothpaste).

269
 NOTES Professional Applied Topical Fluorides (applied 2x/year): 8% Stannous Fluoride, 1.23% Acidulated
Fluorophosphates (APF gel), & 2% Sodium Fluoride.
1. Sodium Fluoride (NaF) (2%)-advantages are neutral/basic pH (9.2), more acceptable taste than
stannous fluoride, and no adverse effect on restorative materials.
2. Stannous Fluoride (SnF2) (8%)-only advantage is it does not etch porcelain restorations. It
tastes bad, stains silicate restorations, and is a non-stable solution. pH is 2.1-2.3 (acidic).
• Causes STAINING of demineralized enamel and porcelain. It may discolor tooth-colored
restorations and margins, and cause staining of teeth in demineralized areas, pits, fissures,
and grooves.
• Stannous fluoride is NOT used in any approved dentrifices in the U.S.
• The main advantage of using an 8% solution of stannous fluoride instead of a 2% solution
of sodium fluoride for a topical fluoride treatment is a single treatment may be given.
3. Acidulated Phosphate Fluoride (1.23%)-has a more acceptable taste than stannous fluoride,
and can be applied to both arches simultaneously. However, it may damage porcelain restorations.
Typically 1.23% concentration is applied by the dentist.
• pH of APF gels falls in the 1-4 range (pH is 3.0-3.5 which is acidic).
• APF is contraindicated on porcelain and composite restorations because it causes pitting
and etching of these materials. Acidulated fluorides should be avoided on implant patients
because they can corrode the surface of titanium implants.
• The most effective way to increase fluoride content in the external tooth layers is a daily
application of 1.23% APF in fitted trays for 4 minutes. However, this is not realistic since we
do not routinely do "daily" applications.

Fluoride Concentrations Found in Other Compounds

Fluoride Type Dentrifice Brush-on Gel (home use) Oral Rinse

0....,
.......... Sodium Fluoride (NaF) 0.24% 1.1% 0.05% daily-swallow
:z: 0
.....
v;~
- 0.2% weekly-expectorate
..... :=0
:=0-
-< C">
Sodium Monofluorophosphate 0.76% NA NA
(NaP03F)
Acidulated Phosphate Fluoride NA 0.5% 0.04% daily-swallow
(APF) or expectorate
Stannous Fluoride (SnF2) NA 0.5% 0.1% daily

*Fluorapatite is the most stable reaction product of a topical application of fluoride.

When painting fluoride on, it is critical to isolate the teeth with cotton rolls. When using fluoride
trays, cotton rolls may be placed in premolar areas to increase patient comfort and help keep the fluo-
ride in place. Patients are asked not to brush, rinse, eat, or drink for 30 minutes after a fluoride treat-
ment so the fluoride is left undisturbed and is able to continue reacting with the hydroxyapatite for
some time after the initial application. Fluoride treatments should be applied for 4 minutes, although
there are now some 1 minute products available on the market.

Appropriate Use of Professionally Applied Fluoride Application Frequency

Sodium Fluoride (NaF) Acidulated Phosphate (APF) Stannous Fluoride (SnF2)

Concentration Solution 2% Gel or solution 1.23% Solution 8%
Fluoride ion % 0.91% 1.23% 1.95%
ppm fluoride 9,040ppm 12,300ppm 19,360ppm
mg/ml fluoride 9.04 12.0 19.36
Efficacy 29% 28% 32%
Taste bland bitter without flavoring astringent
Tooth discoloration none none brown
Gingival reaction none none occasional

270 *The fluoride concentration is most dentrifices ranges between 900-1500ppm.

Beneficial Effects of Fluoride:
1. Interferes or inhibits plaque formation on enamel surfaces. Dental plaque adheres to teeth
because DEXTRANS are insoluble and sticky.
2. Has antibacterial qualities depending on the concentration (fluoride is bactericidal in
high concentrations).
3. Enhances enamel remineralization to help reduce and eliminate early carious lesions.
4. Decreases enamel solubility.
5. Inhibits glycolysis (the process by which sugar is metabolized by bacteria to produce acid).
When glycolysis is inhibited, the caries process is inhibited.

Mechanisms of Fluoride to Inhibit Caries:

1. Topical effect of constant infusion of a low fluoride concentration into the oral cavity
enamel remineralization.
• One of the most effective means of reducing caries activity is by decreasing the solubility of
enamel to the acid attack of bacteria. Enamel demineralization begins when the pH reaches
5.5 (the pH threshold level at which enamel demineralization occurs).
• The main anti-cariogenic effect of fluoride is by enhancing remineralization. Its secondary role
is to decrease demineralization by increasing the resistance of the tooth's outer surface
(enamel). Lastly, the least understood property of fluoride are its antimicrobial properties.
2. Fluoride converts hydroxyapatite fluorapatite by substituting OH' for Fl'. F decreases the
solubility of hydroxyapatite crystal, while increasing the crystal size. Fluoride ion is easily
exchanged with the hydroxyl ion in the lattice structure of enamel because FI is slightly smaller
than OH- with a greater affinity for hydroxyapatite crystals than OH-.
3. Fluoride inhibits glycolysis where sugar is converted into acid by bacteria (fluoride ion inhibits
enzymatic production of glucosyltransferase).

Fluoride mouth rinses are shown to have the greatest effect on NEWLY ERUPTED TEETH, making it
essential to have rinsing continued into the teen years to protect the 2nd and )Cd permanent molars.
• Fluoride rinses are most beneficial to SMOOTH tooth surfaces and there are some benefits to ,...,
C
,...,
."

pits & fissures .. ....-

:z: c
-:Do

• Systemic fluorides are least effective on root surfaces. ....-< ""

(I)

""-
....

C">

During a routine prophylaxis, it is possible that the use of abrasive polishing agents may remove the
fluoride-rich layer of enamel. The greatest concentration of fluoride ions exist on the outermost
layer of enamel (not just beneath the enamel surface). Since this fluoride-rich layer may be inadver-
tently removed while polishing, all patients would benefit from a topical fluoride application after a
routine prophylaxis.
• Dicalcium Phosphate-the toothpaste/dentrifice component most likely to inactivate the fluoride ion.
• Some believe the pumice prophylaxis may be omitted as studies show fluoride can make its way
through the pellicle and plaque to the tooth surface. However, heavy stains may interfere with fluoride
absorption, thus stains should be removed.

Factors to Consider when Prescribing a Child Fluoride Supplement:

• Amount of fluoride in the child's drinking water, child's age, and how responsible the person
administering the fluoride supplement is (whether it be the patient or patient's parents).
• When determining the appropriate dose of systemic fluoride supplement for a child, it is most important
for the dentist to consider the child's age and fluoride content of the drinking water (H2O)'
• Before prescribing topical and/or systemic fluoride, the dentist must consider the child's AGE.

271
 NOTES -

Recommended Dosages of Supplemental Fluoride by Age &

Concentration of Fluoride in Water (ppm)

Child Age < 0.3ppm 0.3-oJppm > oJppm

6 months-3 years O.25mg None None
3-6 years O.50mg O.25mg None
6-16 years 1.00mg O.50mg None

*l.oomg of fluoride supplement should be given to a 6-year old patient in an area where the fluo-
ride is 0.25ppm.
*0.5mg of fluoride supplement should be given to a 3-year old patient in an area where the fluo-
ride is 0.25ppm.

Emergency treatment in the dental office for a child who has accidentally ingested a large amount
of fluoride includes:
• Induce vomiting manually or with the help of Ipecac syrup and call 911.
• Have the patient drink a large quantity of milk or another calcium-containing liquid to decrease
stomach acidity and to form complexes with the fluoride to decrease its absorption.
• Do NOT have the patient drink large quantities of sodium bicarbonate or crush ammonia vaporole
under the patient's nose.

Acute Fluoride Toxicity symptoms may appear within 30 minutes of ingestion and persist for up to
24hrs. Patients may experience nausea, vomiting, diarrhea, and abdominal cramping since 90-95% of
ingested fluoride is absorbed through the stomach and small intestines. Fluorides are mainly elimi-
nated from the body via the kidneys. However, the fluoride that remains in the body is found mostly in
CJ ..,
.., -.::I
skeletal tissue.
:z: CJ
.....
c:;;~
-
..... ::o::r
::o::r-
-< ~ ACUTE FLUORIDE POISONING - is rare, but the most common causes of death are cardiac fail-
ure &respiratory paralysis. Fluoride toxicity shows up in the bones as osteosclerosis.
• Ingestion of 15mg/kg of fluoride can be lethal to a child. The adult lethal dose is 4-5gm.
• In mg/kg body weight, the LETHAL DOSE of fluoride falls in the range of 2o-50mglkg.

If a 6-year old child were receiving fluoridated water in the amount of 3ppm, the result would most
likely be fluorosis, but not systemic toxicity. However, if a child age 6-7 were receiving 8ppm of fluori-
dated water, there is a good chance of systemic toxicity and moderate-to-severe fluorosis.

For an adult, the LETHAL DOSE of fluoride is between 2.5-1 og, with the average lethal dose is 4-5g.
Death has occurred in infants with as little as O.25g (250mg). Death is likely in a child who ingests>
l5mg of F-/kg body weight (i.e. 5 teaspoons of APF gel for a 441b child) . Thus, it is weight dependent.
Most fluoride absorption occurs in the stomach (an acidic pH is required to facilitate this diffusion
process). The minimum does that could caGse toxic signs and symptD'illS (including death), and that
should trigger immediate therapeutic intervention and hospitalization is 5mgF/kg weight =
2.27mgF/lb (this is the "probable toxic dose")

Most effective method to reduce dental caries in the general population is FLUORIDATION of the
communal water supply. The optimal concentration in the communal water supply varies with mean
annual temperature, but is 1ppm in most states. Fluoride supplements are recommended if the
water fluoride content is < 0.7ppm. Fluoride supplements are normally NOT indicated after age 13.
• School water fluoridation optimal concentration is 4.5x that of city water supplies because of less
water consumption at school.
• Achild should STOP taking fluoride supplements at 16-18 years old.
• It is not necessary to prescribe fluoride supplements to a child who is consuming optimally
fluoridated water.
• Children in an elementary school exhibit a high interproximal caries rate. For these children, the
school-based program that will be most effective is fluoride mouthrinse.

272
In communities without fluoridated water supplies, the most cost-effective method of delivering NOTES
fluoride to 6-12 year old children is via school water fluoridation (it is better than tablets, brushing
with fluoride gel, or rinsing with fluoride mouthrinse).

Fluoride Therapies for a 13-year old child prone to decay who lives in a community where the
water is appropriately fluoridated:
• Professionally applied fluoride every 6 months, and fluoride toothpaste.
• Low concentration fl uoride mouth ri nse. High concentration mouth rinses must be professionally
prescribed and require a prescription. These rinses reduce root surface hypersensitivity.
• Dietary fluoride supplements are contraindicated since the community water is appropriately
fluoridated.

DENTAL FLUOROSIS - an "irreversible" diffuse symmetric hypomineralization disorder of

ameloblasts that only occurs with exposure to fluoride when enamel is developing (during the calcifi-
cation period). Dental fluorosis is a toxic manifestation of chronic (low-dose, long-term) fluoride in-
take. Dental fluorosis is not caused by repeated topical application of fluoride .

• Dental fluorosis typically causes "mottled" discoloration and pitting of the enamel of permanent
and deciduous teeth. The severity of mottling increases with an increasing amount of fluoride in the
drinking water. Thus, there is little mottling at a level below O.9-1.0ppm of fluoride in the drinking
water, while children living in temperate zones where the water supply contains a higher content of
fluoride are most often affected .

• If a child lives in a temperate zone most of their childhood (up to age 9-lOyrs.), all permanent teeth
will most likely be affected (remember: 3rd molars begin calcification between ages 7-9yrs, so if the
child moves before this age, the 3rd molars may not be affected).

• Systemic distribution of fluoride may affect tooth morphology. Systemic distribution of fluoride is
accomplished by fluoride in the water, fluoride tablets, and vitamins that contain fluoride. ..... .....
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• Fluorosis may result from excessive fluoride consumed during the mineralization stage of tooth -< C">

development, and can occur in permanent and primary teeth.

When a 15-year old female who has lived in a non-fluoridated area all her life moves to a commu-
nity where the drinking water naturally contains 6ppm of fluoride, an increase in the amount of fluo-
ride stored in her bones is most likely to occur. Moderate fluorosis will not occur, because by age
15, her entire dentition has undergone complete enamel calcification (except possibly the 3rd molars) .

3 Fluorides used in Public Drinking Water Supply: sodium fluoride, sodium silicofluoride, & hy-
drofluosilicic acid (supplied as an aqueous solution in 55 gallon drums and is commonly used at
ground water well houses). The first two fluorides are supplied in bulk, crystalline form, and are regu-
larly used at water treatment plants.
• The use of hydrofluosilicic acid is advantageous because of the relatively inexpensive equipment
required compared to the equipment used with powered components. Hydrofluosilicic acid is added
directly to the water by a chemical dosing system th?t consists of a chemical feed pump,
analyzer/controller, injector, drum scale, and 55-gallon drum of the acid solution. Diluting the acid
prior to adding it to the water is not recommended because of the hazards involved in handling the
acid, and errors associated with dilution.
• When fluoride concentrations in excess of 1.5-3.0mg/L are consumed, a chemical combination can
occur within tooth enamel, resulting in mottled and permanently discolored teeth. Concentrations>
4mg/L can be toxic.

273
 N SEALANTS & FLUORIDE
Placing sealants is a highly effective way to prevent pit and fissure caries. It is safe, but underused
in the private and public dental health care delivery systems. The substantial reductions in dental
decay in the U.S. young population is due to systemic and topical fluorides. The control of smooth sur-
face caries provided by fluorides is critical to the additional effectiveness of sealants. Sealants are
highly effective in preventing pit and fissure caries.
• When sealants are applied correctly, there is a decreased development of new carious lesions and a
decreased progression of pre-existing lesions.
• A close correlation exists between a sealant retention and their effectiveness. The effectiveness of
sealants is equal whether applied by dentists, hygienists, or dental assistants provided that they have
received appropriate training.
• Curing sealant materials occurs one of two ways. Some sealants are chemically cured via
"autopolymerization". These materials are dispensed as two components. As soon as the components
are mixed, polymerization begins. Curing is complete in -60 seconds. Other sealant material is cured
with visible light, but the curing light must be of high quality and should be tested frequently for the
value of light emitted. Retention rates for chemically cured and light cured sealants are similar.
• Low viscosity sealants wet acid-etched tooth surfaces the best.
• Sealants need micro-mechanical retention. The surfaces should be cleaned with a prophylaxis brush
or rubber cup and pumice with water. When the teeth are effectively isolated from saliva
contamination, the surfaces are dried and acid etched by applying 30-50% phosphoric acid solution
for 1 minute. The solution should be gently agitated during application and is then washed away and
dried to leave a frosty-appearing etched surface.
• The properties of sealants are closer to unfilled direct resins than to filled resins (composites) .
Sealants are weaker than filled resins, but their strength is sacrificed allow it to flow into pits and
fissures (its viscosity must be low enough to flow into pits and fissures) .
• The most likely result of inadvertently sealing a small carious lesion in the occlusal surface is the
C ."
I'T'I I'T'I caries is arrested.
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• Research indicates pit and fissure sealants are best retained on maxillary and mandibular premolars .
..... :::c
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-< ... However, maxillary and mandibular 1st molars benefit the most from sealants.

The principal feature of a sealant required for success is ADEQUATE RETENTION. Sealant success is
highly depends on obtaining and maintaining intimate adaptation of the sealant to the tooth surface
to hopefully seal it. Research shows caries protection is 100% in pits and fissures that remain
completely sealed.

Components of Pit &Fissure Sealants:

1. Bis-GMA: monomer that can be diluted with TEGDMA to reduce viscosity.
2. Initiator: Benzyol Peroxide in self-cured sealants and Diketone in visible-light cured.
3. Accelerator: amine is self-cured.
4. Opaque Filler: small amounts of Ti02 (titanium oxide) are added to make the appearance
slightly different from the occlusal enamel.

Sealant materials can be unfilled, filled with opaquer, clear, and colored. However, there is no dif-
ference in retention rates. Filled materials are easier to see and monitor, but clear materials allow
the operator to continue to see the filled fissures. Sometimes operators prefer colored sealants to make
monitoring retention easier. The newest sealant material is "fluoride releasing" where fluoride is re-
leased from the sealant after polymerization. The clinical significance of this is not yet determined, but
the fluoride release is thought to occur at the base of the sealed groove, which provides a fluoride-rich
layer available when remineralization of an incipient lesion occurs.

274
If a topical fluoride is used in conjunction with a pit and fissure sealant, the fluoride is applied
AFTER the sealant. When topical fluoride is used, it is applied either before the conditioner (acid
etchant) or after the sealant. When cleaning the tooth prior to application, do not use glycerine-con-
taining products. Applying fluoride after the conditioner decreases the bond strength. Technique for
Applying Sealants:
1. Gross debridement of enamel surfaces (use plain flour or pumice). Do not use anything that
contains fluoride because it inhibits etching. Rinse thoroughly.
2. Isolate teeth with a rubber dam or cotton roll to keep the tooth dry. Dry isolated teeth thoroughly.
3. Acid etch the teeth with phosphoric acid (30-50% concentration). Apply etchant by gentle dabbing
of the enamel surface. Etching time for permanent teeth is 1 minute (2 minutes for primary teeth).
4. Rinse and dry thoroughly. A properly etched surface appears dull and chalky.
5. Apply sealant (procedure differs with the method of polymerization).
6. Evaluate results, floss the tooth, and check occlusion.

When painting fluoride on, it is important to isolate the teeth with cotton rolls. When using fluoride
trays, cotton rolls may be placed in the premolar areas to increase patient comfort and kept the fluo-
ride in place. Patients should not brush, rinse, eat, or drink for 30 minutes after fluoride treatment so
that the fluoride is left undisturbed and can continue to react with the hydroxyapatite for some time
after the initial application. Fluoride treatments should be applied for 4 minutes, although there are
now some I-minute products available.

Fluoride Concentrations Found in Other Compounds

Fluoride Dentifrice Brush-On Gel (Home Use) Oral Rinse
Sodium Fluoride (NaF) 0.24% 1.1% 0.05% daily-swallow
0.2% weekly-expectorate
Sodium Monofluorophosphate 0.76% NA NA ""
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(NaP03F) .....
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Acidulated Phosphate Fluoride NA 0.5% 0.04% daily-swallow ::c -
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(APF) or expectorate
Stannous Fluoride (SnF2) NA 0.4% O.l % daily

*Fluorapatite is the most stable reaction product of a topical application of fluoride .

HEAD &NECK CANCER patients can benefit by using Sodium fluoride &Stannous fluoride for home-
care custom tray use. The gel contains 1% sodium fluoride or 0.4% stannous fluoride. For maxi-
mum benefit, the gel must be in direct contact with teeth. Fluorides are recommended to protect
cancer patients from post-irradiation caries.
• The fluoride found in commercial toothpastes is not adequate for people who have had head and
neck radiation. These patients must continue to use the fluoride gel as directed for their entire life
to protect their teeth from rampant decay.
• Patient Instructions: the trays containing the fluoride are placed over the teeth for a prescribed
period of time (usually 10 minutes), and the patient cannot eat or drink for at least 30 minutes. This
is usually done at night after toothbrushing and just before going to bed.

Daily use of fluoride gel in custom trays at home is indicated in these situations:
• Rampant enamel or root caries in any age group.
• Xerostomia.
• Head and neck radiation therapy.
• Use on abutment teeth under an overdenture.
• Hypersensitive root surfaces.

275
 Components of Sodium Fluoride Paste Used to Treat Root Sensitivity: sodium fluoride, kaolin,
glycerin (present in paste in equal parts).
• The rationale of desensitization procedures is not fully understood. Some techniques may depend on
denaturation of the superficial ends of Tomes' fibers or nerve endings in dentin . Other procedures are
designed to deposit an insoluble substance on the ends of the fibers or nerves to act as a barrier to
stimuli . Others are designed to stimulate secondary dentin formation to insulate the pulp from
external stimuli.
• Hydrodynamic Theory-the most accepted theory to explain unusual sensitivity and response
of exposed root surfaces to various stimuli which postulates the pain results from indirect
innervation caused by dentinal fluid movement in the tubules which stimulates mechanoreceptors
near the predentin.
• Technique: After cleaning the hypersensitive areas, rub the paste into the exposed root surfaces with
a porte-polisher and orangewood stick or rubber cup for 1-5 minutes. Satisfactory results are usually
obtained. No caustic effects on the gingiva or mucosa result from contact with the paste. However,
it is toxic if accidentally ingested.

Susan is evaluated 8 months after her sealants were applied and lost two of the four sealants that
were placed due to either:
1. etchant was not rinsed thoroughly off the tooth surface.
2. dry field was not maintained and the tooth surface was contaminated with saliva after etching.
3. contaminated air supply to air/water syringe.
4. tooth was not thoroughly dried prior to applying the sealants.

Sealants act as a physical barrier to prevent bacteria from accumulating in pits and fissures of teeth.
• Care is taken not to mix the sealant resin too vigorously prior to placement or to over-manipulate the
sealant resin upon placement. Either of these errors can incorporate air into the sealant resin , causing
a void in the sealant surface. As long as the sealant remains in tact, decay will not develop under it.
• Factors that may influence which teeth are candidates for sealants: presence of interproximal decay,
""
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-< C"> For permanent molar placement, this is usually around age 6 and 12 (give or take 6 months).
• Although sealants are commonly placed on permanent molars, they can be placed on deciduous teeth
when there are deep pits and fissures, or very caries prone teeth that are not likely to exfoliate soon.

Fluoride Facts:
• Fluoride does NOT reduce caries by making enamel harder, but reduces its rate of solubility.
• Substantial reductions in dental decay in the young U.S. population are due to use of systemic &
topical fluorides.
• Fluoride concentration in body fluids is regulated by an equilibrium relationship between bone &
urinary excretion .
• Most fluoride is absorbed in the small intestine and excreted through the kidneys.
• Fluoride passes the placental barrier slowly and is deposited in calcified tissues (i.e. bones).
• At 1.0ppm fluoride is tasteless, colorless, & odorless. 1.0ppm is the optimum fluoride concentration
in community drinking water.
• U.S. Public Health Service sets the optimal fluoride level at 0.7-1.2ppm for public water. Optimal
fluoride concentration in community drinking water depends on the average air temperature and
water consumption. For temperate climates, the optimum is l.0 ppm, and for warmer and colder
climates the amount is adjusted from 0.7 -l.2ppm, respectively.
• Fluoride uptake on teeth depends on the amount of ingested or delivered fluoride in contact with the
tooth during the day.
• Fluoride is deposited in calcified tissues (skeletal) , and normally accumulates slowly in bones as a
person ages.
• Proximal tooth surfaces derive the greatest benefit from fluoridation.
• Dental fluorosis can occur in permanent and deciduous teeth.
• Fluoride's cariostatic effect is produced during the calcification stage of tooth development.
• Fluoride converts hydroxyapatite fluorapatite to decrease enamel's solubility.

276
Fluoride helps teeth in two ways. When children under age 6 ingest fluoride in small doses, it becomes
incorporated in their developing permanent teeth, making it harder for acids to cause demineraliza-
NOTES
tion. Fluoride also works directly on teeth in children and adults by speeding up remineralization
and disrupting acid production by bacteria.

232 mg of fluoride are in an 8.2 ounce tube of toothpaste sold in the U.S. containing -11 OOppm
fluoride ion. Either sodium fluoride or sodium monofluorophosphate contain -1.0mg of fluoride per
gram of toothpaste.

To solve, convert ounces grams (8.2 ounces x 28.35 = 232gm). Since there is -lmg of fluoride per
gram of toothpaste, there are 232mg of fluoride. For tubes sold in other countries, the fluoride con-
centration varies.

Fluorides currently used in dentifrices sold OTe in the U.S: sodium fluoride &sodium
monofl uorophosphate.

Abrasives Used in Dentifrices: silica, calcium carbonate, dicalcium phosphate (may inactivate F-),
and dicalcium phosphate dihydrate.

In relation to teeth, fluoride is characterized as follows:

• Fluoride concentration increases in the external layer of enamel throughout life.
• Fluoride concentration increases during topical application, but decreases for a few days
after treatment.
• Increasing fluoride content in the external tooth layers increases enamel's resistance
to demineralization.
• Fluoride uptake is greater in enamel than in dentin or cementum.

TOOTH TRAUMA & TREATMENT ........

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The alternate loosening and tightening of a deciduous tooth before it is shed due to the alternate re-
sorption and apposition of cementum and bone. If during a routine exam, you notice a permanent
tooth trying to erupt while the primary tooth remains firmly in place, the best treatment is to ex-
tract the primary tooth and allow the permanent tooth to erupt.
• In most cases, proper treatment for an intruded primary anterior tooth is NO TREATMENllmmediate
attention should be given to soft-tissue damage. However, an x-ray of the area should be taken . If the
intruded incisor is contacting the permanent tooth bud, the primary tooth should be extracted.
• If during the first 6 months after the injury, you observe pulpal necrosis (tooth darkens), the tooth
can receive ReT if needed as long as the tooth is sound in the socket and no pathologic root resorption
is evident. If the tooth is asymptomatic, leave it alone.
• Repositioning displaced mobile primary teeth is not recommended. Extraction is recommended due
to potential aspiration in young children.

Discolored primary teeth that are asymptomatic and show no radiographic changes should NOT BE
TREATED. They should be examined periodically by taking a radiograph. Primary teeth often darken (be-
come gray) after injury due to pulp bleeding and diffusion of biliverdin into the dentinal tubules.
• 80% of primary incisors that darken due to injury are asymptomatic. Occasionally, these teeth
will lighten.
• 15% of these teeth will need to be extracted within 1 year due to repeated trauma .
• 85% of these teeth will remain until normal exfoliation .
• As a result of trauma to the primary dentition, there should not be problems with permanent
successors unless the crown is not calcified. In this case, the tooth will be hypocalcified (most
common with mandibular incisors).
• underdeveloped motor coordination is the most common cause of dental trauma in very young
children's primary dentition ages 1 J,l- 2 J,l years old.
• Recently traumatized teeth may give false negative responses to pulp vitality tests. This impaired
nerve conduction may be temporary or permanent, but only time will tell.

277
 NOTES Crown Fracture Classification:
1. Ellis Class I Fracture-a simple crown fracture involving little or no dentin. Treat with
enameloplasty and/or bonding.
2. Ellis Class II Fracture-an extensive crown fracture involving considerable dentin, but not pulp.
The standard of care used to involve covering exposed dentin with calcium hydroxide or a glass
component cement to seal out oral flora . It is now recommended to also place a glass
ionomer restoration.
3. Ellis Class III Fracture-extensive crown fracture with pulpal exposure. Treatment include pulp
therapy via pulp capping, pulpotomy, or pulpectomy, followed by a permanent restoration . Usually,
a Class III fracture in a primary tooth leads to pulpal necrosis. RCT using ZOE paste as a filling
material is indicated. Unlike gutta percha, ZOE resorbs with resorption of the primary
tooth roots.
4. Ellis Class IV Fracture-a fracture where the entire crown is lost. Treatment is pulpectomy. The
tooth restoration involves using a stainless steel or celluloid crown.

Root fractures of primary teeth are relatively UNCOMMON because the more pliable alveolar bone
allows primary tooth displacement. When a primary tooth root fractures, it is treated identical as for
permanent tooth root fractures. However, the prognosis is LESS FAVORABLE. The pulp in a permanent
tooth with a fractured root has a better chance to recover since the fracture allows immediate decom-
pression and circulation is more likely to be maintained.
• Root fractures in the APICAL THIRD are often repaired without treatment (root fractures in the
apical third are more likely to undergo self-repair). Many dentists recommend a relatively lon g
stabilization period of 2-3 months for teeth with fractured roots. A longer stabilizati on period
encourages a more favorable type of healing with calcified tissue. HEAVY WIRES are recommended
when stabilizing teeth with fractured roots. Splinting is NOT recommended in the primary dentition.
• Occlusion should be adjusted so the injured tooth is not further damaged during normal
mastication. Follow-up radiographs and pulp tests are done at frequent intervals during the 6-month
period after the injury. These teeth often remain functional and vital.
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There is no reliable method to determine pulp vitality in the case of a recently traumatized primary
tooth. Often, traumatized teeth do not respond to vitality testing. Pulp vitality testing is NOT routinely
performed in the primary dentition because primary teeth do not respond to such test reliability since
the test requires a relaxed and cooperative patient objectively reporting a reaction .

Congestion of blood within the pulp chamber a short time after injury can often be detected in th e
exam. Shining a bright light on the facial surface and holding the mirror to view the lingual usually
shows a reddish hue which indicates pulpal hyperemia. If this red color change is evident after sev-
eral weeks, it often indicates a poor prognosis. EPT is seldom reliable to determine pulp vitality if
taken immediately after the injury. The thermal test is the MOST RELIABLE, especially in primary
incisors. Failure of a tooth to respond to heat indicates pulpal necrosis.

Panoramic Radiographs are EXCELLENT to demonstrate the following in a YOUNG PATIENT (CHILD):
• Supernumerary teeth, congenitally missing teeth, and axial inclinations of teeth.
• Apical development of permanent teeth and impacted teeth
• View pathologic jaw lesions and mandibular condyles.

The nice thing about panoramic x-rays is they are taken without placing the film in the mouth so it
does not alarm a nervous child. Rather, children are often "entertained" by the panoramic unit.

Adisadvantage of a panorex is the loss of image detail (it is hard to diagnose early carious lesions).
Thus, bite-wing x-rays are required to diagnose carious lesions. For a clinically caries-free child,
the first bite-wing x-ray should be taken when the spaces between the posterior teeth have closed.

278
Inter-proximal caries on primary teeth may result in eventual loss of the primary tooth, loss of NOTES
tooth structure, and arch length loss. Decay in primary teeth must be treated the same as in perma-
nent teeth . To just "watch" this decay can cause loss of tooth structure, and eventual loss of the pri-
mary tooth with resultant loss in arch length.
• Caries is an infectious disease that must be eliminated by removing the caries and restoring or
extracting the tooth. To ensure arch integrity, restoring the involved tooth, if possible is preferred.
• Amalgam is still used to some degree to restore primary teeth. The most important modification
in its use is in the cavity preparation. Properly contoured restorations are important to maintain
proximal contacts and length of the dental arch.
• Composite resin &resin-modified glass ionomers are also commonly used to restore primary teeth.
• Occlusal anatomy of primary teeth is not as defined as permanent teeth anatomy, thus amalgam
preparations can be more conservative.
• Enamel and dentin are thinner in primary teeth, thus amalgam preparations are deeper. The thickness
of coronal dentin in primary teeth is Y2 that of permanent teeth. Pulpal horns of primary teeth are
longer and pointed, thus amalgam preps must be conservative to avoid pulpal exposure.
• Primary molars have an exaggerated cervical bulge that makes the matrix band adaptation much
more difficult. Primary molars have an exaggerated cervical constriction which requires special care
in the formation of the gingival floor in Class II preparations.
• Enamel rods in the gingival third of primary teeth extend occlusally from the DEJ. This eliminates the
need in Class II preparations for the gingival bevel which is always required when preparing Class
II preparations on permanent teeth.

When placing a Class II amalgam in a primary tooth, with isthmus width should be 1/3 of the inter-
cuspal width. If an amalgam fracture occurs, it is most likely to occur here. Other principles in
preparing cavities in primary teeth:
• Class I & II preparations should include areas with caries and that retain plaque, and potential
carious areas (pits and fissures). This "extension for prevention" is only done when restoring with
amalgam . It is not necessary to "extend for prevention" when restoring with composite resin or resin-
modified glass ionomer, it is possible to seal the remaining pits and fissures. ..., ...,
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• Flat pulpal floor. .....-

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• Beveled axio-pulpal line angle to help reduce stress in the amalgam and provide greater bulk of ::a
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material in this area.
• Rounded angles throughout the preparation to result in less concentration of stresses and allows more
complete condensation of amalgam into extremities of the preparation.
• In Class II preparations, the facial and lingual walls of the proximal box should be carried to
self-cleansing areas and should be parallel to the external surfaces and converge slightly.
• The gingival margin is not beveled in Class II preparations because enamel rods in this area
incline occlusally.
• In Class II preparations, the gingival floor is not ideal in most cases as the preparation gets deeper
in this area due to the cervical constriction found in this area on primary molars.

STAINLESS STEEL CROWNS - are considered superior to large multi-surface amalgam restora-
tions, with a longer clinical lifespan. Two common stainless steel crowns are pre-trimmed &pre-
contoured crowns.
• Primary Teeth Indications: extensive carious lesions, hypocalcified teeth, teeth with dentinogenesis
or amelogenesis imperfecta, restoration after pulpotomy or pulpectomy, on an abutment tooth for a
crown and loop space maintainer, or temporary restoration of a fractured tooth.

Tooth Preparation:
• When preparing a primary tooth for a stainless steel crown, the cusps are reduced 1.0-1.5mm to
allow clearance with opposing teeth and to prevent traumatic occlusion after placing the stainless
steel crown.
• Reduce proximal surfaces (mesial &distal); vertical reductions are made and carried gingivally to
the extent that contact with the adjacent tooth is broken.
• Remove all sharp line angles. It is usually not necessary to reduce the buccal or lingual surfaces. This
aids in crown retention (undercut area). However, it may be necessary to reduce the distinct buccal
bulge, especially on the primary 1st molar.
• When festooning and trimming the crown during fitting, greater length is needed in the mesiofacial
bulge region on a primary 1't molar.

279
 When operative or surgical procedures are performed on the mandibular primary or permanent
teeth, the INFERIOR ALVEOLAR NERVE must be blocked by administering the conventional mandibu-
lar block. The supra periosteal injection technique (local infiltration) is sometimes helpful in anes-
thetizing mandibular primary incisors, but cannot be relied on for complete anesthesia of mandibular
primary or permanent molars.
• Local infiltration can be used to anesthetize maxillary primary teeth. Adequate diffusion of the local
anesthetic readily occurs in children because their bones are less dense than in adults.
• The mandibular foramen is located at a level lower than the occlusal plane of the primary teeth in
the child patient. Thus, the injection is made slightly lower and more posterior than for an adult.
• Young children do not always understand what "numb lip" means when you ask them this after a
mandibular block. The best indicator of a profound block is to probe the labial attached gingiva
between the lateral incisor and canine with an explorer. If this is done without a reaction, the child
is anesthetized .

BEHAVIOR MANAGEMENT
A dentist has offered plaque-control instructions to a patient. To ensure the patient understands the
instructions, the dentist should ask the patient to verbalize her understanding.

Between boys & girls, the difference is onset of pubertal growth spurt is 2 years. Girls reach puberty 2
years before boys.

The MOST personal behavior by the dentist is touching the patient gently on the arm.

RUBBER DAM - a main advantage of using a rubber dam is it aids in child management. It seems
to quiet and calm the patient because it acts as a separation/barrier both physically and psych ologi -
"" ,...,
,..., .." cally between the patient and dentist. Thus, the rubber dam works for a very nervous or anxious pa-
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en -t tient. Other Rubber Dam Advantages:
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• Controls saliva and moisture in the operating field .
• Decreased operating time.
• Provides protection from aspiration or swallowing of foreign bodies.
• Child becomes primarily a nasal breather when the dam is in place, enhancing the effects of nitrous
oxide if applicable.
• Contraindications: presence of fixed orthodontic appliances, a patient with congested nasal
passages/nasal obstruction, or a recently erupted tooth that will not retain a clamp.

Management of a child who must undergo dental extractions is based on these factors:
• Child's age &maturity. This often determines the type of anesthesia best suited for the intended
procedure. Children below the age of reason are best managed under general anesthesia, since a
slight amount of discomfort is always associated with the administration of a local anesthetic. It is
very important to have total anesthesia before starting the procedure. Use both buccal & palatal
infiltration on maxillary teeth, and block anesthesia on mandibular teeth with infiltration.
• Avery young child is best managed under general anesthesia (inhalation or in combination with
small doses of IV barbiturates). VERSED is the most common premedication prior to
general anesthesia.
• Premedication with a barbiturate may cause paradoxical excitement in a young child.

• Past medical and dental experiences that might influence the child's behavior.
• Child's physical status.
• Length of time and amount of manipulation necessary to accomplish the surgery.

Post-anesthetic lip biting is a common post-treatment complication in children. After extracting a

tooth on a child, the biggest post-operative concern is preventing lip biting.

280
TELL-SHOW-DO TECHNIQUE - the most important technique of behavioral management in the
pediatric dental patient used to manage an extremely apprehensive 5-year old child. Tell-show-do is
the backbone of the educational phase of developing an accepting, relaxed child patient.

• In this technique, you tell the child what is going to happen, you show the child what is going to
happen, then perform the actual procedure in the mouth.

• Tell-show-do works especially well when treating a child with a different cultural background.

• The clinical examination of the infant and toddler should be accomplished with the parent's
assistance in a non-threatening environment. Most often, it is not necessary nor recommended that
the dental chair be used. The parent and dentist sit facing each other in a knee-to-knee position,
supporting the child with the head cradled on the dentist's lap.

• Aggressive behavior in the dental office is usually a fear reaction . The most realistic approach to
managing a difficult child in the dental office is to attempt to recondition the child through
techniques of applied psychology.

When treating a child who is obviously afraid, the dentist should permit the child to express his fear (iden-
tify the fear) . All behavioral patterns are motivated by anger and fear. The crying child is NOT an abnormal
child. Anger is easier to treat than fear. Fear is most likely exhibited by a young child on his first visit to
the dentist, and is related to anxiety over being separated from a parent. The PARENT (not the dentist),
has the greatest influence on the child's reaction at this initial visit. Child Control Techniques:
• Angry Child: Separate the parent and child, and place the child in the chair abruptly and be firm.
Use "hand-over-mouth" technique (HOME) after getting the parent's permission! Display authority
and command the child's respect by continuing with treatment even if he/she is uncooperative.
Comfort the parent at the end of the visit, and compliment the child at the end of the visit.

• Fearful Child: ,..,

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• Have the parent stand quietly behind the chair. cn~

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• Allow the child to express his fears (identify the fear) .
• Change the child's focus off fear.
• Lastly, sedation.

• Shy, submissive children are often the product of parents who are OVERPROTECTIVE.

MENTALLY RETARDED CHILDREN - when treating mentally retarded children, they can be con-
trolled similar to normal children, since they respond similarly to normal children of the same mental
age. They respond inconsistently, have short attention spans, and are restless and hyperactive when
undergoing dental care ..Useful procedures when treating a mentally retarded child:
• Keep appointments short, and schedule the patient early in the day, since staff, dentist, and patient
are less fatigued earlier. Speak slowly and in very simple terms and listen carefully to the patient.
Ask the patient if there are any questions about anything you will be doing.
• Give a tour to the patient before attempting any treatment. Introduce the patient to the
office person nel.
• Give only one instruction at a time. Reward the patient with compliments after the procedure is
successfully completed .
• Dentist should assess the degree of mental retardation by consulting with the patient's physician
before starting dental treatment.

281
 American Academy of Pediatric Dentistry's
Standard of Care for Behavior Management
Management Type Description Objectives Indications Contra indications

Communicative
Management
Tell-Show-Do Explanation Allay fears, shape All patients who All patients who
tailored to the patient's can communicate can communicate
cognitive level, response, and give regardless of their regardless of their
followed by behavior method of method of
demonstration, expectations communication communication
then the actual
procedure

Voice Control Modulation on Gain patient's Uncooperative or Uncooperative or

voice volume, attention, avert inattentive, but inattentive, but
tone, or pace to negative or communicative communicative
influence and avoidance child child
direct patient's behaviors,
behavior establish authority

Positive Process of Reinforce desired Any patient Any patient

Reinforcement shaping a behavior
patient's behavior
through
""
...., ....,
."
appropriately
.....
::z
-:co -
"" timed feedback
en .....
..... =
=- (i.e. praise, facial
-< C")
expression).

Distraction Diverting patient's Decrease Any patient Any patient

attention from the likelihood of
perceived unpleasant
unpleasant perception or
procedure threshold

Non-verbal Conveying Enhance Any patient Any patient

Communication rei nforcement and effectiveness of
guiding behavior other
through contact, communicative
posture, & facial management .
expressions techniques; gain
or maintain
patient's attention
& compliance

282
EHfiPTER 7

283
 N Primary Teeth Occlusion:
• Flush Terminal Plane-the NORMAL relationship of the primary molars in the deciduous (primary)
dentition. The terminal plane relationship of primary second molars determines the future antero-
posterior position of the permanent first molars.
• Mesial Step-the primary dentition's equivalent to an Angle Class I malocclusion.
• Distal Step-the primary dentition's equivalent to an Angle Class II malocclusion (retruded mandible).
• An equivalent of Angle's Class III is almost NEVER SEEN in the primary dentition because of the
normal pattern of craniofacial growth where the mandible lags behind the maxilla.

The EDGE-TO-EDGE position of permanent maxillary &mandibular first molar cusps is the MOST
COMMON initial relationship (when primary molars are in a flush terminal plane). This will most
likely become a Class I molar relationship by both molars drifting forward ("early mesial shift"),
with the mandibular molar drifting two times farther than the maxillary molar.

While erupting, the permanent teeth move OCCLUSALLY &BUCALLY. Also, during active tooth erup-
tion, there is apposition of bone on all surfaces of the alveolar crest and on the bony socket walls.
• Important: the maxillary arch is slightly longer than the mandibular arch. The sum of the M-D
diameter of the maxillary permanent teeth is -128mm, and is 126mm for the mandibular
permanent teeth.

OVERBITE - the VERTICAL overlapping of maxillary anterior teeth over the mandibular anterior teeth .

OVERJET - the HORIZONTAL projection of maxillary anterior teeth beyond the mandibular anterior
teeth. Labial-axial inclination of the maxillary incisors.
• Reverse Overjet-associated with Class III skeletal patterns with more than 2 maxillary anterior teeth
in linguoversion.

PHYSIOLOGIC OCCLUSION - while it is not necessarily an ideal Class I occlusion, it is an occlu-

sion that adapts to the stress of function, and can be maintained indefinitely.

PHYSIOLOGIC TOOTH MOVEMENT - an example is mesial drifting of a permanent molar into a

C)
space created by the premature loss of a primary molar. Important: permanent molars have a natural
::c
-< tendency to drift MESIALLY.
::c
C)
CI
Q
:z:
:::!
PATHOLOGIC OCCLUSION - occlusion that cannot function without contributing to its own de-
C")
en struction, and may manifest itself by any combination of excessive tooth wear without sufficient
compensatory mechanisms, TMJ problems, pulpal changes ranging from pulpitis to necrosis, and
periodontal changes.
• Pathologic tooth movement-tooth movement caused by pathologic conditions.

MALOCCLUSION - malocclusion is MOST OFTEN HEREDITARY. There may be a disproportion be-

tween the size of the maxilla & mandible, or between the jaws and tooth size resulting in overcrowding
of teeth or in abnormal bite patterns. Supernumerary teeth, malformed teeth, impacted or lost teeth
that erupt in an abnormal direction may cause malocclusion. Less frequent causes of malocclusion
are thumb sucking or tongue thrusting habits.

Incipient Malocclusion Signs:

• Lack of interdental spacing in the primary dentition. The significance ilf the lack of spacing related
to the increased M-D width of the permanent teeth.
• Crowding of permanent incisors in the mixed dentition. Since arch perimeter increases after the
incisors erupt and is small in the maxilla and essentially non-existent in the mandible, arch growth
cannot usually contribute to further dental alignment.
• Premature loss of primary canines (especially in the mandibular arch) . Premature loss of the
mandibular primary canine reflects insufficient arch size in the anterior region . As such, the crowns
of lateral incisors during eruption impinge on the primary canines' roots and cause them to resorb.
When the canine is shed, the midline will shift in the direction of the lost tooth, and there is lateral
and lingual migration of the mandibular incisors.

284
• 3 Planes of Space To Classify Malocclusion: Antero-posterior, Transverse, &Vertical.
NOTES
• The incidence of malocclusion in a HOMOGENOUS population is generally LOWER than in a
HETEROGENOUS population (where the incidence is higher). Dental arch form is ultimately
determined by the interaction of environmental influences on the genetic pattern.

SEVERE malocclusion may compromise all aspects of oral function (speech, swallowing, and mas-
tication). There may be difficulty in masticating if only a few teeth meet, and jaw discrepancies may
force adaptive alterations in swallowing. It can be difficult or impossible to produce certain sounds,
and speech therapy may require some preliminary orthodontic treatment. Referral to a speech thera-
pist is helpful as both patient and parents can benefit. Even less severe malocclusions can affect
mastication , swallowing and speech, not so much by making function impossible, but by requiring
physiologic compensation for the anatomic deformity.

• Patients with anterior open-bite may have difficulty making speech sounds "th, sh, ch"
due to distortion. An anterior open-bite can also create a lisp, making it difficult to
pronounce "s" & "z" sounds.

• A large diastema between maxillary incisors can create a lisp, making it difficult to pronounce
Us" & "z",

• Irregular incisors (especially lingual position of maxillary incisors), creates a difficulty to

produce sounds ''t'' & "d".

• Due to distortion, there may be difficulty in making speech sounds "F" & "V" in a Skeletal
Class III.

SKELETAL OPEN-BITE ("LONG FACE SYNDROME") - a type of malocclusion that is most

often associated with MOUTH BREATHING. Factors associated with chronic mouth breathing include
narrow face & oropharyngeal space, chronic rhinitis (inflammation of the mucous membranes of the
nose), chronic tonsillitis, allergies, and a deviated nasal septum .
• The earliest possible diagnosis of a skeletal open-bite is essential because the condition is not self-
correcting, and usually worsens with time. Anterior open bites can be classified as a form of Q
:::a
.....
apertognathism (an open-bite deformity). AS ACHILD MATURES, THEIR FACIAL PROFILES BECOMES ::c
Q
LESS CONVEX. co
Q
:z:
:::!
C")
There is no set rule as to when a malocclusion should be treated. The age of treatment depends on CI>

the problem. Malocclusions are more identifiable in children ages 7-9 because the eruption of per-
manent incisors reveals tooth-arch length discrepancies.

Steiner Analysis:
1. SNA angle-the angle formed at the intersection of 2 lines (one line from sella turcica (S) to nasion
(N), and the other line from nasion to Point A). These two lines show the maxilla's position relative
to the cranial base. Steiner indicates in a good skeletal pattern, the SNA angle is _82°.
• SNA> 82° = maxillary prognathism.
• SNA < 82° = maxillary retrognathism.

2. SNB angle-the angle formed by the intersection of line SN & NB. It defines the sagittal location
of the mandibular denture base. Steiner states an 80° angle is compatiblewith skeletal harmony.
• SNB angle> 80° = mandibular prognathism.
• SNB angle < 80° = mandibular retrognathism.

3. ANB angle-the norm for this critical angle is 2° (it is the difference between SNA &SNB norms) .
A Class I skeletal profile has a 2° ANB angle.
• ANB angle> 4° = Class II skeletal profile.
• ANB angle < 0° (negative angle) = Class III skeletal profile.

285
 ANGLE'S MALOCCLUSION CLASSIFICATIONS (PERMANENT MOLAR RELATIONSHIPS) - the
MESIOBUCCAL CUSP of the maxillary first molar serves as the REFERENCE POINT in identifying Angle's
Class I, II, & III occlusions.
1. Class I (A) Malocclusion: MB cusp of the maxillary first permanent molar occludes with (lines
up with) the buccal groove of the mandibular first permanent molar. Also, maxillary centrals
overlap mandibular centrals. THE MOST COMMON OCCLUSION (-70% of the population) and is
associated with an ORTHOGNATHIC FACIAL PROFILE where the nose, lips, & chin are
harmoniously related.
• Class I (A) canine relation: maxillary permanent canine occludes with the distal half of the
mandibular canine & mesial half of the mandibular first premolar (maxillary canine lies
between the mandibular canine & first premolar) .
• Cephalometric analysis of Class I malocclusions indicates an ANB angle < 4° (indicates a
harmonious skeletal profile and sagittal haromony between the maxillary and mandibular
dental arches) .
• The MOST COMMON CAUSE of Class I malocclusion is a discrepancy between tooth structure
and amount of supporting bone length.
• The MOST PREVALENET characteristic of Class I malocclusion is CROWDING due to
insufficient alveolar arch length to accommodate all teeth in ideal alignment and in a good
sagittal position. When a diagnosis is made that crowding does exists,and this crowding>
4mm in the mandible, extractions are often required to attain an excellent, stable result.
However, the decision to extract teeth depends greatly on performing a mandibular space
analysis which is usually performed (referral) to the orthodontist.
• When the space lacking is < 4mm, in most cases, it is obtained by carefully stripping some
interproximal enamel from each anterior tooth. Aspace deficiency> 4mm indicates
extraction to correct the malocclusion.

2. Class II (B) Malocclusion (Retrognathism = Overbite): mandibular first permanent molar's

buccal groove is DISTAL to the MB cusp of the maxillary first permanent molar (the mandible is
"distal" to the maxilla). The MB cups of the maxillary first molar is between the mandibular first
molar & second premolar. The lower jaw and chin may appear small and withdrawn. The
mandibular incisors occlude even more posterior to the maxillary incisors so that they may not
touch at all. Associated with a RETROGNATHIC FACIAL PROFILE where the convexity is due to
c::> the relative prominence of the maxilla compared to the mandible. The mandibular incisors will
::a
.....
:::I: most likely be tipped forward. This is less common (-25% of population) . An SNB angle < 78 0

c::I
c::I
c::I
indicates mandibular retrognathism, while an SNA angle < 82 0 indicates maxillary retrognathism.
:z:
::!
C")
(;)
The big difference between Division I & II is in a Division II, the maxillary laterals are tipped labi-
ally & mesially.
• Class II, Division I: a distal relationship of the mandibular first permanent molar's buccal groove
to the MB cusp of the maxillary first permanent molar & maxillary incisors (maxillary central &
lateral incisors are in extreme labioversion (protruded).
• In most Class II, Division I malocclusions, the body of the mandible and its superimposed
dental arch are in a DISTAL relationship to the maxilla, and the maxillary incisors are usually
in a labial axial inclination. Also, the relationship of the maxillary first molars and canines to
their mandibular counterparts is such that the DB cusp of the maxillary first molar occludes
in the buccal developmental groove of the mandibular first molar, and the maxillary canines
occlude mesial to the mandibular canines. Besides the labial-axial inclination of the maxillary
incisors (overjet), various aberrations in the individuaJ alignment of the teeth (i.e. crowding)
can be superimposed on this class.

• Class II, Division II: a distal relationship of the buccal groove of the mandibular first permanent
molar to the MB cusp of the maxillary first permanent molar and maxillary laterals being tipped
labially and mesially (sometimes overlapping the centrals) . Its a malocclusion where the body of the
mandible and its superimposed dental arch are also in distal relationship to the maxilla, while the
molar & canine occlusion are the same as Class II Division I. The DB cusp of the maxillary first
. molar occludes in the buccal developmental groove of the mandibular first molar, and maxillary
canines occlude mesial to mandibular canines. The maxillary centrals are near normal antero-
posteriorly or slightly in linguoversion (usually retruded), and maxillary lateral incisors are usually
labiomesially flared and overlap the central incisors. An impinging overbite may also exist.

286
• When the distocclusion occurs on ONLY ONE SIDE OF THE ARCH, this UNILATERALITY is called a NOTES
"subdivision" of its division (Class II, Division I Subdivision where ONE SIDE of the maxillary arch
is in a Class II relationship with its occluding mandibular quadrant, while the other side is in a
Class I relationship). The protruded maxillary incisors (centrals &laterals) and maxillary overjet and
other anterior aberrations are usually confined to one side of the maxillary arch.

• "Sunday Bite" -a term given to the forward postural position of the mandible adopted by people with
Class II profiles in an effort to improve their esthetics.

• Class II (B) canine relation: mandibular canine's distal surface is DISTAL to maxillary canine's
mesial surface. The maxillary canine is mesial to the mandibular canine.

ECTOPIC ERUPTION - occurs when a tooth erupts in the WRONG PLACE (most commonly occurs in
the eruption of maxillary first molars & mandibular incisors), and is much more common in the
maxilla, and often associated with a developing skeletal Class II malocclusion.

• Ectopic eruption occurs in 2-6% of the population and spontaneously corrects itself in -
60% of cases.

• Ectopic eruption of a permanent maxillary first molar is often treated by a BRASS WIRE separating
device placed between the primary second molar & permanent first molar to cause the permanent
first molar to tip distally.

• If the eruption path of the maxillary first molar carries far too mesially at an early stage, the
permanent molar cannot erupt and the primary molar root can be damaged. The mesial position of
the permanent molar means the arch will be crowded unless the child receives treatment. Important:
this mesially inclined position of the permanent molar makes it susceptible to decay. If it shows
signs of caries, extract the adjacent primary second molar immediately. The resultant space can
then be maintained as part of orthodontic treatment.

• Ectopic eruption of mandibular lateral incisors (which occurs more commonly than mandibular
1't molars), can cause transposition of the lateral incisor & canine. A poor eruption direction of the
canine, sometimes leading to impaction is often observed, but is usually due to the eruption path C)
:=
being altered by a lack of space. .....
::z:
C)
C)
C)

3. Class III (C) Malocclusion (Prognathism =Underbite): occurs when the body of the mandible :z:
::!
n
and its superimposed dental arch are in a MESIAL relationship to the skull base & maxilla. The ~

maxillary first molar occludes distal to the mandibular first molar, while the maxillary canine is
an exaggerated distal relationship to the mandibular canine. mandibular first permanent molar's
buccal groove is MESIAL to the MB cusp of the maxillary first permanent molar (MB cusp is
between the mandibular first &second molars). The chin may protrude like a bulldog. Mandibular
incisors overlap a'nterior to the maxillary incisors (mandibular incisors are forward to the maxillary
incisors). Maxillary incisors are usually tipped lingually.LEAST COMMON MALOCCLUSION « 5%).
Associated with a PROGNATHIC FACIAL PROFILE (MANDIBLE) where the mandible is markedly
forward past the maxilla giving a concave midfacial appearance (the mandible protrudes forward,
and the mandibular teeth extend over the maxillary teeth).
• Class III subdivision: a Class III relationship of the teeth on one side, with a Class I
relationship on the other side.
• On a cephalometric analysis, all Class III malocclusions have an SNA angle> 84°
(maxillary prognathism).
• Due to distortion, there may be difficulty in making speech sounds "F" & "V" in a
Skeletal Class III.
• Reverse Overjet-associated with Class III skeletal patterns with more than 2 maxillary
anterior teeth in linguoversion.

287
 PSEUDO-CLASS III MALOCCLUSION - malocclusion where the mandibular incisors are forward
of the maxillary incisors in centric occlusion, but the patient can bring the mandible back without
strain so that the mandibular incisors can touch the maxillary incisors (this ability is often consid-
ered diagnostic). Thus, this type is a milder form of the "true" Class III malocclusion, and is more
amenable to conservative orthodontic movement, while a "true" Class III malocclusion often requires
surgical correction .

• The existence of a FORWARD SHIFT of the mandible during closure to avoid incisor interference
is found in "Pseudo" Class III malocclusions. To avoid teeth interference, the patient can adopt a
jaw position on closure that is forward to normal (this may look like a Class III position in the absence
of a "true" skeletal Class III relationship. Thus, it is called a "pseudo" Class III malocclusion . In
most cases they have an edge-to-edge bite.

• Treatment: involves eliminating the CO-CR discrepancy early in the treatment to avoid abnormal
wear and abnormal growth influences. Occlusal interferences and anterior cross bites are treated
subsequently.

• Bimaxillary Dentoalveolar Protrusion-present when the teeth protrude in both jaws. In this condition
you will see severe dental and lip protrusion accompanied by severe lip strain which is needed to
bring the lips into closure.

• Class III (C) canine relation: mandibular canine's distal surface is MESIAL to maxillary canine 's
mesial surface. The maxillary canine is DISTAL to the mandibular canine.

CROSSBITES - occur when some of the teeth move on the "wrong side of the track". Crossbite can
be unilateral (on one side), or bilateral (on both sides), and can occur anteriorly or posteriorly. Cross-
bites are associated with a jaw-size discrepancy, hereditary (genetics), reverse over-jet, and a
scissor bite. Crossbites are NOT associated with tongue thrusting.
• Anatomical (Skeletal) Crossbite-usually demonstrates a smooth closure into centric occlusion.
• Functional Crossbite-usually caused by thumb sucking does not demonstrate a smooth closure
into CO.

C> Orthodontic treatment to correct a crossbite in children should start as early as possible. Maxil-
.....
""
::c
C>
lary expansion-is the first step of treatment to broaden the maxilla with an "expander" appliance.
CI
C>
:z:
This palatal expander is fixed to the roof of the mouth and is widened each night for 1-2 months with
...
:::!
en
a turn key, and remains in the mouth for -3 additional months to allow the bone to harden in its new
position.

Braces may also be placed on the maxillary teeth during the palatal expansion to eventually close the
"gap-tooth grin" that develops as the maxilla is expanding. Once expansion is complete, the child
may need to wear a full set of braces for 1-2 years to achieve an ideal occlusion.

SCISSOR BITE (BILATERAL LINGUAL CROSSBITE) - results from a narrow mandible or wide
maxilla. Milder cases may involve only maxillary first premolars. Severe cases may require contraction
of the maxilla or expansion of the mandible.

ANTERIOR CROSSBITE in the primary dentition often indicates a skeletal growth problem & a devel-
oping Class III malocclusion. Anterior crossbite can be caused by a labially situated supernumerary
tooth, traumatic injury, or an arch length discrepancy.

• However, anterior crossbite of one or more permanent incisors may suggest a localized discrepancy
and a condition that should almost always be treated in the mixed dentition state, or as soon as it
is identified . It is NOT a self-correcting condition .

• It is most often associated with prolonged retention of a primary tooth. Delayed treatment can
lead to serious complications (Le. loss of arch length). The most essential facto~r related to
correcting an anterior crossbite is the amount of M-D space available. It is easily retained once
it is corrected .

288
• Premature exfoliation of a primary canine may indicate an arch length deficiency. Premature loss of NOTES
a primary mandibular canine may cause a lingual collapse of the mandibular anterior teeth .

• A corrected anterior crossbite is BEST RETAINED by the normal incisor relationship that is achieved
from the treatment (the overbite), not from appliances.

• CLASSIC SYMPTOMS of a digit sucking habit: anterior crossbite, crossbite, proclination of maxillary
incisors, constriction of the maxillary arch (not expansion) retroclination of mandibular incisors, and
a Class II malocclusion.

OPEN BITE - a malocclusion (abnormal bite) where some teeth (usually the front teeth) cannot be
brought into contact with their opposing teeth . Tongue thrusting DOES NOT cause crossbites or open
bites. Atongue thrust swallow is the result of displaced incisors (not the cause). Recent studies
show that "tongue thrust swallowing" does not cause open bite as there is no tongue force on the
teeth during swallowing even though the tip of the tongue is placed forward. The tendency to place
the tongue forward originates from the need to attain an oral seal. By placing the tongue between the
teeth (in cases of anterior open bite) an oral seal is formed during swallowing. Thus, the forward posi-
tion of the tongue during swallowing is due to the anterior open bite, and the reverse is not true "a
tongue thrust swallow thus is considered the result of displaced incisors, not the cause".

ANTERIOR OPEN BITE - is the most common sequelae of a digit sucking habit. Unilateral cross-
bites can also occur. Increased pressure from the buccinator muscles during sucking constricts the
maxillary arch. Other mechanical forces cause the maxillary incisors to procline & mandibular incisors
to retrocline. As the hand rests on the chin, it retards mandibular growth, causing a Class II profile.

• Most of the time, anterior open bite is ASYMMETRICAL with normal posterior occlusion.

• Anterior open bites are much more common in African Americans than Caucasians.

• Deep bites are much more common in Caucasians.

POSTERIOR CROSSBITE after prolonged thumb sucking &ANTERIOR CROSSBITE in mildly prognathic
children are usually seen with displaced teeth related to functional shifts. C)
::c
--I
::z::
C)
c
• Prolonged sucking habits often produce a mildly narrow maxillary arch and a tendency toward C)
:z:
bilateral crossbite. Children with this condition usually shift the mandible to one side on closure to :::!
C">
gain better function, which can guide permanent molars, or later guide premolars into a cross bite tI>

relationship.

• A young child with a tendency toward a Class III malocclusion will have end-to-end contact of the
primary incisors. Atrue anterior crossbite in the primary dentition is rare because mandibular growth
LAGS BEHIND maxillary growth. The primary incisors wear down rapidly, and an anterior shift of the
mandible to escape occlusal interferences rarely occurs until the permanent incisors begin to erupt.
A pattern of anterior displacement of the mandible may develop when the permanent incisors come
into contact, however, producing an anterior crossbite from the shift.

POSTERIOR CROSSBITE in the MIXED DENTITION should be corrected ASAP and be thoroughly diagnosed
as either a dental, functional, or skeletal crossbite and may be associated with a mandibular shift.

• Posterior crossbite may be corrected with a palatal expansion which causes diastema formation
between the central incisors and expands the nasal floor. Tooth movement and skeletal expansion
are inevitable when the mid palatal suture is widened with a palatal expander.

• It is important to correct posterior crossbites (which are related to the TRANSVERSE PLANE OF
SPACE) and mild anterior crossbites in the FIRST STAGE of treatment, even if the permanent 1st
molars have not erupted. Severe anterior crossbites are usually not corrected until the SECOND
STAGE of conventional treatment.

• THE MOST COMMON ACTIVE TOOTH MOVEMENT in the primary dentition is to CORRECT APOSTEIROR
CROSSBITE (a transverse plane of space problem).
289
 MAXILLARY MANDIBULAR PLANE ANGLE (MMPA) - the angle between the mandibular plane
(Go-Me line) & maxillary plane (ANS-PNS line) whose normal value is 27° (+ 4°) . The greater MMPA,
the longer the anterior facial height.
• There is also an interaction between face height & antero-posterior position of the mandible. All other
factors being equal, a long face predisposes the patient to Class II malocclusion, while a short face
predisposes the patient to a Class III malocclusion.

The mandibular plane angle is visualized clinically by placing a mirror handle or other instrument
along the border of the mandible.
• ASTEEP mandibular plane angle correlates with LONG anterior facial vertical dimensions & anterior
open bite malocclusion. A long face predisposes the patient to Class II malocclusion.
• AflAT mandibular plane angle correlates with SHORT anterior facial vertical dimensions (height)
& anterior deep bite malocclusion. Ashort face predisposes the patient to a Class III malocclusion.

POOR MAN'S CEPHALOMETRIC ANALYSIS - a facial profile analysis that delinates the same
information as that obtained from lateral cephalometric radiographs. The difference is there is greater
detail obtained from the lateral cephalometric. However, the Poor Man's Cephalometric Analysis is a
vital diagnostic technique for primary evaluation as it is a quick, simple, and inexpensive technique
that readily gives the following information:
1. anteroposterior position/proportion of the jaws relative to each other.
2. lip posture (competent/incompetent) and incisor prominence.
3. vertical facial proportions.
4. inclination of the mandibular plane angle.

*Within the lower 1/3 of anterior face height, the mouth should be -1/3 of the way between the
nose & chin.

Cephalometries in Orthodontics are used for diagnosis, analysis of treatment results, and longitudi-
nal study of growth. Cephalometries is useful to assess tooth-to-tooth, bone-to-bone, &tooth-to-
bone relationships. Serial cephalometric film can show the amount and direction of growth .

• The lateral head radiograph (cephalometric radiograph) must be compared with the "normal" lateral
C)
;:c radiographs to form an accepted norm. Linear & angular measurements are obtained using known
.....
::c
C)
anatomical landmarks in the lateral head radiography of the patient. These measurements are then
CI
C)
:z:
compared with measurements considered within normal limits and in that way enable the orthodontist
..,
::::!
en
to assess aberration in the dentition and jaw structures that result in malocclusion .

• Analysis of cephalometric radiographs is NOT limited to hard structures (i.e. bone & teeth), but
include measurements of soft tissue structures (i.e. nose, lips, soft tissue chin).

• Superimposition in longitudinal cephalometric analysis is on a reference plane and registration point.

This best demonstrates the growth of structures furthest from the plane and the point. The most
stable area to evaluate craniofacial growth is the anterior cranial base because of its early
cessation of growth.

• A lateral cephalograph usually shows magnification with up to 7-8% magnification which is

considered acceptable. The resulting double shadows are traced, and the average is used for
measurements.

290
CEPHALOMETRIC LANDMARKS: NOTES
1. Bolten (Ro)-the highest point in the upward curvature of the retrocondylar fossa of the
occipital bone.
2. Baison (Ra)-the lowest point on the anterior margin of the foramen magnum, at the base of
the clivus.
3. Articulare (Ar)-the intersection of 3 radiographic shadows, inferior surface of the cranial base,
& posterior surfaces of the necks of the mandibular condyles.
4. Porion (Po)-the midpoint of the upper contour of the metal ear rod of the cephalometer.
5. Sphenooccipital synchondrosis (SO)-the junction between the occipital & basisphenoid bones.
6. Sella (S)-the midpoint of the cavity of the sella turcica.
7. Pterygomaxillary fissure (Ptm)-the point at the base of the fissure where the anterior &
posterior walls meet.
8. Orbitale (Or)-the lowest point on the inferior margin of the orbit (floor of orbit).
9. Anterior nasal spine (ANS)-the tip of the anterior nasal spine. The point above the root
the maxillary central.
10. Point A(Subspinale)-innermost point on contour of the mandible between the incisor and
bony chin.
11. Point B (Supramentale)-innermost point on contour of the mandible between the incisor
and bony chin.
12. Pogonion (Pog)-the most anterior point of the chin's contour (on the mandibular sym physis).
13. Menton (Me)-the most inferior point on the mandibular symphysis (the bottom of the chin).
14. Gonion (Go)-the lowest, most posterior point on the angle of the mandible with the
teeth in occlusion.
15. Nasion (Na)-anterior point of the intersection between the nasal and frontal bones.

FRANKFORT-HORIZONTAL PLANE - constructed by drawing a line connecting PORION & OR-

BITALE. FHP is the best representation of the NATURAL ORIENTATION OF THE SKULL.

TO PREDICT THE TIME OF PUBERTAL GROWTH SPURT while treating jaw mal-relationships in a grow-
ing child, the orthodontist can get the most valuable information from a WRIST-HAND RADIOGRAPH.
The physiologic age (developmental age) is judged by determining the skeletal development. Wrist-
hand radiographs offers the best aid to do this by examining the ossification &development of the c:::>
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wrist's carpal bones, hand's metacarpils, and finger's phalanges to give the orthodontist an idea re- .....
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garding the chronology of skeletal development. Comparing the overall pattern observed in the hand- c:::>
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wrist radiograph, with age standards in a reference atlas, does this. ::::!
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• ulnar sesamoid or hamate bones are landmarks to obtain an estimate of the timing of the
adolescent growth spurt. Wrist-hand radiographs in the dental office are obtained using a standard
cephalometric cassette and dental radiograph.

• The state of physical maturity or skeletal development co-relates well with the jaw growth.
Orthodontist use this information to predict the amount of expected jaw growth. After sexual maturity,
much less growth is expected, thus growth modification is not attempted .

• Hand-wrist radiographs are LESS useful in evaluating if growth has stopped or is continuing
(patient's position on the growth curve). Serial Cephalometric radiographs are used for this purpose.

291
 MIXED DENTITION - the dentition phase when some of the teeth in the oral cavity are permanent,
and some are primary. The earliest indication of a mixed dentition consists of the primary dentition
& permanent mandibular first molars. Supervising a child's development of occlusion is MOST
CRITICAL from ages 7-1 Oyrs (mixed dentition stage).
• Mixed Dentition Analysis (transitional dentition analysis)-an analysis performed during the mixed
dentition to predict the amount of crowding AFTER the permanent teeth erupt. It determines the
space available vs. space required. It is performed using a boley gauge, study models, and a
prediction table. The analysis is based on a correlation of tooth size (one may measure a tooth or group
of teeth and predict accurately the size of the other teeth in the same mouth .

Performing a Mixed Dentition Analysis:

1. Measure the M-D diameter of the mandibular incisors and ADD them together.
2. Measure the space available for the mandibular incisors.
3. Subtract #1 from #2 (a negative number indicates CROWDING in the incisor region).
4. Measure the space available for the canine and premolars on each side of the arch.
5. Calculate from the prediction table the size of the canine and premolars.
6. Subtract #6 from #5 on each side (again, a negative number indicates CROWDING).
7. By this step, there are 3 numbers that are added : (a (-) number =
crowding; a (+) number = space).
1. number for incisor crowding or excess space.
2. number for the right canine and premolar crowding or excess space.
3. number for the left canine and premolar crowding or excess space.

For the MAXILLARY ARCH, mandibular incisors are used to predict the size of maxillary canines & pre-
molars. Follow the same steps as for mandibular teeth.

MOYERS' MIXED DENTITION ANALYSIS - the size of unerupted canines & premolars is pre-
dicted from knowing the size (M-D width) of the mandibular incisors that have already erupted into the
mouth early in the mixed dentition. Maxillary incisors are not used in any of the predictive procedures,
since they show too much size variation . Mandibular incisors are measured to predict the size of maxil-
lary and mandibular posterior teeth.

o If mandibular anterior crowding is noted during the mixed dentition phase, the most appropriate ap-
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o proach to management is to take study models and perform an arch length analysis. This mandibular
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incisor crowding usually results from a tooth size-arch length discrepancy.
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PRIMATE SPACES - spaces found in the primary dentition. Spacing is normal throughout the ante-
rior part of the primary dentition, but is MOST NOTICABLE in these two locations:
• Maxillary arch: primate space located between the lateral incisors & canines.
• Mandibular arch: primate space located between canines and 1'1 molars.

Primate spaces are normally present from the time the primary teeth erupt. Developmental spaces
between the incisors are often present from the beginning, but become larger as the child grows and as
alveolar processes expand. Generalized spacing of the primary teeth is required for proper alignment
of the permanent incisors. This spacing is most frequently caused by growth of the dental arches.

If spacing is present, it is possible that DRIFTING of the adjacent teeth will occur if there is a loss
of a primary incisor. However, if no spacing exists, and the primary anterior teeth were in contact be-
fore the lost incisor, a collapse in the arch after the loss of one of the primary incisors is almost cer-
tain. This is not true in the case of a lost permanent incisor as space closure occurs rapidly whether
spacing is present or not prior to the primary tooth loss. Space maintenance would be indicated.
• Important: one of the MOST COMMON CAUSES OF MALOCCLUSION IS INADEQUATE SPACE
MANAGEMENT AFTER EARLY LOSS OF PRIMARY TEETH.

Relative to the primary mandibular canines, the permanent mandibular canines ERUPT IN A FACIAL
(LABIAl) direction or are often right in line with the primary canines. If there are eruption problems,
•
these teeth can be displaced either lingually or labially, but they are usually displaced LABIALLY if
there is not enough room to accommodate them within the arch. The mesial inclined plane of the pri-
mary maxillary canine articulates with the distal inclined plane of the primary mandibular canine. This
is the normal relationship.
292
In both maxillary and mandibular arches, the permanent incisor tooth buds lie LINGUAL & APICAL
(inferior) to the primary incisors. This results in a tendency for mandibular permanent incisors to
erupt somewhat lingually, and in a slightly irregular position (this occurs in children who have normal
dental arches and normal spacing within the arches). Permanent teeth normally move OCCLUSALLY
& BUCCALLY while erupting.
• The maxillary arch is slightly longer (-128mm) than the mandibular arch (-126mm).

LEEWAY SPACE - the DIFFERENCE in the total of the M-D widths between the primary canine, first
molar, and second molar, AND permanent canine, first premolar, and second premolar. The permanent
successors are usually SMALLER than their primary predecessors.
• Mandibular leeway space averages 3-4mm & the Maxillary leeway space averages 2-2.5mm.
The important factor is that some space will be available in the posterior part of the mouth .
This leeway space serves to at least accommodate the permanent canines (which are usually
larger than primary canines).
• During the canine-premolar transition period, the permanent first molars generally move MESIALLY
into the leeway space after the primary second molars are shed, thus causing a loss in arch length.
This is called "the late mesial shift of a permanent first molar" .

SERIAL EXTRACTION - a procedure that involves the orderly removal of selected PRIMARY & PER-
MANENT TEETH in a predetermined sequence. Serial extraction is primarily indicated in SEVERE CLASS I
malocclusion in the mixed dentition that has insufficient arch length. It benefits children who have an
arch-length discrepancy. Important: severe arch space deficiency in the permanent dentition (>
1Omm) almost always requires extractions to properly align teeth. Serial Extraction Stages:
1. Primary Canines are removed 1st
2. Primary 1st Molars are removed 2nd
3. Permanent 1't Premolars are removed last (usually).

6-15 months is the interval between extractions. To aid in support and retention during serial extrac-
tion treatment, a LINGUAL ARCH is used in the mandible and HAWLEY APPLIANCE in the maxilla. This
is usually followed by full orthodontic treatment. THE KEY TO SUCCESS IS TO EXTRACT THE 1't PREMO-
LARS BEFORE THE PERMANENT CANINES ERUPT.

In serial extraction procedures, concerns about eruption sequence are usually related to the eruption o
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pattern of the permanent mandibular canines & first premolars. After extracting the maxillary first ::c
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premolar in a serial extraction procedure, the maxillary canines' path of eruption will usually be down- ""
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ward and backward. :::!
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MOST COMMON IMPACTED ANTERIOR TEETH are MAXILLARY CANINES. Failure of a permanent tooth to
erupt may damage the roots of other teeth and create a severe orthodontic problem . Orthodontic con-
sultation is indicated when first observed on a radiograph. An impacted canine or other tooth in a
teenage patient can usu?lIy be brought into the arch by orthodontic traction after being surgically ex-
posed. In older patients, there is an increasing risk that the impacted tooth has become ankylosed.
Even adolescents have a risk that surgical exposure of a tooth will cause ankylosis.

3 Principals when Treatment Planning an Impacted Tooth:

1. The prognosis is based on the extent of displacement and surgical trauma required for exposure.
2. During surgical exposure, flaps should be reflected so that the tooth is ultimately pulled into the
arch through keratinized tissue (NOT through alveolar mucosa).
3. Adequate space should be provided in the arch BEFORE attempting to pull the impacted tooth
into position .

Research suggests the association of impacted canines with missing lateral incisors or shortened
roots of lateral incisors. The distal aspect of the lateral incisors root guides the eruption of canines.

293
 NOTES SUPERNUMERARY TEETH - extra teeth that develop in excess of the normal complement of teeth
that can occur in the maxilla or mandible, but are most common in the maxilla in the midline of the ante-
rior teeth, and sometimes distal to the molars. Supernumerary teeth have a 2: 1 predilection for MALES.

• MOST COMMON SITE of a SUPERNUMERARY TOOTH IS BETWEEN MAXILLARY CENTRAL INCISORS.

• Mesiodens-an extra tooth that occurs between the maxillary central incisors. Mesiodens are usually
small peg-shaped teeth (microdontia) that do not resemble the normal teeth of the site. An impacted
mesiodens can cause a diastema between the maxillary central incisors, while an inverted mesiodens
can cause delayed eruption of the maxillary central incisors.

• Supernumerary teeth can cause crowding of the normal teeth and can delay permanent tooth eruption.

• Diagnosis: to localize a supernumerary or impacted tooth and its relationship to other teeth, take two
or more periapical radiographs at different angles, and an occlusal view film.

• Treatment: surgically removing the supernumerary teeth and observing the progress of the
permanent teeth.

• Conditions associated with multiple supernumerary teeth : Gardener's syndrome, Down's

syndrome, Cleidocranial dysplasia, &Sturge-Weber Syndrome.

OLIGODONTIA - absence of one or more teeth. More common in females, and often associated
with a smaller than average tooth-size ratio.

Space Maintenance: A 9 year old patient had an extraction of the primary mandibular first molar.
The ideal treatment at this time is PLACE A SPACE MAINTAINER. Although this can be done with ei-
ther fixed or removable appliances, fixed appliances are preferred in most situations because they
eliminate the factor of patient cooperation. If the space is unilateral, it can be managed by a unilat-
eral fixed appliance ("band & loop" space maintainer). If molars on both sides have been lost, and the
permanent incisors have erupted, it is usually better to place a lingual arch space maintainer.

An 8 year old child with a PULPALLY INVOLVED primary second molar comes into your office The
IDEAL and best approach to manage this case is to TREAT THE PULP and RETAIN the tooth as a
space maintainer BECAUSE there is no prefabricated space maintainer that is as good as the natural
tooth . In this case, proper pulpal therapy followed by a restorative procedure is needed on this tooth to
allow it to function as a space maintainer.
• The natural tooth will preserve ARCH LENGTH & INTEGRITY better than any prefabricated space
maintainer.
• If a primary tooth is lost, an orthodontic evaluation is indicated to determine whether space
maintenance is needed. This decision is based on the patient's skeletal and dental development (i.e.
if a 10 year old child loses the primary first molar, no treatment is usually needed, since the
permanent first molar usually erupts between ages lD-12yrs).

GENERALIZED CAUSES OF FAILED OR DELAYED ERUPTION - Hereditary Gingival Fibro-

matosis, Down's syndrome, &Rickets. Generalized eruption failure or "primary failure of eruption" is
caused by the failure of the eruption mechanism itself. The involved teeth do not erupt spontaneously
and are not amenable to any orthodontic recourse. Fortunately, the condition is rare.
• Hyperparathyroidism, however, causes premature exfoliation (loss) of primary teeth.

LOCALIZED CAUSES OF FAILED OR DELAYED ERUPTION - congenital absence, abnormal po-

sition of the crypt, lack of arch space (crowding), supernumerary teeth, and dilacerated roots.

294
Effects of Environmental Influences during Growth &Development of the face, jaws, and teeth:
• Patients who have excessive overbite or anterior open bite usually have posterior teeth that are infra-
NOTES
erupted or supra-erupted respectively.
• A non-nutritive sucking habit causes malocclusion only if it continues during the mixed dentition
stage.
• Negative pressure created in the mouth during sucking is not a cause of maxillary arch constriction.
• Adenoids that lead to mouth breathing, cannot be with certainty considered an etiologic agent of a
long-face pattern of malocclusion as studies show most of the long-face population do not have
nasal obstruction.

98% of 6-year olds, &49% of 11-year old children have a MAXILLARY (MEDIAN) DIASTEMA caused
by either a tooth-size discrepancy, mesiodens, abnormal frenum attachment, or a normal stage of
development.
• The diastema closes as the permanent canines erupt. The greater the spacing, the LESS likely a
maxillary central diastema will completely close on its own.
• As a general rule, a maxillary central diastema of 2mm or less will usually close spontaneously, while
total closure of a diastema initially greater than 2mm is unlikely. If the space is 2mm or less, and
maxillary laterals are in a good position, it is most likely the result of a normal developmental process.
• If the diastema is caused by an abnormal frenum, it is best to align the teeth orthodontically and
then do a frenectomy (this is usually not done until the permanent canines erupt).
• Methods to Close a Diastema: using a lingual arch with finger springs, a Hawley appliance with
finger springs, or using cemented orthodontic bands with inter-tooth traction.

6 Types of Tooth Movement Accomplished with Orthodontics:

1. Tipping-the tooth crown moves in one direction, while the root tip/apex is displaced in the
opposite direction due to rotation or pivoting of the tooth around the axis of resistance (axis of
rotation) which is located somewhere in the apical 113 of the root. Tipping is best accomplished
with a removable appliance and most easily with anterior incisors.
2. Translation (bodily movement}-a coupled force is applied to the crown to control root movement
in the same direction as crown movement (force is applied through the tooth's center of
resistance). Translation is very difficult to accomplish.
3. Extrusion-displacement of the tooth from its socket in the direction of eruption.
4. Intrusion-tooth movement into the socket along the tooth's long axis. Intrusion is very difficult o
to accomplish. ....
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5. Torque-controlled root movement F-L or M-o while the crown is held relatively stable (M-D root o
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movement is also called "uprighting"). :z:
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6. Rotation-revolving the tooth around its long axis. Recurring tooth rotations after orthodontic C">
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correction occur due to the persistence of the elastic supracrestal gingival fibers (mainly free
gingival & transseptal fibers). Need adequate retention to prevent relapse. Thus, supracrestal
fibers are commonly associated with relapse after orthodontic rotation of teeth.
• An appropriate candidate for post-orthodontic circumferential supracrestal fibrotomy is a
ROTATED maxillary lateral incisor. Circumferential supracrestal fibrotomy-a minor surgical
procedure where a simple incision into the sulcus is made to the crest of bone to incise all of
the collagen fibers that are inserted into the tooth root. Cutting the collagen fibers
eliminates relapse potential due to collagen fiber retraction and allows new fibers to form
to help retain the tooth in its new position.

On the side TOWARD where the tooth is being moved, osteoclasts are breaking bone down, while on
the side of the root from where the tooth moves osteoblasts that are remodeling/forming bone.

One of the most important aspects of orthodontic therapy is RETENTION. After malposed teeth have
been moved into the desired position they must be mechanically supported until the hard & soft tis-
sues have been thoroughly modified in structure and function to meet the new position's demands.
Once the desired occlusal results are achieved, and the hard tissues are in normal function, the next
step is to maintain or modify the soft tissues in the retention phase. Important: most clinicians be-
lieve the collagen fibers in the supra-alveolar tissue are primarily responsible for relapse of ortho-
dontically rotated teeth and for redevelopment of spaces between orthodontically moved teeth.

295
 Collagen fibers are the main components of attached gingiva. When teeth are orthodontically moved,
collagen fibers stretch like rubber bands to adjust to the new position. However, like rubber bands, the
fibers have a strong tendency to return to their former position (pulling the teeth with them as they go).

The rationale for RETENTION in orthodontics (accomplished with fixed or removable retainers) is to
allow reorganization of gingival & periodontal tissues, minimize changes due to growth, and to main-
tain the teeth in unstable conditions. Maintaining the treatment outcome after orthodontic treatment
is one of the most difficult aspects of the entire treatment process. Retention is necessary because:
1. gingival and periodontal tissues are affected by orthodontic tooth movement, and require time
for reorganization when the appliances are removed .
2. changes produced by growth may alter the orthodontic treatment result.
3. teeth may be in an inherently unstable position after treatment so that soft tissue pressures
constantly produce a tendency for relapse. Thus, gradual withdrawal of an orthodontic appliance
is of no value. The only possibilities are accepting relapse or using permanent retention.
Fortunately, only the first two reasons apply to most orthodontic patients, and maintaining the
teeth's position until remodeling of the supporting tissues is complete and growth has stopped
allows a stable orthodontic result without further retention .

Anterior cross bite is EASILY RETAINED after orthodontic correction by the overbite achieved during
treatment.

ORTHODONTIC APPLIANCES - can irritate the gingiva, act as plaque harbors, and make proper
oral hygiene difficult to perform. Prolonged orthodontic treatment has long been associated with
causing inflammatory periodontal disease. However, if meticulous oral hygiene is maintained at all
times during orthodontic treatment, periodontal health can be maintained.
• When a patient (young or old) is in active orthodontic treatment, and the gingiva is inflamed, the
dentist should encourage better oral hygiene. It may be useful to recommend using water irrigation
devices to help flush food debris away from the orthodontic brackets.
• For an orthodontic appliance to be effective in TRANSLATING TOOTH ROOTS it MUST be capable of
EXERTING ATORQUE.

FIXED ORTHODONTIC APPLIANCES - offer controlled tooth movement in all 3 PLANES OF

SPACE. 4 basic components of a fixed appliance are BANDS, BRACKETS, ARCHWIRES, &AUXILLARIES
(elastics or ligatures to hold the archwire in the brackets). ALLOYS used for orthodontic archwires:
stainless steel, chromium-cobalt, & titanium.
• The properties of stainless steel wires used for archwires can be controlled over a wide range by
varying the amount of cold working annealing during manufacturing. Steel is softened by annealing
and is hardened by cold working (work hardening).
• Chromium-cobalt alloys are advantageous because they can be supplied in a softer, thus more
formable state, and can be hardened by heat treatment after being shaped. The heat treatment
increases strength significantly.
• Titanium alloys offer a highly desirable combination of strength, springiness, & reasonably good
formability.

Properties of an IDEAL WIRE MATERIAL for orthodontic purposes should possess high strength, high
range, high formability, and low stiffness (stiffness of orthodontic wires is a function of the wire's
length & diameter, and the wire's alloy composition. The material should be weldable or solderable,
so hooks or stops can be attached to the wire. Loops & Helices are incorporated into archwires to in-
crease the activation range.

QUAD HELIX - a FIXED appliance that consists of 4 helices (2 anterior & 2 posterior) used for POS-
TERIOR CROSS-BITE cases with a digital-sucking habit.

UNBUFFERED PHOSPHORIC ACID (35-50%) - used as an ETCHING AGENT for 1 minute be-
fore direct bonding of orthodontic brackets. After etching, the tooth surface has a FROSTED appear-
ance. When etching, the tooth surface cannot be contaminated with saliva that promotes immediate
remineralization, until bonding is complete to avoid re-etching. DO NOT USE topical fluoride before
etching as FLUORIDE DECREASES ENAMEL SOLUBILITY.

296
Indications for using BANDS instead of bonded brackets:
• To provide better anchorage for greater tooth movement.
• For teeth that need both lingual and labial attachment.
• Teeth with short clinical crowns.
• Tooth surfaces that are incompatible with successful bonding.

BAND CEMENTATION - glass-ionomer cements (resin or non-resin based) due to their fluoride
releasing properties and retentive strengths, are fast replacing zinc phosphate cement. The cold
slab ("frozen slab technique") is used to mix the cement on regardless of the cement that is used to
allow a greater amount of powder into the cement liquid, to produce a stronger cement.

INDIRECT METHOD OF BONDING BRACKETS to a tooth over the direct method:

• Advantages: reduced chair-side time, accurate placement on teeth, controlled resin thickness
between the tooth & bracket interface, and easier clean-up during bonding & de-bonding.
• Disadvantage: indirect bonding is more complex, more technique sensitive, & requires extra
precautions than direct bonding.

Indirect Bracket Bonding Procedure:

1. take an accurate alginate impression and pour it with orthodontic model stone to be used
as a working model.
2. draw vertical lines on the teeth to aid in bracket placement, and a separating media is applied .
3. brackets are then loaded with a filled resin paste and cured.
4. after its initial set, individual positioning of a tray with silicone is prepared by applying it over
the bracketed teeth on a plaster model.
5. entire set-up is placed in warm water to dissolve the separating media.
6. silicone tray is then removed from the plaster model with brackets embedded in it.
7. brackets are cleaned under running water making sure that pads have cured resin.
8. enamel is etched, conditioned, and unfilled resin is applied . Unfilled resin is also applied to
cured resin on the base of the bracket pads.
9. silicone tray with embedded brackets is then positioned on the teeth being bonded and held
in position until the initial set of unfilled resin is reached.

The control of "flash" (excess resin) makes clean-up easier, and the controlled thickness of it accu-
rately expresses the built-in prescription of the appliance. Also, in situations where visibility is a
problem (Le. lingual appliances), this technique is almost always used.

Types of Fixed Appliances:

• Lingual Archwire Appliance & Whip-Spring Appliance
• Fixed-Space Maintainers & Palatal-Separating Devices
• Edgewise Mechanism
• Light-wire, twin wire, & universal appliances

FIXED EDGEWISE APPLIANCE - the MOST WIDELY USED APPLIANCE TODAY by orthodontists. In
its essential form, the mechanism consists of bands on all teeth, tubes on the last molar, and brackets
on all other teeth. One labial arch is used at a time. The ultimate labial arch wire is .0125 x .028 in di-
ameter, and the narrow dimension (edge) fits precisely into the bracket slot (which is .022inch wide
from top to bottom) . It finds its greatest application in treating comprehensive malocclusions of the
adolescent permanent dentition.
• VARIATIONS of the basic Edgewise Appliance: includes double (tandem) brackets (Siamese twin
brackets), & narrow slotted brackets, 0.18 from top to bottom. Astraight wire appliance is a version
of the edgewise appliance with several features that allow placement of an ideal rectangular archwire
without bends.
• Edgewise Appliance Components:
• Siameses twin bracket (used on maxillary anterior teeth).
• Broussard buccal tube (allows for the use of the segmented arch technique used to intrude teeth).
• Straight wire bracket and a bracket with a .0222 x .028 rectangular slot. The bracket slot size
of .022 inch allows a wide range of wire sizes to be used. The alternate slot size is .018 inch,
which can also upright the molar, but limits the wires sizes available. The tipped 2nd molar should
be banded because the considerable posterior masticatory forces produced can easily shear off
bonded brackets.
297
 N • The time required to UPRIGHT AMOLAR takes between 6-12 months (a severely tipped molar or
molar that requires mesial movement to shorten the pontic space requires longer treatment). AFixed
Edgewise Appliance is usually used for MOLAR UPRIGHTING. Molar Uprighting Facts:
• Aseverely lingually tipped mandibular molar is MORE DIFFICULT to control and upright properly.
• Molar uprighting treatment in high angles cases results in excessive bite opening (increases
vertical dimension of occlusion VDO).
• Stabilization (retention) should last until the lamina dura &POL reorganize which takes -2
months for simple uprighting, and up to 6 months for uprighting and osseous surgery or grafts.
This retention (stabilization) is provided by an appliance or well-fitting provisional restoration to
stabilize the tooth positions and allow for reorganization of the POL. Slow progress in molar
uprighting in an adult patient is most likely due to occlusal interferences.

Conditions that can complicate MOLAR UPRIGHTlNG:

• High mandibular plane angle (one of the most significant complications because if the molar is
uprighted unsuccessfully, it can cause an increased open bite, and loss of anterior guidance) .
• Presence of periodontal disease.
• Poor crown-to-root ratio and/or short roots.
• Root resorption.
• Significant CR to MIC discrepancy.
• Severe lingual inclination of the tooth in addition to the mesial tipping.
• Occlusal plane disharmony (i.e. extruded maxillary & mandibular molars).
• Open bite.
• Severe skeletal discrepancies.

Acommon dental condition that can benefit from orthodontic treatment prior to prosthetic treat-
ment is the long-term loss of a mandibular permanent 1'1 molar which causes tipping, migration &
rotation of adjacent teeth into the edentulous space. The best way to upright a 2nd molar that drifted
mesially is tipping its crown DISTALLY and opening up space for a pontic to replace the missing first
molar, rather than attempting to move the 2nd molar mesially to close the space.

ANORMAL ANGULATION of a molar is desirable because it improves the direction & distribution of
occlusal forces, alveolar contour, crown-to-root ratio, and the periodontal environment by eliminating
o plaque-retentive areas. It decreases the amount of tooth reduction required for parallelism of the
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abutments and the possibility of endodontic, periodontic, or more complex prosthodontic procedures. It
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increases restoration durability due to better force distribution .
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en WHIP-SPRING APPLIANCES - used to DE-ROTATE one or two teeth.

Space Maintainers that REPLACE ONE PREMATURELY MISSING PRIMARY TOOTH:

1. "Band &Loop" Space Maintainer-most often used when the PRIMARY FIRST MOLAR must be
prematurely extracted . Used after a unilateral loss of a primary first molar. It consists of a band
that is usually cemented to a primary second molar. Attached to the band is a loop that extends
to the canine's distal surface. The loop prevents mesial migration of the primary second molar.
Note: limited strength allows only single tooth-space maintenance.
2. Distal Shoe Space Maintainer-used when a primary second molar is lost BEFORE the
permanent first molar erupts (typically children under age 5 or 6).
• Premature loss of a primary maxillary second molar usually produces a Class II molar
relationship on the affected side. DISTAL SHOE SPACE MAINTAINER may help alleviate this
potential problem. This maintainer extends backwards from the primary first molar crown,
and subgingivally to the mesial line of the unerupted first permanent molar, thus preventing
mesial migration.

Space Maintainers that REPLACE MULTIPLE PREMATURELY MISSING PRIMARY TEETH:

1. Lingual arch space maintainer-the primary second molars or permanent first molars are banded.
Typically, the "lingual arch" space maintainer is comprised of two bands that are cemented to
the primary second molars or permanent first molars with a loop of wire that rests on the cingula
of the incisors. Used to maintain space when multiple primary teeth are missing and the
permanent incisors have erupted. It does NOT restore function, and should be made
completely passive.

298
 2. Nance appliance (transpalatal appliance)-used for BILATERAL LOSS of primary maxillary
molars. An acrylic button rests on the palate, and is attached to bands that are bilaterally
cemented on the permanent maxillary molars. This appliance prevents MESIAL ROTATION &
DRIFTING of the permanent maxillary molars to which it is attached.
3. Partial Denture-most useful for bilateral posterior space maintenance when permanent incisors
have not erupted. Also used for missing anterior teeth when esthetics are a concern.

REMOVABLE orthodontic appliances-are generally restricted to TIPPING teeth.

1. Active Removable Appliances: includes extraoral traction devices (head gears, face masks, chin
cups), lip bumpers, active plates (Schwartz appliance & anterior spring aligners), and vacuum
formed appliances.
2. Passive Removable Appliances: bite planes, occlusal splints, and retainers.

Removable Orthodontic Appliance Components:

1. retentive component-retains the appliance in function, and consists of various clasps
(i.e. Adam's crib).
2. framework (baseplate)-made of acrylic and provides anchorage.
3. tooth-moving elements-are either springs or screws.
4. anchorage component-resists force of active components (i .e. acrylic base-plate). Anchorage
components can also cause desired or undesired tooth movements.
5. active components (tooth moving components)-springs, screws, or elastics.

Indications of Removable Appliances: retention after comprehensive treatment, limited tipping

movements, & growth modification during the mixed dentition.

HAWLEY RETAINER - the MOST COMMON REMOVABLE RETAINER used is orthodontics. It incorpo-
rates clasps on molar teeth and a characteristic outer bow with adjustment loops that span from ca-
nine-to-canine.
• Palatal coverage of a removable plate like a Hawley retainer makes it possible to incorporate a BITE
PLANE lingual to the maxillary incisors to CONTROL BITE DEPTH. This design is important for any
patient who once had an EXCESSIVE OVERBITE. Palatal coverage with acrylic is the major source
of anchorage in the Hawley appliance.
• Hawley retainer can be made for the upper & lower arch. The lower retainer is fragile and may be
difficult to insert because of undercuts in the premolar region. A patient may have difficulty
pronouncing linguoalveolar consonants for a few days after receiving a maxillary Hawley until the
tongue adapts to the palatal coverage.

BEGG APPLIANCE - uses round wires that fit loosely into the bracket's vertical slot.

FRANKEl'S APPLIANCE - a REMOVABLE functional appliance used for abnormal (hyperactive)

soft tissue patterns.

HEADGEAR - used to maintain EXTRA-ORAL ANCHORAGE& TRACTION. The -required force for an-
chorage is 250g for 10hrs/day. The required force for traction is 500g for 14-16hrs/day. One of the
greatest advantages of using extraoral anchorage (headgear) is it PERMITS POSTERIOR MOVEMENT
OF TEETH IN ONE ARCH without adversely disturbing the opposing arch.
• Headgear extra-oral components: neck strap, chin cup, & head cap.
• Headgear intra-oral component: facebow which has an outer & inner bow. The length & position of
the outer bow is set according to the inner bow. The inner bow relates to the center of resistance of
the tooth and effects anchorage and/or traction.
• For use with URA, the direction of force above the occlusal plane aids in retention.

4 Basic Headgears: cervical-pull, straight-pull, high-pull, & reverse-pull. These are selected based
on the direction of force (pull) needed.
1. High-pull headgear: produces a DISTAL & UPWARD force on the maxillary teeth & maxilla. This
headgear consists of a head cap connected to a face-bow. This type of headgear has a more
direct effect on the anterior segment of the arch. Indicated for Class II, Division I malocclusions
that have an open bite.

299
 2. Cervical-pull headgear: consists of a neck strap connected to a face-bow to produce a DISTAL
& DDWNWARD force against the maxillary teeth & maxilla. Major disadvantage: possible
extrusion of maxillary molars. Likely results include an open bite, and move first molars distally,
and decrease forward growth of the maxilla. Indications: Class II, Division I malocclusions.
3. Straight-pull headgear: similar to cervical-pull headgear, but this appliance places a force in
a straight distal direction from the maxillary molar. like cervical-pull headgear, straight-pull
headgear is indicated for Class II, Division I malocclusions (when bite opening is undesirable).
4. Reverse-pull headgear: UNLIKE ALL OTHER HEADGEAR BECAUSE IT HAS AN EXTRAORAL
COMPONENT supported by the chin, cheeks, forehead, or combination of these structures.
Indicated for Class III malocclusions (where protraction of the maxilla is desirable).

FINGER SPRINGS - best method for TIPPING maxillary &mandibular ANTERIOR TEETH. Finger
springs are attached to a removable appliance. The most common problems associated with these
simple removable appliances are lack of patient cooperation, poor design leading to a lack of re-
tention, and improper activation. An undesirable common side effect of a finger spring is the ten-
dency for the root apex to move in the direction opposite from the crown.
• Z-Springs-can also be used for tipping anterior teeth, but deliver excessively heavy forces & lack
range of motion.
• Maxillary incisor rotation is not commonly treated during the mixed dentition stage, but is BEST
TREATED after all permanent teeth have erupted (in the early permanent dentition) with SIMPLE
REMOVABLE APPLIANCES. However, if the incisor is in anterior cross bite, it should be corrected ASAP
(while it is erupting).
• When using BUCCAL COIL SPRINGS to try and regain space by pushing a tooth mesially or distally,
be careful because what commonly occurs is ROTATION of that tooth, rather than actual movement.
• The force generated in the spring is DIRECTlY proportional to the distance that an orthodontic spring
is deflected and the radius (r) of the wire. The force is INVERSELY proportional to the spring's length.

F = d r4
13

LOOSE REMOVABLE APPLIANCES - include functional appliances and functional jaw

orthopedic appliances.
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o FUNCTIONAL APPLIANCES - Frankel, Bionator, Clark's Twin Block, Herbst, & Activator. Functional
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en 1. Tissue-Borne Functional Appliance: Frankel's Functional Appliance-the only TISSUE-BORNE
FUNCTIONAL APPLIANCE whose function is to expand the arch by "padding" against the
pressure of the lips & cheeks on the teeth and postures the mandible forward and downward.
2. Tooth-Borne Functional Appliances:
• Activator: advances the mandible to an edge-to-edge position to induce mandibular growth
to correct a Class II malocclusion. The maxillary teeth are prevented from erupting by the acrylic
shelf, while mandibular posterior teeth are free to erupt. This improves the deep-bite seen in
Class II cases .
• Bionator: similar to the activator in function , but its design is a trimmed-down version of the
activator to make it more comfortable to wear.
• Herbst Appliance: can be fixed or partially removable. Ametal-rod & tube-telescopic apparatus
are attached bilaterally to the maxillary first molars & mandibular first premolars to help
posture the mandible forward and induce growth. Jasper modified Herbst by replacing the
telescopic apparatus with a flexible plastic open coil spring.
• Clark's Twin Block: a two-piece acrylic appliance that postures the mandible forward with
help of occlusally inclined guiding planes and bite blocks. The vertical separation of the jaws
is also configured by the height of the bite blocks.

A7 year-old child with good occlusion has a LINGUALLY LOCKED maxillary permanent central incisor.
There is sufficient room for the tooth. To treat this condition properly, the dentist should CORRECT
THE CONDITION IMMEDIATELY WITH ASIMPLE APPLIANCE. Ideally, this anterior crossbite should have
been corrected BEFORE it reached the occlusal plane (while it was erupting). The most probable etio-
logic factor for this happening is PROLONGED RETENTION OF PRIMARY MAXILLARY INCISORS.

300
• Cross-elastics from the maxillary lingual to mandibular labial can be used to correct a single-tooth
crossbite. Amaxillary removable appliance can also be used. When elastics are used to move teeth
they should be ATTACHED DIRECTLY TO THE APPLIANCE COMPONENTS.
• Anterior Crossbite (especially crossbite of the incisors), is RARELY FOUND in children who do not have
a skeletal Class III jaw relationship. A crossbite relationship of 1 or 2 anterior teeth, however, may
develop in a child who has good facial proportions. Maxillary lateral incisors tend to erupt to the lingual,
and may become lingually trapped especially in the presence of severe crowding. In this situation,
extracting the adjacent primary canines usually leads to spontaneous correction of the crossbite. It is
important to evaluate the space situation before attempting to correct any anterior crossbite. If enough
space is available to accomplish this movement, a maxillary removable appliance is usually the best
mechanism to correct a simple anterior crossbite that requires a tipping movement. Anterior
crossbite in a primary dentition usually indicates a SKELETAL GROWTH PROBLEM.

FIRST ORDER BEND - a bend of an orthodontic wire in the HORIZONTAL PLANE.

Cartilage Growth Occurs 2 Ways:

1. Appositional Growth-by the recruitment of fresh cells, chondroblasts, from perichondral stem
cells and the addition of new matrix to the surface. The perichondrium consists of a fibrous outer
layer and chondroblastic inner layer.
2. Interstitial Growth-occurs by the mitotic division & deposition of more matrix around chondrocytes
already established in the cartilage. Examples of sites that grow by interstitial growth include the
mandibular condyle, nasal septum, and spheno-occipital synchondrosis.
• Hyaline Cartilage-differs from bone in that hyaline cartilage may grow by
INTERSTITIAL GROWTH.

BONE FORMS by either Endochondral ossification or Intramembranous ossification. Bone formation

begins in the embryo where mesenchymal cells differentiate into either fibrous membrane or carti-
lage. Do not confuse bone growth & bone formation. Once bone is formed, it then GROWS by apposi-
tional growth (growth by the addition of new layers on top of previous formed layers). This leads to two
paths of bone development.
1. Intramembranous ossification-takes place IN membranes of C.T. Osteoprogenitor cells in the
membrane differentiate into osteoblasts, and a collagen matrix is formed which undergoes
ossification. The maxilla & mandible are formed this way. c
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• FLAT BONES of the skull & part of the clavicle are formed by INTRAMEMBRANOUS OSSIFICATION. .....
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2. Endochondral ossification-is how the remainder of the skeleton forms and takes place within a c
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hyaline cartilage model. Cartilage cells are replaced by bone cells (osteocytes replace
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chondrocytesl, organic matrix is laid down and calcium and phosphate are deposited. V>

Endochondral ossification is mainly responsible for formation of SHORT & LONG BONES
(i.e. ethmoid, sphenoid, & temporal bones of the skull).

BONE GROWTH occurs ONLY BY APPOSITIONAL GROWTH which below the covering periosteal layer
of bone. Periosteum con·sists of a fibrous outer layer & a cellular inner layer of osteoblasts, which lay
down bone. Due to its rigid structure, interstitial growth is not possible.
• A major site of growth of the mandible is the CONDYLE. Mandible growth occurs by cartilage
proliferation at the condyles, and by apposition & resorption of bone at the mandible surfaces.
Resorption occurs along the anterior surface of the ramus (creates space for mandibular molars),
while bone apPosition occurs along the posterior surface of the ramus. However, the mandible's
MAIN GROWTH SITE is in the CONDYLAR CARTILAGE. The "V principal" of growth is best illustrated
by growth of the mandibular ramus. Important: growth at the mandibular condyle during puberty
usually results in an increase in posterior facial height.
• Mandibular growth involves a synchronous & selective deposition and resorption of bone from
membrane surfaces and interstitial & appositional growth changes in the condyle. The MAIN GROWTH
THRUST is in an UPWARD & BACKWARD direction causing the body of the mandible to move
DOWNWARD & FORWARD. In this process, bone is deposited along the posterior aspects of the ramus
and in the condylar area .

301
 NOTES • Bone deposition in the MAXILLARY TUBEROSITY REGION is responsible for LENGTHENING OF THE
MAXILLARY ARCH. The maxillary arch elongates, moves posterior, and increases in height. Bone
deposition in the tuberosity region is responsible for the lengthening (elongation) of the maxillary arch.
The posterior movement is due to resorption of the labio-alveolar surface, and apposition of the
lingual surface. Alveolar growth is responsible for an increase in the height of maxillary bones.
• Posterior movement predominates in the tuberosity area. The primary movement of the alveolar
region & palate is downward, the nasal region moves forward, and zygomatic process moves
posteriorly and laterally.
• Growth of the maxilla and its associated structures occurs from a combination of growth at
sutures, and direct remodeling of the surface of the bone.

• In a young child, the ALVEOLAR PROCESS grows in height &length to accommodate the developing
dentition. Alveolar process bone exists ONLY TO SUPPORT TEETH. If a tooth fails to erupt, alveolar
bone will never form in that area. If a tooth is extracted, the alveolus resorbs after the extraction
until finally the alveolar ridge completely atrophies.

• The space between the jaws into where the teeth erupt is provided by growth at the mandibular
condyles (especially the molars). Condyle is a major site of vertical growth in the mandible. Many
arguments have been made about the condyle's function in mandibular growth. Most agree that
soft-tissue development carries the mandible forward and downward, while condylar growth fills
in the resultant space to maintain contact with the base of the skull.

• In infancy, the ramus is located at about the spot where the primary first molar will erupt. Progressive
posterior remodeling creates space for the second primary molar and then for the sequential eruption
of the permanent molar teeth. More often than not, however, this growth stops before enough space
has been created for eruption of the 3'd permanent molar, which becomes impacted in the ramus. After
age 6, the greatest increase the mandible size occurs distal to the first molars.

LATE MANDIBULAR GROWTH - is the theory that best explains why there is a strong tendency
for mandibular anterior crowding in the late teens and early 20's. The current concept is that late
incisor crowding develops as the mandibular incisors and possibly the entire mandibular dentition,
move DISTALLY relative to the body of the mandible late in mandibular growth.
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en • Mandible undergoes more growth in the LATE TEENS than the maxilla.

The MOST RAPID LOSSES IN ARCH PERIMETER are usually due to a MESIAL TIPPING & ROTATION of
the permanent first molar after removal of the primary second molar. When the primary second
molar is lost, ALWAYS MAINTAIN SPACE until the second premolar arrives.

• If a permanent 1st molar is extracted on a child before the permanent second molar erupts, th~best
approach is to allow the second molar to erupt and allow mesial drifting to occur naturally as this
will usually fill in the space.

• A space maintainer can be removed as soon as the permanent tooth begins to erupt through
the gingiva.

• MOST RELIABLE INDICATOR of readiness of eruption of a succedaneous (permanent) tooth (and

the need for a space maintainer) is the EXTENT OF ROOT DEVELOPMENT determined by radiographic
evaluation. Aspace maintainer is NOT required if eruption of the succedanous (permanent) tooth
is imminent.

302
EHfiPTER fi

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303
 N ACRYLIC RESINS
Mechanical properties of resins are influenced by:
1. MW of the polymer.
2. Degree of cross-linking (need difunctional monomers that contain two areas for reaction).
3. Composition of monomers used to prepare the polymer.
4. Acrylic resins EXPAND when immersed in water and become DISTORTED when dried out.

Acrylic Resin Components:

1. Powder (polymer): polymethyl methacrylate (PMMA) polymer, benzoyl peroxide initiator,
and pigments.
• Cross-linking agents contribute greatly to the strength of the polymer.

2. Liquid (monomer): pure methyl methacrylate (MMA) monomer, hydroquinone inhibitor, cross-
linking agents, and chemical activator (dimethyl-p-toluidine) which is only present in self-cured
resins to cause polymerization .
• Other monomers (liquids) used in dentistry are ethyl methacrylate, vinyl ethyl methacrylate,
and epimine resins. These are less irritating to the pulp.
• Inhibitors are added to monomers to help prevent polymerization during storage.
• Excessive shrinkage may occur if too much monomer (liquid) is added to the polymer (powder).

HEAT-CURED MATERIALS - heat is used as an accelerator to decompose benzoyl peroxide (initia-

tor) into free radicals which initiate the polymerization of MMA PMMA. The polymerization process con-
tinues as new PMMA is formed as a matrix around residual PMMA powder particles.

• Methyl Methacrylate (MMA)-the liquid monomer that is the most frequently used polymer system
in dentistry. The polymerization reaction of MMA is exothermic (gives off heat).

• Polymerization range is the temperature range of -60°C (140°F) to noc 070°F) at which the major
part of polymerization occurs in a heat-cured resin .

• Heat-cured resins have LESS residual monomer and higher MW than self-cured resins, thus are
STRONGER and have superior color stability.

SELF-CURED MATERIALS (AUTO-CURED, COLD-CURED) - a chemical activator like di-

methyl-p-toluidine (a tertiary amine) is added to the monomer (MMA) to decomposes the benzoyl per-
-c oxide initiator into free radicals. These free radicals initiate the polymerization of MMA & PMMA. The
""
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::c • Polymethyl Methacrylate (PMMA)-the acrylic powder polymer used in self-cured resins.
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distorting the denture is less.

COMPLETE DENTURES
Denture Design Characteristics:
1. Stability-the quality of a restoration to be firm, steady, constant, and not subject to change
position when forces are applied. In dentures, stability is the relationship of the denture base to
bone that resists dislodgement of the denture in a horizontal direction.
• Stability involves resistance to horizontal, lateral, &torsional forces (most important).
• All components of an RPD, except the retentive clasp tip, contribute to stability.
2. Support-resistance to vertical seating forces provided by rests and denture bases. For RPDs,
support is given by occlusal rests and edentulous ridge areas. Support is the MOST important
design characteristic for oral health.

304
 3. Retention-that quality in a restoration that resists the force to gravity, sticky foods, and forces NOTES
associated with mandibular movement. Direct and indirect retainers provide retention. Clasps
placed in undercut areas of abutment teeth provide retention.
4. Reciprocation-the means by which one part of a restoration is made to counter the effects
created by another pa rt.
• In the mesial rest, guide plane and I-bar design, reciprocation is achieved by rigid plating,
minor connectors, guide planes extended around the vertical line of abutments, contact areas
of proximal teeth, and by reciprocal clasp arms.
• Reciprocation refers to the function of the lingual clasp arm (reciprocal clasp arm) to
counteract forces exerted by the buccal clasp arm (retentive clasp arm).
• Reciprocation is the means by which one part of the metal framework OPPOSES the action of
the retainer in function. Reciprocation is achieved by opposing flexible retainers with guide
planes, minor connectors, rigid clasp arms, or plating. If true reciprocation is to occur, the
reciprocating element MUST BE PLACED OPPOSITE the direct retainer, and must contact the
abutment as the retentive tip passes over the tooth's height of contour.
5. Bracing-horizontal force transmission by placing rigid portions of clasps or other parts of the
RPD in non-undercut areas of abutment teeth.
6. Guidance-during insertion and removal obtained by contact of rigid parts of the framework with
areas on axial tooth surfaces parallel to the path of insertion.

Current concepts of impression making of complete dentures recommend using a technique that:
• Affords placement and control of the impression material in recording border tissues (border molding).
• Results in minimal tissue displacement under the denture (registers the tissues in its
passive position).
• Is dependent on the oral conditions present.
• Best impression technique for a patient with loose hyperplastic tissue is to register the tissue in
its PASSIVE position. There must be intimate contact of the impression material with the tissue.

Custom Tray &Border Molding:

• The custom tray fabricated on the preliminary cast is trimmed -2mm short of the mucosal
reflection and frenae . This is done by first checking the borders in the mouth and then trimmed
down. This allows a uniform thickness of 2mm of modeling compound when the borders are molded .
However, the primary indicator of the accuracy of border molding is the stability and lack of
displacement of the tray in the mouth.
• The custom tray for a final mandibular or maxillary complete denture impression should have a
spacer with stops to insure the tray will be seated in proper relationship to the arch, and to ensure
adequate room for the impression material. The space is created with wax covered by aluminum foil
over the master cast prior to forming the tray.
• Primary indicator of the accuracy of border molding is: stability and lack of displacement of the
custom tray in the mouth.
• Border molding is completed in two stages. The molding should approximate the borders and should
be slightly overextenaed . Excess compound is trimmed from inside and outside of the custom tray.
The remaining modeling compound is then refined by repeating the process. The final form of the
border molding should represent an accurate impression of the peripheral tissues. The border
modeling compound should have a smooth, polished appearance.
• The MOST critical area in the border molding procedure for a maxillary denture is the
MUCOGINGIVAL FOLD above the maxillary tuberosity area as this area is extremely important for
maximal retention. Other critical areas are the labial frena in the midline and frena in the bicuspid
area. Overextension in these areas often leads to decreased retention and tissue irritation.
• When border molding a mandibular custom tray that will be used for a final denture impression , the
distofacial extension is determined by the position and action of the MASSETER MUSCLE and the
distolingual extension is limited by the action of the SUPERIOR CONSTRICTOR MUSCLE.

The distolingual extension of the mandibular impression for a complete denture is limited by the
action of the superior constrictor muscle.

305
 NOTES Dislodgement indicates overextension and the border molding process should be refined in the of-
fending area. The labial and buccal are common areas of overextension in the mandibular impres-
sion. This is suspected when the impression raises when the mouth is opened. Thus, after border
molding a mandibular custom tray, it is important to check for dislodgement to detect areas of
OVEREXTENSION of the custom tray. Techniques to check for dislodgement:
• Pull gently upward on the patient's cheek.
• Pull the lower lip gently forward in a horizontal direction.
• Have the patient open widely.
• Have the patient move the tongue into the right and left buccal vestibules.
• Have the patient protrude the tongue to touch the lower lip and move the tip of the tongue from one
corner of the mouth to the other corner.

Overextension of a mandibular denture base in the distofacial area causes dislodgement of the den-
ture during function as the result of the action of the MASSETER MUSCLE. An overextended distobuc-
cal corner of a mandibular denture will push against the MASSETER during function. This is a very
common area of overextension, thus should be checked very well when delivering the mandibular den-
ture.

Buccinator muscle lies under the denture flange in this area, but the fibers run anteroposterior in a
horizontal plane and their action is weak. The masseter muscle's anterior fibers pass outside the
buccinator at the DB corner of the mandibular denture and will push against the buccinator during
function causing dislodgement.

The most likely tissue reaction to gross overextension of a complete denture that has been worn for a
long time is EPULIS FISSURATUM (caused by an ill-fitting denture flange).
• The cleft-like lesions of epulis fissuratum are caused mainly from overextension of denture flanges.
The overextension may result from long-term neglect or settling subsequent to residual ridge
resorption. Traumatic occlusion of natural teeth opposing an artificial denture may also cause an
epulis fissuratum.

DENTURE STOMATITIS - a localized or generalized chronic inflammation of the denture-bearing

mucosa. Clinically present as redness and burning sensation . Discomfort may be or may not be pres-
ent. Trauma and secondary fungal infection are the most likely causes.
• Treatment: improved oral hygiene, tissue rest, anti-fungal therapy (Nystatin), resilient tissue
conditioners, and new, well-fitting dentures.

The most important reason to treat hyperplastic tissue before constructing a complete or RPD is to
""CI provide a firm, stable base for the denture. Ways to treat hyperplastic tissue include:
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U) • Tissue rest, soft reline of the existing dentures, change in denture habits (not wearing them
::z: 24hrs/day), or surgical removal of tissue (for extensive tissue changes).
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INFLAMMATORY PAPILLARY HYPERPLASIA - frequently observed under an ill-fitting denture,
especially those with a relief chamber. The hyperplasia is produced in response to irritation from
denture movement and accumulating food debris. The masses present as painless, firm, pink or red
nodular proliferations of the mucosa. Candida Albicans may contribute to the inflammation.
r
• Most patients are unaware of its presence. It usually involves only the HARD PALATE, but may
also involve the residual ridges. IPH treatment depends on the size of the lesions. Although the
nodules are not completely reversible, smaller papilla usually regress with treatment (removing the
denture, soft relines, good oral hygiene, and nystatin therapy).

• Denture-induced fibrous hyperplasia (Epulis Fissuratum), due to clefts found in the hyperplastic
tissue, is also related to the chronic trauma produced by an ill-fitting denture. It occurs in the
vestibular mucosa where the denture flange contacts tissue. It appears as PAINLESS FOLDS of
fibrous tissue surrounding the overextended denture flange. If the amount of hyperplasia is minimal,
tissue conditioning, fabrication of new dentures, and a change in denture habits may be sufficient
to arrest tissue changes. However, surgical excision is usually required.

306
Masseter muscle's superficial layer originates from the maxilla's zygomatic process and inserts at
the angle and lower lateral side of the ramus of the mandible.

PTERYGOMANDIBULAR RAPHE - a TENDON that lies between the buccinator &superior

constrictor muscles.

HAMULUS - a thin, curved bony process extension of the medial pterygoid plate of the sphenoid
bone that serves as the superior attachment of the pterygomandibular raphe (tendon).

HAMULAR NOTCH - a thin cleft between the maxillary tuberosity & hamulus (a maxillary denture
must extend into the hamular notches).

FOVEA PALATINI - a group of mucous gland ducts whose location varies, but usually appears
slightly posterior to the junction of the hard and soft palates near the midline.

Palatoglossus, superior pharyngeal constrictor, mylohyoid, and genioglossus muscles are influential in
border molding the LINGUAL border of the mandibular impression for an edentulous patient.

Primary difference between border molding with ZOE impression material vs. modeling plastic is
ZOE impression material must be border molded during one insertion and within the material's
setting time (as opposed to two insertions with modeling compound).

• The ease and accuracy of the border molding depends on: an accurately fitting custom tray,
control of bulk and temperature of the modeling compound, and a thoroughly dried tray.

• Accurate adaptation of the denture base to the mucosa increases retention of a complete denture.

• Modeling Compound (plastic) has a relatively LOW thermal conductivity.

• In complete denture fabrication, the size and shape of the bony fossae and menisci and muscular
influence regulates the paths of the condyles in mandibular movements.

MAXILLARY COMPLETE DENTURE - the primary support areas for a complete MAXILLARY den-
ture are the residual ridges. The secondary support areas are the palatal rugae .

If a patient complains "when I smile, my upper denture doesn't hold", the area of the denture base
needs to be adjusted is the buccal notch &buccal flange due to excessive thickness of this area.
As the buccal frenum moves posteriorly during smiling or other facial expressions, it encroaches on the
denture border that is too thick, causing the denture to become loose.
• Test the borders for overextension by slowly seating the denture. If you observe premature contact with
frenae or vestibular ·tissues as the denture continues toward its final position, then the border is
probably overextended. Adapt a thin roll of disclosing wax to the denture border. Seat the denture and
instruct the patient to exert vigorous muscle function. In about 1 minute, the wax will soften and is
displaced by muscular action across the overextended denture border.
• The complaint that the denture becomes loose when the mouth is wide opened (i.e. yawning), could
be due to the distobuccal flange of the denture being too thick. This may interfere with the movement
of the coronoid process.
• If a patient complains of sore gums and aching muscles at the bottom of the face after wearing
dentures for several hours, opposing teeth of the denture have sufficient space. Reduce the VDO.
• Tingling or numbing sensation at the corner of the mouth or lower lip after a few days of denture
wearing is caused by excessive pressure from the lower buccal flange in the region of the mental
foramen.

307
 N Posterior Palatal Seal (Maxillary Complete Denture):
• Outline and depth of the posterior palatal seal is different for every patient.
• Posterior palatal seal varies in outline and depth according to the palatal form of the patient.
• Aposterior palatal seal is necessary when fabricating a complete denture on a patient with
a flat pa late.
• The posterior palatal seal should never be removed .
• The middle of the seal should be .5mm deep extending 3mm on both sides of the midline.
• The sea l is 1.5mm deep lateral to the middle of the seal and should extend up to the medial
boundary of the pterygomaxillary (hamular) notches.
• Excessive depth of the posterior palatal seal usually results in unseating of the denture.
• The WIDTH of the seal anterior to posterior is characterized by a concave surface, 3mm wide
in the midline, and 6mm wide in the mid-lateral areas.
• Placement of the posterior palatal seal is always done by the dentist and is never delegated to a
lab technician .

Posterior Palatal Seal Functions:

1. completes the border seal of the maxillary denture.
2. prevents food impaction beneath the denture's tissue surface.
3. improves the denture's physiologic retention.
4. the seal compensates for polymerization and cooling shrinkage of the denture resin
during processing.

Posterior Palatal Seal Landmarks:

• Posterior outline is formed by the "ah" line (vibrating line) and passes through the two
pterygomaxillary (hamular) notches and is close to the fovea palatini. The vibrating line is not a line,
but more of an area. The vibrating line dictates the distal palatal termination of the maxillary
complete denture record base.
• In determining the posterior limit of a maxillary denture base the hamular notch is ON the
posterior border.

• Anterior outline is formed by the "blow" line (valsalva line), located at the distal extent of the hard
palate.The blow line is usually anterior to the vibrating line which freely moves when the patient
attempts to blow through the nose when it is squeezed tightly. The blow line is a close approximation
to the junction of the hard and soft palate.

Changes usually evident on the maxillary arch in a patient who wears a complete maxillary denture
and LACKS posterior occlusion include:
-c • Excessive amount of hyperplastic tissue present on the anterior portion of the maxillary ridge.
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• Poor bone structure in the anterior part of the maxilla.
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• Fibrous tuberosities.
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C) • The patient's chief complaint is looseness of the maxillary denture, and that they can no longer
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see their upper teeth on the denture. These signs and symptoms are caused by a lack of posterior
en
occlusion .

A patient wearing a maxillary complete denture and mandibular bilateral distal-extension RPD may
show a decreased VDO and exhibit a prognathic facial appearance. When a complete maxillary den-
ture opposes natural mandibular anterior teeth , the maxillary anterior ridge often become very
FLABBY.

When the posterior maxillary buccal space is entirely filled with the denture flange, interference
may occur with movement of the coronoid process which may interfere with the denture upon open-
ing of the mouth. This causes dislodgement of the maxillary denture.

In an edentulous patient, the coronoid process can LIMIT the thickness of the denture flange in the
maxillary buccal space.

308
An edentulous patient has slight undercuts on both tuberosities and on the facial of the anterior max- NOTES
illa. To construct a satisfactory maxillary complete denture, the dentist should reduce both tuberosity
undercuts because undercut tuberosities will interfere with seating of the denture.
• Maxillary anterior undercuts are very common and present no special problems unless accompanied
by large bilateral posterior undercuts. Even this situation can usually be managed by reducing the
inner surfaces of the denture lateral to the tuberosities.

• Maxillary sinus appears to enlarge throughout life if it is not restricted by natural teeth or dentures.
As the sinus enlarges, the tuberosity moves downward. If there is no contact with the retromolar pad
at the VDO, the tuberosity must be reduced.

• If a low tuberosity is not removed before constructing new dentures, an accidentally underextended
mandibular denture will probably be made and limited space to position posterior teeth will occur.

• Submucosal Vestibuloplasty-is usually performed on the maxillary arch to improve the available
denture base area. This procedure is favored because no raw tissue surface remains to granulate and
re-epithel ia Iize.

PALATAL TORI - bony enlargements located at the midline of the hard palate, occurring in -20-
25% of the population, and are more prevalent in women. They reach maximum size by age 30-
40yrs, and because the torus is usually covered by thinner and less resilient mucosa than the residual
ridge, it may act as a fulcrum and cause rocking of the maxillary denture.
• Because the soft tissues over the torus are generally thin with a poor blood supply, post-operative
healing is slow. It is best to cover the operated site with a surgical stent lined with a sedative
dressing. If a patient is having all maxillary teeth extracted at once, it is best to also remove the tori
at that time.

• Palatal tori NOT usually removed for denture fabrication. However, mandibular tori are usually
removed prior to denture fabrication . Conditions that warrant palatal tori removal include:
1. impinges on the soft tissue.
2. is so large that it fills the vault and prevents formation of an adequate denture base.
3. is undercut
4. extends so far posteriorly interfering with the posterior palatal seal.
5. is psychologically disturbing to the patient (cancerphobia) .

MANDIBULAR COMPLETE DENTURE - in the MANDIBULAR arch, the primary support area is
the buccal shelf because of its bone structure and its right angle relationship to the occlusal
plane. The residual ridges if large and broad, are also considered primary support areas.

• The second peripheral seal area for a mandibular complete denture is the anterior lingual border.

• When fabricating a mandibular complete denture for a patient with a "knife-edged ridge" you need
maximal extension of the denture to help distribute occlusal forces over a larger area.

• Marked RESORPTION of the alveolar ridge will occur if a mandibular complete denture base
terminates short of the retromolar pad. Important underextension of the peripheral border of a
complete mandibular denture decreases tissue-bearing surfaces, thus affecting denture stability.

• Underlying basal bone (under the retromolar pad) resists resorption (does not resorb). Covering
this area also provides some border seal. An overload of the mucosa occurs if the bases covering the
area are too small in outline.

• Important: mandibular dentures do not rely on suction from a peripheral seal for retention (maxillary
dentures do), but rely on denture stability in covering as much basal bone possible without impinging
on muscle attachments. The active border molding performed by the lips, cheeks, and tongue
determines the peripheral areas of a mandibular arch, thus establishing maximal basal bone coverage.

• Mandibular molars should NOT be placed over the ascending area of the mandible because the
occlusal forces over the inclined ramus dislodge the mandibular denture.
309
 Thin mucosa is found in mylohyoid area & over mandibular tori (mandibular dentures) and on the
midline of the palatal vault and over a torus palatinus (maxillary dentures).

Mandibular tori, sharp prominent mylohyoid ridges, and epulis fissuratum should be evaluated for sur-
gical removal before the fabrication of new dentures begins.

Oenture Fabrication Errors:

• Most common cause or POROSITIES in a denture is due to insufficient pressure on the flask during
processing. Acrylic resin used for denture repairs should be under 20-30psi air pressure while being
processed to help eliminate porosities. If present, these porosities usually occur in the THICKEST
part of the denture. Self-cured resins are generally used for repairs instead of heat-cured resins
since there is less risk of distorting the denture.

• Porosity in a heat-activated acrylic resin denture base is most frequently caused by lack of
pressure on the resinous mass.

• When there is a rapid elevation in temperature causing vaporization of the liquid, the vapor becomes
trapped as gas bubbles.

• Porosities also occur if the packing and processing of the powder and liquid resin is too plastic
(stringy or sandy). This permits the liquid to vaporize and does not allow sufficient pressure during
closure of the flask.

OCCLUSION RIMS -the resultant product after adding base-plate wax to a record base to approxi-
mate the tooth position and arch form expected in the completed denture. Purpose of occlusion rims:
• Determine and establish the patients VDO (vertical dimension of occlusion) .
• Make maxillo-mandibular jaw relation records.
• Establish and locate the future position of the artificial teeth.

When recording CR for an RPD, the occlusion rim is attached to the completed partial denture metal
framework instead of to a record base as used with a complete denture.

In a complete denture patient, when the teeth, occlusal rims, and central bearing point are in con-
tact, and the mandible is in centric relation, the lENGTH of the face is the occlusal vertical dimen-
sion.

Correct VOO is evaluated using 4 methods:

.,
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1. evaluating the overall appearance of facial support .
I:)
."
...... 2. visual observation of space between the occlusal rims at rest.
:::I:
I:) 3. measurment between dots on the face (placed on the tip of nose and chin with a Thompson stick)
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::! 4. observation when the "s" sound is enunciated accurately and repeatedly to ensure adequate
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speaking space between the occlusal rims/occlusal plane.

*Excessive vertical dimension of occlusion may result in trauma to the underlying supporting tis-
sues. A closed vertical dimension is the most likely cause of cheilosis in patient who wears a com-
plete denture and whose medical history is non-contributory. r

The inferior surface of the maxillary occlusion rim should be PARAllEl to CAMPER'S LINE (the
line/plane running from the inferior border of the nose ala to the superior border of the tragus of the ear).
• Significance of Camper's line: the occlusal plane, established by the surfaces of the wax occlusion
rims is parallel to Camper's line and the interpupillary line.

• The posterior determinants of occlusion (2/3 the height of the retromolar pads) have the greatest
effect on the setting of mandibular 2nd molars.

FRANKFORT HORIZONTAL PLANE - extends from the outer canthus of the eye to the ear tragus.
Commonly used in orthodontics for cephalometric analysis.

310
For complete dentures, correct OVD (occlusal vertical dimension), thickness of the anterior border, and NOTES
teeth position affect the correct POSITIONING OF THE LIPS.

An incorrect OVD causes a patient to overclose and have a poor facial profile. To correct this problem,
the dentist should increase the OVO and decrease the interocclusal distance.

If a patient's OVD is increased, an adverse condition that may arise is the straining of the closing (el-
evator) muscles.

If at the tooth try-in appointment the teeth need to be adjusted to correct centric occlusion, the best
way to correct CO is to take a new CR record and remount.

Changes associated with the edentulous state:

• Deepening of the nasolabial groove and narrowing of the lips.
• Prognathic appearance and an increase in the columella-philtral angle.
• Loss of the labiodental angle and decrease in the horizontal labial angle.

Degenerative joint disease is often seen in denture wearers, but may be age-related rather than re-
lated to the state of the dentition.

All new dentures should be evaluated 24hrs after delivery to correct any undetected errors. Tissue
trauma attributed to denture function manifests as hyperemia , inflammation, ulceration, and pain.
The basic sequence of the clinical procedure for a 24hr recall appointment is:
1. remove the dentures from the mouth and thoroughly examine the mouth.
2. ask the patient about the areas of tissue trauma that have been observed .
3. permit the patient to describe additional complaints.
4. After collecting all of the diagnostic information, the dentist can then determine the source
of the problem and cure.

During the first few days after inserting complete dentures, the patient should expect some difficulty
in masticating most foods and excessive saliva due to reflex parasympathetic stimulation of the
salivary glands. Over time, this will subside and return to normal.

IMMEDIATE DENTURES - when treatment planning a patient for mandibular and maxillary imme-
diate dentures, the ideal treatment method is to fabricate the maxillary and mandibular immediate
dentures simultaneously to avoid setting the maxillary teeth to the likely mal positions of the remain-
ing mandibular teeth.

• If the master casts are altered in an immediate denture procedure (e.g. elimination of gross
undercuts), it is advisable to construct a second denture base that is transparent (using a surgical
stent or template). The stent is placed over the ridge after the teeth are extracted. Pressure points
and undercuts are readily visible and surgical ridge correction can be performed .

• Duplicating a master cast to construct a surgical stent/template that is to be used at the time of
immediate denture insertion is best made after wax elimination and after the cast is trimmed.

Recommended 2-step schedule for tooth removal prior to delivery of immediate complete dentures:
1. Step 1: extract all posterior teeth EXCEPT a maxillary first premolar and its opposing tooth. This
leaves a posterior "stop" to maintain the VDO.
2. Step 2: after the posterior residual ridges exhibit acceptable clinical healing, the 2nd treatment
phase (denture fabrication) can begin. Anterior teeth are extracted at the time of
denture insertion.

To help the patient get through the first day of wearing immediate dentures, instruct them to not
remove the dentures, eat soft foods, and return in 24hrs for the first adjustment/evaluation.

311
 NOTES Pre-extraction guides for selecting artificial teeth for edentulous patients: teeth of close relatives,
diagnostic casts, radiographs, photographs, and extracted teeth.
1. Photographs: provide general information about the tooth width and outline form.
2. Diagnostic casts: teeth form can be very well determined from previous diagnostic casts of
natural teeth if available (check with the patient's previous dentist).
3. Intra-oral radiographs: tooth size and form can be determined, but beware because radiographs
can be distorted and usually are larger images of the teeth.
4. Teeth of close relatives: when no other means are available to get an idea of the form, size, and
shade of teeth to be used, records of the patient's children's teeth can help. It may also help in
determining the teeth arrangement.
5. Extracted teeth: sometimes patients keep their extracted teeth, which could be an excellent
source and aid to delineate tooth form , to help in the tooth selection process.

Methods for selecting denture teeth include saving extracted teeth: using pre-extraction records,
photographs, &following the lines placed on the occlusal rims.

Primary role of ANTERIOR TEETH on a denture is ESTHETICS. Spaces, lapping, rotation, and color
changes can be judiciously used to create a natural appearance.
• Setting anterior teeth either too far lingually or facially to satisfy esthetic concerns should NOT be
done. When selecting teeth, pre-extraction records are extremely valuable. Maxillary and mandibular
anterior teeth should NOT contact in centric relation .
• The error that most often contributes to poor esthetics of dentures is the practice of placing maxillary
anterior teeth directly over the edentulous ridge.
• Setting maxillary and mandibular anterior teeth so they contact in CR produces an unsatisfactory
arrangement of artificial teeth for complete dentures.
• The outline of anterior teeth should harmonize with the form of the face. Convex profile faces should
have a similar convex labial surface of anterior teeth . Broader contact areas of teeth look more natural
on dentures as they seem more compatible with advanced age.
• For best esthetics, maxillary anterior teeth in a complete denture are usually arranged FACIAL TO
THE RIDGE. Setting anterior teeth directly over the ridge usually causes poor esthetics of dentures.
Also, it is important to have accurate adaptation of the border seal and adequate bulk of the maxillary
facia l flange for good esthetics. VDO affects the lip support as well. Maxillary central incisors are
the MOST important teeth for esthetics. Their placement controls the midline, speaking line, lip
support, and smiling line composition.
• For most patients, the labial surface of the central incisor should be -8mm anterior to the center of
the incisive papilla . The labioincisal1/3 of the maxillary central incisors should support the lower lip
when the teeth are in occlusion .
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o
en
In general, FUNCTIONAL needs overshadow esthetic needs when selecting POSTERIOR TEETH. Do not
......
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set mandibular molars over the ascending area of the mandible because occlusal forces in the area
CJ
o will dislodge the mandibular denture.
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n
en
The size of POSTERIOR TEETH for a RPO is determined primarily by the amount of useful posterior
tooth space and characteristics of the denture-supporting tissues. Other factors releva nt to select-
ing posterior RPD teeth include:
1. occluso-gingivallength: the MOST important factor in determining poste~ior tooth length is the
available interarch space.
2. mesiodistal width: the total MD space available for the posterior teeth is determined by
measuring from the distal of the lower canine to the point where the mandibular residual ridge
begins to slope upward .
3. bucco-lingual width: the BL width is narrowed in relation to the missing natural tooth. It is
thought that reducing the area of the occlusal table decreases stress transferred to the denture
support area during food bolus penetration. Also, reducing the B-L width increases tongue space.
4. shade: the shade of posterior teeth is usually selected to harmonize with the anterior teeth .
5. occlusal surface form: it appears that no superior tooth form or arrangement is identified . Thus,
it is logical to use the least complicated approach that fulfills the patient's needs.
6. materials: plastic bonds well to the acrylic resin. Thus, plastic teeth are retained better than
porcelain teeth.

312
Common Errors Made When Arranging Denture Teeth:
• Setting mandibular anterior teeth too far forward to meet the maxillary teeth.
NOTES
• Failure to make canines the turning point of the arch.
• Setting mandibular first premolars buccal to the canines.
• Establishing the occlusal plane by an arbitrary line on the face.
• Not rotating anterior teeth enough to give an adequately narrower effect.

The primary reason for using PLASTIC teeth in a denture is because plastic teeth are retained well
in acrylic resin .

Lower 1/3 of a patient's face appears too short and there is apparent loss of the vermilion border of
the lips. The procedure indicated to correct this situation is increasing the occlusal vertical
dimension (VDO).

Immediate Complete Denture Advantages:

• Amajor advantage with immediate dentures is the ability to duplicate the position of the
natural teeth.
• Continuously acceptable esthetics. Immediate dentures are esthetically advantageous in that the
patient is never without either natural or artificial teeth.
• Improved speech adaptation. Immediate dentures require only one period of speech adaptation,
while conventional denture treatment requires two (one after extractions and another after the
dentures are delivered).
• Protects the extraction sites from trauma. Dentures act as a type of bandage over the clot filled
sockets.
• Continuously acceptable masticatory function. The patient retains some semblance of chewing
ability during the healing process.
• Prevents tongue enlargement. When natural teeth are lost and not replaced, the tongue expands into
the available space.

Immediate Complete Denture Disadvantages:

• MAJOR disadvantage of immediate denture therapy is not being able to have an anterior tooth try-
in to evaluate esthetics (anterior tooth try-in is impossible).
• Relining/rebasingthe denture is required in 8-12 months. Relining is simple, but must be carried
out within 8-12 months depending on the rate of alveolar ridge resorption. Also, increased post-
delivery soreness for a few days can be encountered.
• Increased post-insertion care (including relining or remaking the dentures). Contour changes occur
in the residual ridge during the 8-12 month healing period.
• Increased post-delivery soreness. The combination of post-extraction pain and denture-related
trauma often produces greater discomfort during the first few days after insertion.
• Greater complexity of clinical procedures (i.e. border molding and final impressions are more
difficult when natural teeth remain).
• Higher total cost of treatment due to the need for relines and repeated equilibration of the occlusion .

Immediate dentures should be scheduled for RELINES at 5 months and 10 months post-extraction.
Recontouring of the healing ridge progresses rapidly for 4-6 months and does not stabilize in form until
10-12 months post-extraction. Due to this, immediate dentures become progressively more ill-fitting.
They should be relined 5 months and 10 months after delivery to compensate for contour changes. This is
a general timeline, as each case must be evaluated monthly and if necessary, relines performed .
• Reline Indications: any denture when diagnostic information indicates a rel ine a will effectively
solve the patient's chief complaint (when the denture record base adaptation is the major defect in
the prosthesis.
• Reline Contraindications: when there is excessive overclosure of vertical dimension (a large
decrease in VDO). In this case, new dentures are indicated at the proper vertical dimension.

After relining dentures, if a patient constantly returns for adjustments due to sore spots on the ridge,
check the occlusion because the relining may have changed the CR contacts.

313
 N Errors in occlusion are checked most accurately by REMOUNTING the dentures on the articulator
using remount casts and new interocclusal records.
• When a previously edentulous aged patient who now wears a complete maxillary denture against
the 6 mandibular anterior teeth for many years, it is very common to have to do a reline every so
often due to the loss of bone structure in the ANTERIOR maxillary arch. This is evident by a flabby
maxillary anterior ridge (loss of osseous structure in the anterior maxillary arch).
• Aflabby, maxillary anterior ridge under a complete denture is frequently associated with retained
natural mandibular anteriors.
• A dentist relined a patient's maxillary complete denture. This patient returned repeatedly for
adjustments of the erythematous areas on the ridge crest. The most likely causes of these areas
are a loss of even centric relation contacts.

COMPLETE OVEROENTURE - a denture whose base is constructed to cover all of an existing resid-
ual ridge and selected roots. Retained roots help prevent resorption of the alveolar ridges, improve
denture retention, and allow the patient some proprioceptive sense of "naturalness" in function of the
dentures. Thus, the MOST important benefit of an overdenture (root-retained denture) is preserva-
tion of the alveolar ridge.

• It is not always necessary to cover a root beneath an overdenture. However, if a root is not covered,
the exposed surfaces are highly susceptible to decay. The patient's oral hygiene must be impeccable
to prevent root decay.

• Retained roots are the most common findings when taking routine panoramic radiographs or
patients who wear complete dentures (not necessarily overdentures).

The first step in the treatment of abused tissues in a patient with existing dentures is to patient ed-
ucation. The patient should understand the cause of the tissue deterioration and the eventual outcome
if the process is not arrested.
• If the constant wear of unacceptable dentures is causing the tissue abuse, the most efficient
preliminary treatment is to remove the dentures. However, business and social commitments may not
permit removal for extended periods. Thus, resilient tissue conditioning materials can be used to
assist in the tissue recovery program. Other procedures recommended as treatment aids for abused
tissues are massage and warm saline rinses.

Potential Problems with New Dentures:

1. Cheek Biting which is caused by:
• Posterior teeth set edge-to-edge. Treat by reducing facial surfaces of mandibular molars to
.." create proper horizontal overlap .
""
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en • Inadequate VDO. Treat by relining dentures at the corrected VDO, CR remount, and fabricate
.....
::c
c:::> a new denture.
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• Biting corners of the mouth. Treat by resetting the canines and premolars.
:::! 2. lip Biting-may be caused by reduced muscle tone and/or a large anterior horizontal
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overlap (overbite).
3. Tongue Biting-may be caused by having posterior teeth set too far lingually.
4. Generalized speech difficulty with complete dentures is usually caused by faulty tooth position
and/or faulty palatal contours.
• Speech problems due to faulty tooth position are avoided by placing the denture teeth as close
as possible to the position of the natural teeth. Note: the most effective time to test for
phonetics is at the time of the wax try-in of the trial denture (usually the 4th appointment) .
• Faulty palatal contours are corrected by trial and error. Add wax to increase contours and
reduce as needed to improve articulation of sounds.

Patient edentulous for many years often have more distorted speech than patients who have been
edentulous for a short time due to a loss of tonus of the tongue musculature.

Impaired healing, poor tissue tolerance, and rapid bone resorption might be anticipated in an uncon-
trolled diabetic patient.

314
Sounds:
• "S" sound: mandibular incisal edges should be even with or just behind the incisal edges of the
maxillary teeth. Most people form the "s" sound with the tip of their tongue approaching the anterior
palate and lingual surfaces of the maxillary teeth. These sounds bring the mandible and maxilla
close together. "S" sounds are the speech sounds that bring the mandible closest to the maxilla.
• If a patient complains that when he/she tries to make an "s" sound, it sounds like "th", the two
most probable causes of this problem is either the maxillary incisors are set too far palatally, or the
palate is made too thick.
• Words with the sibilant sound (hissing sounds) are pronounced correctly with the incisal edges of
maxillary and mandibular almost touching. These sounds are usually produced between rest and the
occluding position.
• "Th" sound: when forming this sound, the tongue should protrude slightly (2-4mm) between the
maxillary and mandibular anterior teeth.
• "F" & "V" sounds: formed by the incisal edges of the maxillary teeth and lower lip (incisal edges
should just touch the wet/dry line of the lower lip).
• "P" & "B" sounds: are formed totally by the lips.
• If the teeth are set too far lingually, the "t" will sound like a "d". If the teeth are set too far labially,
the "d " will sound more like a "t". Apatient who wears complete dentures is having difficulty trouble
pronouncing the letter "t" due to incorrect positioning of the maxillary incisors.
• Increased VDO is the usual cause of contacting/clicking of posterior teeth when a patient speaks.
• Ahigh palatal vault or a constricted palate can cause whistling sounds. Whistling during speech with
dentures (complete or RPD that replaces the incisors) can be caused by either insufficient vertical
overlap (overjet), excessive horizontal overlap (overbite), or the area palatal to the incisors is
improperly contoured.

A patient returns to your office a few days after delivery of new dentures and complains of generalized
irritation of the basal seat. The cause could be attributed to:
• Premature occlusal contacts (the MOST common cause of generalized irritation of the
basal seat).
• Lack of denture hygiene
• Nutritional and hormonal imbalance.
• Excessive VDO
• Acrylic spicules, inaccurate denture bases, and trapped food can all cause ulcers. To correct, either
reduce the spicules and/or reline if the denture base is inaccurate.

A patient who wears a complete maxillary denture complains of a burning sensation in the palatal
area of their mouth. This indicates too much pressure being exerted by the denture on the INCISIVE
FORAMEN.

A burn ing sensation in the mandibular anterior area is caused by pressure on the MENTAL FORAMEN.

A patient having difficulty swallowing may have insufficient interocclusal space (decreased freeway
space caused by excessive VDO) .

The best dietary advice for an elderly denture patient is to eat foods rich in proteins and vitamins A, C,
D, & B complex. Learning to chew food satisfactory with new dentures requires at least 6-8 weeks to
establish new memory patterns of the facial and masticatory muscles.

Res idual ridges can be ruined by using denture adhesives and home reliners. Thus, patients should be
warned about their uses. These agents can modify the position of the denture on the ridge and cause
changes in the VDO and CR.

At the first appointment after insertion of complete dentures, the presence of generalized soreness on
the crest of the mandibular ridge is MOST likely due to improper occlusion (premature occlusal con-
tacts). To identify prematurities, the best method in the mouth is to use warm disclosing wax by in-
serting the wax bilaterally and have the patient close into CR. The prematurities will show up as
windows in the wax. Once CR is complete, check eccentric movements.

315
 FACE BOW - a caliper-like device used to record the patient's maxilla/hinge axis relationship
(opening and closing axis) and to transfer this relationship to the articulator during the mounting of
the maxillary cast. If the transfer is done properly, the arc of closure on the articulator should duplicate
the patient's true arc of closure.
• Before an accurate face-bow transfer record can be made on a patient, the location of the hinge axis
point (axial center of opening-closing), must first be determined.

• The facebow transfer is NOT a maxillo-mandibular record. Rather, it is a record used to orient the
maxillary cast to the hinge axis on the articulator. The facebow transfers the maxilla/hinge axis
relationship to the articulator during mounting of the maxillary cast.

• Aface-bow transfer record DOES NOT: allow the dentist to locate the hinge axis, nor record CR more
reliably, nor position the maxillary cast properly in relation to the mandibular cast, nor transfer the
cast to the articulator maintaining the proper interocclusal relationships present in the mouth .

• This hinge-axis face bow transfer enables the dentist to alter VDO on the articulator. When altering
VDO (either via restorations or with dentures), casts should be mounted on the hinge axis. Hinge
Axis Face Bow-used to record opening and closing of the mandible.

• When the maxilla/hinge axis relation is transferred to the fully adjustable articulator, it may be
necessary to obtain the precise tracing of the paths followed by the condyle. Pantograph-an
instrument that carries out this task using two face bows (one attached to the maxilla , the other to
the mandible using a clutch that attaches the teeth in the respective arches).

• It is critical to mount a patient's casts on a true hinge axis when the dentist plans to change the
VDO through restorations.

• The preferred method to preserve the face-bow transfer is TAKING APLASTIC INDEX because it
avoids possible distortion of wax. When fabricating dentures, two methods can be used to preserve
the face-bow transfer.
t. Taking a plaster index of the occlusal surfaces of a maxillary denture before removing the
denture from the articulator and cast.
2. Placing a piece of tOx wax on the occlusal surfaces of the mandibular teeth and closing the
articulator in centric relation. Chill the wax, drop the incisal guide pin to touch the incisal guide
table (do not change) .

• The primary purpose of a plaster index of the occlusal surfaces of a maxillary denture before
removing the denture from the articulator and cast is to PRESERVE THE FACE-BOW TRANSFER.

• Several varieties of arbitrary face-bows are available, and are all based on an average location of
the hinge axis and yield an error of 2mm or less in most patients. Arbitrary rotational centers are
generally located over measured points on the face or by some type of earpiece. One average
measurement (from the ear tragus ear to the outer canthus of the eye) places the rotational point 13mm
anterior to the distal edge of the ear tragus along a line from the superior-inferior center of the tragus,
to the outer canthus of the eye. The condylar styli of the face-bow are then placed directly over the dots.

ARCON ARTICULATOR (ARTICULATED CONDYLE) - an articulator that has its condylar ele-
ments on the lower member of the articulator and condylar path elements on the upper member. The
angle between the condylar inclination and occlusal plane is FIXED on this articulator.

• Commonly used for diagnostic mounting of study casts to allow examination of occlusal contacts
in the retruded contact position and analysis of tooth contacts during excursive movements of the
mounted models.

• Occlusal records in right and left lateral excursions are necessary for setting both the medial and
superior condylar guides.

• Fabrication of cast and porcelain restorations to ensure correct tooth contacts in occlusion and
mandibular movements.

316
NON-ARCON ARTICULATOR (NON-ARTICULATED CONDYLE) - has the condylar elements on
the upper member of the articulator and condylar path elements on the lower member. The angle be-
tween the condylar inclination and occlusal plane is NOT fixed on this articulator. This design is more
popular to fabricate dentures. The following clinical records are required to mount the casts and set
the articulator elements.

• An occlusal record in the retruded contact position is necessary so that the lower cast can be
correctly related to the maxillary cast for mounting on the lower component of the articulator.

• Occlusal records in protrusion and right &left lateral excursions are required to set the sagittal
condylar guidance angles.

DIABETES - associated with delayed healing, rapidly progressing periodontal disease with marked
alveolar bone loss, increased calculus formation, and is a predilection for periapical abscesses.

• Mucosal bleeding (bleeding disorders) are NOT associated with diabetes.

• Even controlled diabetics present problems for the prosthodontist. The oral mucosa is prone to
developing sore spots that heal poorly and often become secondarily infected.

• When constructing dentures for patients with any debilitating disease: have maximal extension,
narrow occlusal table, non-pressure impression technique, do not use porcelain teeth, establish a
good occlusion, reinforce oral hygiene, and place the patient on a 6-month recall (sooner if needed
to reinforce oral hygiene).

REMOVABLE PARTIAL DENTURES (RPDs)

To determine if the alveolar bone can withstand occlusal forces of an RPD, an x-ray should be taken of
the abutment teeth and bone level surrounding these teeth. Periodontal health of the abutment teeth
and maintaining the health of the supporting tissues is best achieved by maintaining tissue support
(preserving denture bone support) of the edentulous areas.The total occlusal load applied to an RPD
is influenced by occlusal surface area, occlusal efficiency, & number of existing teeth.

When surveying casts, the clinician/technician must perform an important step to correctly record the den-
tures path of insertion, the position of the survey line, and location of undercut and non-undercut areas. To
do this, TRIPOD MARKS should be placed on the cast to record the cast's orientation to the surveyor. "'C
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• Tripod marks-3 spots placed at 3 different locations around abutment teeth from a single point of ""
view, ensure reproducible orientation of the cast to the surveyor.
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• Dental Surveyor-an instrument used to determine the relative parallelism of oral anatomy. Areas ""
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used for support CANNOT be determined by surveying. When surveying casts, the correct procedure n
is to first adjust the tilt to permit the establishment of guiding planes. The anterior edentulous space '"
will frequently dictate the angulation needed. Normally, some recontouring of the proximal walls of
abutment teeth is needed to improve guideplane alignment. These alterations are accomplished by
disking the proximal surface parallel to the path of insertion.
• Tilting the cast during surveying changes the path of insertion, position of survey line, and location
of the undercut and non-undercut areas of each tooth.

317
 N KENNEDY CLASSIFICATIONS - based on the MOST POSTERIOR EOENTUlOUS AREA to be re-
stored. Although Class III &IV RPDs are entirely supported by abutment teeth, Class I &II RPDs are
supported by abutment teeth, the residual ridge, subjacent tissues, and fibrous C.T. overlying the alve-
olar process. The alveolar ridge resorption under the distal extension RPD is of concern and is reduced
by maximizing coverage of these supporting areas.
• Important: periodontal damage to abutment teeth is avoided with firm tissue support (maintaining
a stable base-tissue relationship).

KENNEDY CLASS I (BILATERAL DISTAL EXTENSION) - patient is missing posterior teeth on

both sides of the arch. Supported by abutment teeth, the residual ridge, subjacent tissues, and fibrous
C.T. overlying the alveolar process

KENNEDY CLASS II (UNILATERAL DISTAL EXTENSION) - patient is missing posterior teeth on

one side of the arch. Supported by abutment teeth and the residual ridge, subjacent tissues, and fi-
brous C.T. overlying the alveolar process

KENNEDY CLASS III - unilateral edentulous spaces bound by teeth (i.e. patient is missing both
premolars on one side of the arch and a 2nd premolar and lsI molar on the other side of the arch). It is
a unilateral edentulous area with natural teeth natural teeth remaining both anterior and posterior to
it. This is a tooth-borne RPD type because it depends entirely on abutment teeth for support.

KENNEDY CLASS IV - anterior teeth are missing and across the midline (i.e. patient is missing
teeth from the right canine to the left canine). It is a single, but bilateral (crossing the midline), eden-
tulous area located anterior to the remaining natural teeth. This is a tooth-borne RPD type because it
depends entirely on abutment teeth for support .

Any other additional edentulous area is referred to as a modification (except Class IV). For example, if
a Kennedy Class I (bilateral distal extension) has another edentulous area in the anterior region, it is
then called a Class I, modification I.

Applegate's Rules for Applying the Kennedy Classification:

1. Rule 1: classification is done after not before extractions are done.
2. Rule 2: if a 3rd molar is missing and will not be replaced, it's not considered in the classification.
3. Rule 3: if a 3'd molar is present and not to be used as an abutment, it's not considered in
the classification.
4. Rule 4: if a 2nd molar is missing and will not be replaced, it's not considered in the classification .
5. Rule 5: the most posterior area always determines the classification.
.." 6. Rule 6: edentulous areas other then those determining the classification are called modifications
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::c 7. Rule 7: the extent of the modification is not considered, only the number of additional
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edentulous areas.
:::! 8. Rule 8: there are no modification areas in a Kennedy Class IV.
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Craddock Classification-based on the denture type.

• Type I mucosa borne
• Type II tooth borne
• Type III mucosa and tooth borne

Major and Minor connectors MUST BE RIGID for functional stresses applied to the RPD to be evenly
distributed throughout the mouth.

MAJOR CONNECTOR - the unit of an RPD that connects the parts of the prosthesis located on one
side of the arch to parts on the opposite side of the arch. The major connector must be RIGID so
stresses applied to any single portion of the denture may be effectively distributed over the entire sup-
porting area. Major connectors should be designed and located with the following guidelines:
• They should be free of movable tissues and should not impinge on gingival tissues.
• Relief should be provided.
• Bony and soft tissue prominences should be avoided during placement and removal.

Major connectors most frequently encounter interferences from lingually inclined mandibular premolars.
318
Mandibular Major Connectors: NOTES
1. Lingual Bar-more popular than a labial bar. A lingual bar is placed so its upper border is at least
4mm below the gingival margins. When severely tipped premolars and molars are present, an
alternate framework design or crowns are recommended.
• Lingually inclined mandibular premolars interfere most frequently with mandibular
major connectors.
2. Lingual Plate-a lingual bar that has been extended upward to cover the cingula and interproximal
spaces between mandibular anterior teeth. It should be thin and follow the contours of the teeth
and embrasures. The upper border should be located at the middle 1/3 of the lingual surface of
the teeth and extend upward to cover interproximal spaces to the contact point.

Linguoplate Indications:
• To avoid a high lingual frenum or when there is no space in the floor of the mouth .
• A lingual plate is preferred over a lingual bar connector when there is no space in the floor of
the mouth.
• Use if you have a vestibule that is < 5mm.
• Mandibular tori that cannot be removed.
• To support/stabilize periodontically weakened teeth.
• To serve as retention for lower anterior denture teeth when the prognosis for the natural teeth is
guarded. When anticipating possible replacement of mandibular anterior teeth class I situations
where ridges have undergone excessive vertical resorption.
• Severe anterior crowding is a contraindication for using a linguoplate.

3. Labial Bar-are seldom requ ired . Should be 3mm below gingival margins. Indications:
• Trauma and congenital deficiencies occasionally produce dental arrangements where only a
labial connector is feasible.
• Use with lingually inclined mandibular anterior teeth or with large lingual tori.

Maxillary (Palatal) Major Connectors: major connectors of a maxillary RPO may be beaded to produce
a positive contact with the tissue.
1. Single Palatal Bar-are objectionable because they lack rigidity. Their use is limited to tooth-
borne restorations for bilateral short span edentulous areas. The wide, thin bar (strap) is more
rigid with less bulk compared to a narrow bar. The palatal bar is usually transpalatal , connected
to the first molars, and used to maintain width and increase anchorage.
2. Palatal horseshoe-shaped plate-only used when a large, inoperable torus prevents using
other designs.
3. Anterior-posterior palatal bar-the MOST RIGID palatal major connector that can be used in
almost any maxillary partial denture. To attain symmetry, both anterior and posterior connectors
should cross the midline at right angles rather than on a diagonal. If the palatal bar is too thick,
the patient may have difficulty in pressing food backward for swallowing.
4. Palatal Plate Connector-a thin, broad connector that can be used for simple edentulous areas
and full palatal coverage. This connector covers more tissue which produces added retention
from atmospheric pressure and interfacial surface tension .

DISTAL EXTENSION RPD - can be unilateral or bilateral, but always receives its support from the
residual ridge, tissue-bearing areas, selected abutment teeth, and the fibrous C.T. overlying the
alveolar process.

• The most important factor in determining the success of distal extension RPOs (bilateral and
unilateral) is proper coverage over the residual ridge. Coverage of the free-end should extend over
the retromolar pad to create stability of the RPD and to minimize torquing forces on the abutment teeth .

• Unilateral Distal Extension RPO-a removable partial denture in which part of the functional load is
carried by the residual ridge at one end of the denture base segment, while the other end of the base
segment is supported by natural teeth.

319
 • First step in relining a distal extension RPD is to verify the fit of the framework. Th is is done fi rst
even if you are also relining a maxillary complete denture that is opposing this distal extension.
When relining, apply finger pressure to the rests &indirect retainer to establish proper placement
at the impression stage. If the indirect retainers are not seated as the extension bases are
depressed, the bases need relining.

• If a patient complains of sensitivity to percussion on an abutment tooth of a distal extension RPD,

the most likely cause is the OCCLUSION on this abutment. Deflective occlusal contacts can also
cause a feeling of "looseness" to the denture.

• For an extension-base RPD, the most important to maintain the remaining supporting tissues is
preserving denture base support.

ALTERED CAST TECHNIQUE - the purpose is to record the form of the edentulous segment
without tissue displacement and to accurately relate the edentulous segment of the teeth via the
metal framework. The goal is to provide maximum support for the RPD denture base, thus maintain-
ing occlusal contact to distribute occlusal load over both natural and artificial dentitions, while mini-
mizing movement of the base that would create leverage on the abutment teeth.

• Altered cast technique helps obtain soft tissue support to aid abutments in resisting functional
stresses. It is a secondary impression system that uses the metal framework to hold customized
impression trays for the edentulous areas.

• Impression materials cannot record anatomic form of the teeth and physiologic form of the soft
tissue in a functional relationship simultaneously. To achieve these objectives, the altered cast
technique can be used. After the trays are fabricated and trimmed, the peripheries of the plastic
trays are border molded to the physiological form of vestibular mucosa. Impressions are then made
with a free-flowing material, and edentulous segments of the master cast are re-poured.

Altered Cast Advantages:

• the tray doesn't contact the tissues.
• the tray is maintained perfectly in one position during impression making.
• muscle molding ensures proper border extension of the denture base.
• impression records the edentulous ridge tissues in the exact form that they will assume
when the finished RPD is in place on the teeth.
• The only pressure on the tissues during impression making is resistance to movement or flow
of the impression material.
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VI STRESS-BREAKER - a device that relieves the abutment teeth to which an FPD or RPD is at-
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tached, of all or part of the forces generated by occlusal function. When a stress-breaker is incor-
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the residual ridge and only minimal transfer of functional stress to the abutment teeth occurs.
Since vertical and horizontal forces are concentrated on the residual ridge, increased ridge resorption
frequently occurs. Relining the free-end saddle area must be done when needed to prevent excessive
ridge resorption. When a stress-breaker is placed on a pontic's distal surface, occlusal forces tend to
unseat the key from the key.

Types of Stress-breakers:
1. Wrought-Wire Retentive Clasp (gold or cobalt-chromium)-the simplest form of stress relief.
This has a flexible connection between the direct retainer and denture base.
• Wrought-wire clasp Advantages: higher yield strength, greater flexibility, more ductile
and resilient.
• Awrought wire clasp has a tensile strength at least 25% greater than the cast alloy from
which it was made. Wrought-wire clasps have greater flexibility and adjustability than the
cast clasps.
• Wrought-wire clasps are tougher than cast clasps, and have greater tensile strength than
cast clasps, thus can be used in smaller diameters to provide greater flexibility without fatigue
and ultimate fracture.

320
 • Important: having been formed by being drawn into a wire, the wrought-wire clasp has greater NOTES
toughness & ductility than a cast clasp arm. The clinical effect of this is increased capacity
for deformation of the wrought-wire without breaking (greater flexibility).
• However, the yield strength of both gold and chromium-cobalt alloy wrought wires can be
drastically reduced by simply subjecting the wire to too much heat. If the heat is high enough,
the fibrous microstructure of the wrought wire disappears and is replaced by a grain or
crystalline microstructure. This heating process is called "recrystallization" or "gain growth"
and is a most undesirable occurrence in wrought-wire retainer arms.
• The terminal end of the retentive arm is optimally placed in the middle of the gingival 1/3
of the clinical crown. However, it is acceptable to place it at the junction of the gingival and
middle 1/3 of the clinical crown. When the partial is completely seated, the retentive arm
should be passive and applying no pressure on the teeth.
• Wrought wire is incorporated into the RPD by soldering it to the minor connector, meshwork,
incorporating it into the wax pattern, or is embedded into the acrylic resin (makes it the
most flexible).
• 20-gauge wrought-wire in 2x more flexible than an 18-gauge wire
• 20-gauge cast clasp into an .010 undercut is an alternative to wrought wire

2. Split-bar major connector (Ticonium "Hidden-Lock")-has a flexible connection between the

direct retainer & denture base.
3. Stress-breakers with a movable joint between the direct retainer and denture base:
• DE hinge, Dalbo attachment, Crismani attachment, and ASC-52 attachment.

CAST METAL- any metal melted and cast into a mold (i.e. inlay crown or clasp). When the casting is
cold-worked to provide the required article or appliance (i.e. wire), it is called a "wrought metal" in con-
trast to a cast metal. Many mechanical properties of the wrought structure are superior to the cast
structure (i.e. tensile strength, hardness, and strength). Thus, a wrought structure with a smaller cross-
section than a cast structure may be used as a retainer arm (retentive) to perform the same function.

• ELONGATION-most important mechanical property involved when a base metal RPD

clasp is adjusted.

• A cast wire (compared to a wrought wire of similar composition) has less yield strength, less
flexibility, less ductility and resilience. Wrought wire generally has superior mechanical properties
because the cast wire contains unavoidable porosities, which has a weakening effect. When the
cast ingot is drawn into a wire, the small pores and blebs may be collapsed, and welding may occur
so that such defects disappear.

INDIRECT RETAINER (RESTS, MINOR CONNECTORS, PROXIMAL PLATES) - functions to

prevenUcounteract vertical dislodgement of the distal extension base of an RPD away from the tis-
sues (dislodging forces) caused by sticky foods and tissue rebound. It is an anti-rotational device
fabricated by a rest/connector combination and placed as far forward from the embrasure clasp as
possible. It counteracts the upward rotation of the edentulous base and serves as a 3rd reference
for seating the framework and making altered cast impressions. The indirect retainer may be omit-
ted in some designs (i.e. tooth-borne RPDs).

• Indirect retainers also serve another function . In their absence, upward dislodgement of the distal
expansion bases would be accompanied by downward motion of the anterior part of the major
connector. By preventing this downward movement, it PROTECTS SOFT TISSUES from impingement
by the major connector.
• An indirect retainer should be placed as far from the distal extension base as possible in a prepared
rest seat on a tooth capable of supporting its function.
• An indirect retainer pertains to RESTS that augment mechanical retention. Rests should be placed
on abutment teeth next to the edentulous areas for maximum support when designing a tooth-borne
partial (Class III or IV). These rests limit the denture's movement in a gingival direction.
• Minor Connector-the connecting link (or tang) between the major connector or base of the RPD and
other units of the prosthesis (clasps, indirect retainers, and occlusal rests). Minor connectors
have 2 functions:
1. transfer functional stress to the abutment teeth.
2. transfer the effect of the retainers, rests, and stabilizing components to the rest of the denture.
321
 N Indirect Retainer Design:
• The greater distance between the fulcrum line and IR, the more effective the IR.
• IR should be at right angles to the fulcrum line.
• IR should be placed in rest seats to direct forces through the long axis of the tooth.
• An indirect retainer located FARTHEST from the clasp tips located closest to the edentulous area
provides the best leverage against lifting/dislodging of the denture base. As unseating occurs in
the edentulous segments, a ling through the rests located furthest from the retentive clasp tips acts
as the fulcrum in a Class III lever system. Moving the fulcrum line still further from the clasp tip
improves the mechanical advantages of the lever arm system. By maintaining this position , the most
distant rests augment the retentive action of the clasp, and indirectly contribute to retention . Thus,
the term "indirect retainer" refers to rests, which augment mechanical retention.
• As the denture base moves upward, the most anterior rest (which is the direct retainer), resists
downward movement. This increases the direct retainer's effectiveness. Direct retainers must be
effective for an indirect retainer to function.

RESTS - the primary purpose of any rest (occlusal, cingulum, or incisal) is to provide VERTICAL
SUPPORT for the RPD.
1. Occlusal Rest: the primary design-quality of the occlusal rest that categorizes it as a "positive"
rest is the fact that it forms acute angles with the minor connectors that connect them to the
major connectors. This defines the positive rest and permits maximum bracing.
• Occlusal rests must be rounded (spoon-shaped) to permit functional movement.
• Occlusal rests are prepared primarily to RESIST vertical forces of occlusion.
• Rest preparations are started with a BALL-SHAPED DIAMOND or carbide of appropriate size.
Reduce and round the marginal ridge area of the occlusal rest (this reduces the chance of
fracture of the metal rest). Lower the marginal ridge so there will be sufficient strength in the
origin of the rest seat without interfering with the opposing occlusion. Athickness of 1.5mm
is needed for adequate bulk and strength. The rest width occupies the middle 1/3 of the
occlusal surface. The rest floor should slope down toward the center of the tooth and be
spoon-shaped. The rest's outline form resembles a saucered spoon with the apex
toward the tooth's center.
• The rest should allow not tilting of the appliance, should prevent movement of the RPD, and
should transmit stress down the tooth's long axis.

2. Cingulum Rest-a vertical stop on an ANTERIOR TOOTH whose lingual anatomy lends itself to
ready preparation for a positive seat. Not all teeth have sufficient cingulum contour to receive
a seat. Cingulum rests are usually confined to preparation on MAXILLARY CANINES since these
teeth have a gradual lingual incline and prominent cingulum. Sometimes, cingulum rests can be
placed on maxillary central incisors. The lingual slope of the mandibular canine is usually too
steep for an adequate cingulum rest to be placed in enamel.
• A cingulum rest is more esthetic than an incisal rest.
• The resulting stress relayed to the abutment with a cingulum rest has less torquing influence
than an abutment with an incisal rest.

3. Incisal Rest-used when other preffered support is not available. The high placement of this rest
is not very esthetic. The distal incisal rest is usually less esthetically visible than a mesial
incisal rest. Never place an incisal rest so deep that it interferes with the proximal contact.

Direct Retainers:
1. Intracoronal attachment-the MOST esthetic direct retainer for a RPD.
2. Clasps (Extracoronal Retainers)-the most common direct retainer used for RPDs. They provide
retention based on the resistance of metal to deformation. There are two types of extracoronal
retainers (Suprabulge &Infrabulge retainers).
1. Suprabulge Retainers (Clasps)-originate from ABOVE the survey line (usually from an occlusal
rest), and angle downward across the clinical crown until the tip is located in a prescribed
amount of undercut. It approaches an undercut from above the crown's height of contour.
Types of supra bulge retainers:

322
 • circumferential clasp: composed of a buccal &lingual arm originating from a common body.
Usually one arm is retentive, while the other arm functions in bracing. This clasp is used to
engage undercuts located on the side (mesial-distal) of the tooth opposite to the site of the rest.
• ring clasp: encircles nearly all of a tooth to engage an undercut located on the same side of
the tooth as the rest. It is not used where the caries rate is high or where esthetic
considerations are important.
• embrasure clasp: used when no edentulous space exists at the clasp assembly site.
• reverse-action clasp (hairpin clasp): may be used to engage an undercut located on the
same side of the abutment as the rest, or on any posterior tooth, but it covers a lot of tooth
surface and may compromise esthetics.
• extended arm clasp: a circumferential clasp that extends to neighboring teeth to provide
increased splinting and to engage a more favorably located undercut.
• ~ and ~ clasp: consists of one circumferential clasp emanating from the rest area and
another arm from the minor connector on the opposite side.

2. Infrabulge Retainers (Roach, I, J, U, L, T Bar Clasps)-approaches a crown undercut from

BELOW the tooth's height of contour. They are clasps that originate from below the survey line.
They are metal projections emanating from the denture base struts in the framework, and
course through the denture base and project parallel to the mean plane of the gingiva until they
make a gentle right angle turn. They then cross the gingiva and come to rest upon the abutment
tooth in a specific undercut area below the survey line. Infra-bulge retainers MUST NOT be
placed into tissue undercuts nor should contact the abutment of any place except at the
specified undercut.

Advantages of infrabulge retainers compared to suprabulge retainers:

• More efficient retention.
• Less distortion of coronal contours and less tooth contact.
• Cleaner and less prone to caries
• Esthetically superior in most cases.
• Greater adjustability.

Disadvantages:
• Are more bothersome/irritating to vestibular tissues.
• Too flexible for effective bracing.
• Can be esthetically objectionable in patients with a high lip line.
• Where there are not enough guideplanes to positively establish the path of insertion, opposing cross-
arch undercuts can be used. In these cases, the effectiveness of infrabulge clasps is diminished
because the unseating motion (without guideplanes) is rotary, vertical, and horizontal.

• Most common infra-bulge retainers: I, J, U, L, Tbar clasps. These bar clasp arms & circumferential
clasp arms (suprabulge retainer), provide retention by the resistance of metal to DEFORMATION,
rather than frictional resistance created by the contact of the clasp arm to the tooth.

3. Intracoronal Retainers-another direct retainer sometimes used for RPDs. These are attachments
built into the contour of a crown (casting) to produce mechanical and frictional retention. By
eliminating the need for a visible retentive clasp, these retainers give optimal esthetics and
provide vertical support through the rest seat located more favorably in relation to the horizontal
axis of the abutment teeth.
• Intracoronal retainers are not used when an RPD depend on an edentulous area for support
(distal extension). Intracoronal retainers may provide a rigid connection between the denture
and abutment (fine for tooth-borne RPDs). However, in distal extensions, functional motion
must be permitted without torquing the abutment teeth.

Awire-gauge is selected based on its active length. Ashort arm clasp « 7mm) should be made in a
20-gauge wire or finer for optimum function below its proportional limit, since < 7mm is a short
arm clasp and shorter length clasps must have a finer gauge of wire for optimum flexibility.

323
 Flexibility of a retentive clasp arm depends on:
1. clasp length: a clasp's flexibility varies directly with the cube of its length. Thus, increased
length results in a marked increase in flexibility.
2. clasp thickness: as a clasp becomes thicker, its flexibility decreases by a cube ratio.
3. clasp width: as a clasp's width increases, its flexibility decreases by a ratio of 1:L
4. clasp cross-sectional form: a round form is equally flexible in all directions. In contrast, a Yz
round form flexes readily only when the stress is applied perpendicular to the flat surface.
5. clasp taper: a uniform taper allows increasing flexibility toward the clasp tip.
6. clasp material: different materials flex more than other materials. *wrought wire retentive arms
have increased flexibility.

• Failure of partial dentures due to poor clasp design is best avoided by altering tooth contours.

• When a RPD is completely seated, the retentive terminals of the retentive clasp arms should be
passive and applying no pressure on the teeth.

RECIPROCATION - refers to the function of the lingual clasp arm (reciprocal clasp arm) to
counteract forces exerted by the buccal clasp arm (retentive clasp arm).

Reciprocation is the means by which one part of the metal framework OPPOSES the action of the re-
tainer in function. Reciprocation is achieved by opposing flexible retainers with guide planes,
minor connectors, rigid clasp arms, or plating. If true reciprocation is to occur, the reciprocating ele-
ment MUST BE PLACED OPPOSITE the direct retainer, and must contact the abutment as the reten-
tive tip passes over the tooth's height of contour.

CLASP ASSEMBLY - consists of a retentive clasp arm, reciprocal (stabilizing clasp arm), plus
any minor connectors and rests from which they originate or with which they are associated.
• Reciprocal Clasp-Arm functions on an RPO: reciprocation, stabilization, and auxiliary indirect
retention (bracing) .

• With reciprocal clasp arms, when positioning cast clasps on abutment teeth, the horizontal undercut
is considered a significant measurement and height of contour is considered a controlling factor in
clasp positioning. Reciprocal clasp should contact the tooth on or above the height of contour.

• Altering the natural tooth form to allow effective clasping may involve producing guiding planes or
changing the location of the height of contour. Facial and proximal contours of premolars and
molars most often need to be altered. Crown fabrication may be necessary to provide the appropriate
contour.

• Guiding planes serve to ensure predictable clasp retention. Failure of partials due to poor clasp
retention design can be avoided by altering tooth contours. Guiding planes serve to assure
predictable clasp retention.

• In general, you should NOT use retentive areas on the buccal & lingual of the same tooth. Reciprocal
bracing on the lingual, and retentive portion of the clasp on the buccal is more desirable.

• All clasps should be designed to permit insertion and removal without applying excessive force.

Fundamental Principles of a Clasp Assembly:

1. Clasp should be completely passive and its retentive function is activated only when dislodging
forces are applied to the RPD.
2. Each retentive clasp must be opposed by a reciprocal (bracing) clasp arm or another RPD
element capable of resisting horizontal forces exerted on the tooth by the retentive arm.
3. Each clasp must be designed to encircle more than 180 0 (more then Yz the circumference) of the
abutment tooth.
4. The rest should only provide vertical support.

324
PRECISION ATTACHMENT RESTORATION - an attachment pre-constucted with metal male &
female portions that fit together in a precise fashion with little tolerance. It may be rigid in function ,
or may incorporate a movable stress control unit to reduce the torque on the abutment.
• Semi-Precision Attachment-a cast into the crown and RPD. The female portion is usually made of
preformed plastic positioned into the wax form and then cast. The male portion is cast with the RPD
framework. The female and male parts fit together with much more tolerance than with a precision
attachment, resulting in less retention .

Advantages:
• The provide retention without an unsightly display of metal.
• The functional load is dispersed down the long axis of the abutments by virtue of the low central
loading at the base of the attachments.
• The restorations permit the patient access to all areas of the tissues when the denture is not in place.
• If both sides of the dental arch have this type of restoration, and are joined by a rigid major connector,
excellent bilateral stabilization is provided by the abutments.

Disadvantages:
• Precision attachment restorations are difficult to repair.
• They must never be used in a distal extension RPD without using a stress-breaker (the primary
indication for precision attachments is when teeth are present on both ends of the edentulous area).
• Full cast crowns must be prepared on all abutments.
• They cannot be used with short clinical crowns or when the pulp is large (requires extensive
tooth reduction).
• Both clinical and laboratory procedures require special skill.
• The metal parts wear and lose retention.
• The cost is much greater.

BASE METAL ALLOYS - have a lower density than Type IV (extra hard) gold alloys. This low density of
base metal alloys makes the casting process difficult. Compared to gold alloys, base metal alloys have:
• Higher resistance to deflection in thin segments.
• Higher modulus of elasticity.
• Much higher melting point temperature (2300°F to 2600°F).
• Lower yield strength, lower specific gravity, and lower density.

ADVANTAGES OF USING RPD CAST CHROMIUM-COBALT ALLOYS - is corrosion resistance,

high strength, low specific gravity. However, chromium-cobalt alloys are very inflexible (they have
virtually no ductility or malleability after they are cast).
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Popularity of the chromium-cobalt alloys for fabricating RPD cast frameworks is due to their low den- ~
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sity (weight), high modulus of elasticity (stiffness), low material cost, and corrosion resistance. CI
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• The form of chromium-cobalt alloy connectors is flat, broad, and reinforced along the borders by the :z:
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BEAD on the tissue surface. The beading process maintains tissue contact and provides additional C")
en
strength (for maxillary major connectors).
• Causes of chromium-cobalt RPD framework fracture: work hardening, shrinkage porosity, low
percent elongation, & excessive carbon in the alloy.

Composition of Chromium Base Metal Alloys for RPDs:

1. Chromium-constituent responsible for CORROSION RESISTANCE in cobalt-chromium alloys by
producing a passivating film for corrosion resistance. Ensures the alloy will resist tarnish and
corrosion by forming a complex chromium oxide film . An RPD made of a base metal alloy is
resistant to tarnish and corrosion because of its surface oxide layer.
2. Cobalt-increases the alloy's rigidity, contributes to the framework's strength, rigidness,
and hardness.

325
 3. Nickel-increases ductility. Nickel in the composition of base metal alloys is responsible for the
alloy's ductility. It is also measured as a percentage of elongation and determines how much
margins can be closed via burnishing.
• Nickel is the metallic component of a RPD with the greatest potential for allergic reactions
in the mouth.
4. Minor constituents-carbon has a pronounced effect on the strength, hardness, and ductility.
Tin, indium, and other readily oxidized minor components of the alloy function to
improve bonding.

ADA classifies alloys as follows:

• Type I: used for small inlays.
• Type II: larger inlays & onlays.
• Type III: onlays, crowns, and short-span FPDs.
• Type IV: thin veneer crowns, long-span FPDs &RPDs.

BRITTLE - a material with high compressive strength, but low tensile strength .

SPECIFIC GRAVITY - is a property of gold alloys that exceeds a base-metal alloy in numerical value.
Adentist determined it would be necessary to adjust a patient's denture teeth to correct the centric oc-
clusion at the wax try-in appointment. This dentist should make a new CR record and remount.

• Elongated grains in the microstructure of a wrought wire indicates that it has been cold worked.

• SUPPORT is the design characteristic of an RPD that is most important to oral health.

• A patient complains of "looseness" with a new bilateral distal extension RPD probably due to
deflective occlusal contacts.

• Important considerations when preparing an RPD abutment to receive a crown are the path
of draw, location of the rests, orientation of guiding planes, and placement of the porcelain
metal finish lines.

The recommended treatment for a patient who has lost 4 maxillary incisors some time ago and has
suffered excessive ridge resorption is a removable partial denture (RPD). If excessive ridge resorp-
tion has occurred after tooth loss in the anterior region, the pontics required to replace these teeth may
be very unesthetic. An RPD with its tissue colored acrylic base can provide this esthetic consideration.
Other situations where an RPD is specifically indicated rather than a fixed bridge:
."
:= 1. Distal Extension: if several teeth must be replaced and no posterior abutment is present, then a
CI
~ RPD must be used (another option is implants). It is possible, however, to cantilever one tooth in
::c
CI a fixed bridge if at least two very sound teeth exist anterior to the space.
""
CI
:z: 2. Long span edentulous area: sufficient abutment teeth are not present to support the occlusal
...
:::!
V>
forces, which would be placed on the fixed bridge .
3. Periodontally involved abutment teeth: the bracing and cross-arch stabilization of a RPD in
this case, makes it the ideal treatment.
4. After recent extractions: a temporary RPD may be provided until tissues have had time to heal
property and fixed bridgework can be done.
5. Economics: may force the use a RPD as an interim solution to a problem that must eventually
be solved with fixed prosthodontics.

PAGET'S DISEASE (OSTEITIS DEFORMANS) - a chronic bone disorder where the bones becomes
enlarged and deformed. The exact cause is unknown, but it is often discovered in the dental office
because the patient's dentures do not fit due to widening of the alveolar ridges.
• Characterized by excessive breakdown of bone tissue, followed by abnormal bone formation. The new
bone is structurally enlarged, but weakened with heavy calcifications.
• Involvement of the skull may enlarge head size and cause hearing loss and blindness if the cranial
nerves are damaged by the bone growth .
• Dental Considerations: Relieving the tissue surface of the dentures and relining with resilient
materials can extend the life of the dentures. However, remaking the dentures frequently is
unavoidable.
326
Notes:
• Children who wear dentures and acromegaly patients with dentures often need their dentures relined
or remade to allow for bone growth.
• Diseases of bone growth or expansion are much rarer than diseases of bone loss.
• Osteoporosis is the most common change associated with systemic disease. Osteoporosis is a
generalized defect in which the quantity and quality of bone in the skeleton is reduced.

FIXED PARTIAL DENTURES (FPD)

CROWN & BRIDGE
When treatment planning for fixed prosthodontics, studying diagnostic casts can provide you with
this information:
1. Length of the abutment teeth can be accurately gauged .
2. True inclination of the abutment teeth.
3. Mesial or distal drifting, rotation , and F-L displacement of potential abutment teeth are
clearly seen.
4. Allows an unobstructed view of the edentulous areas and an accurate assessment of the
span length and its occluso-gingival dimension .
5. Arch curvature in the edentulous region can be determined in order to predict if the pontic(s)
will act as a lever arm on the abutment teeth.
6. Athorough evaluation of wear facets, their number, size, and location is possible when viewed
on casts. Excessive wear on occluding surfaces of teeth is usually caused by disharmony
between CO (MICP) and CR.

Presence of periodontal pockets and crown-to-root ratio of potential abutment teeth CANNOT
be determined by studying diagnostic casts. You must do a clinical exam and take x-rays to
obtain this information .

Porcelain Veneer Indications:

1. Covering labial surface defects like enamel hypoplasia.
2. Masking discolored teeth like tetracycline staining, discoloration after loss of tooth vitality.
3. repair structural damage like fractured incisal edges.
4. improve tooth contour (i.e. peg-shaped lateral incisors).
5. reducing spaces in cases when orthodontics are inappropriate.

-c
PORCElAIN VENEER CONTRAINDICATIONS - severe imbrication of teeth, traumatic occlusal :::c
c:::>
contacts, unfavorable morphology, insufficient tooth structure and enamel. A patient with a high ~
::c
c:::>
caries index, short clinical crown, and minimal horizontal overlap are not candidates for partial veneer C1
c:::>
crowns. Rather, the restoration of choice is a full PFM crown . :z:
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:::!
en

Technique for Inserting Porcelain Veneers:

1. the veneer should be tried in wet with a drop of water or glycerine to check for fit. A reliable
estimate for the possible post-cementation appearance with try-in pastes can also be done.
2. the veneer fit surface is cleaned to remove saliva contamination or try-in composite.
3. if the fit surface has not previously been treated with silane and protected with light-cured
unfilled resin , this should be done at this stage.
4. clean the enamel surface with pumice and water.
5. while protecting adjacent teeth with matrix strips, the enamel is acid-etched.
6. etched surfaces are washed and dried, and a layer of unfilled bond resin is applied and
thinned with oil-free air.
7. an appropriate shade of light-cured composite is applied to the fit surface of the veneer
which is "puddled" into place on the tooth surface.
8. gross excess of composite is removed and light-curing is completed.
9. remaining excess composite is removed with finishing diamond burs, discs, strips, and the
margins finely polished.
10. patient should return for a follow-up appointment in 1 week.

327
 Advantages of Partial Veneer Restorations (3/4 &7/8 crowns):
*
• The primary reason for choosing a crown over a full cast crown is TOOTH STRUCTURE IS SPARED.
• Agreat deal of the margin is in an area accessible to the dentist for finishing and to the patient for
cleaning.
• Less of the restoration margin is in close proximity to the gingival crevice, thus decreasing the
chance of periodontal irritation.
• Can be more easily seated completely during cementation. With at least part of the margin visible,
complete seating of a partial veneer crown is more easily verified by direct vision.
• If it is ever necessary to do an electric pulp test (EPT) on the tooth, a portion of the enamel is un-
veneered &accessible.

The path of insertion of an anterior % crown should parallel the incisal 112-2/3 of the labial surface,
not the tooth's long axis. If the path of insertion is made parallel to the tooth's long axis, the labio-
incisal corner will be sacrificed and an unnecessary display of gold will result. Two factors must be
*
done to successfully produce an anterior crown with a minimal display of gold:
1. Path of insertion and groove placement.
2. Placement and instrumentation of extensions. Proximal extensions must be done with thin
diamonds and hand instruments from a lingual approach to minimize gold display. They should
be extended facially to a cleansable area without destroying the tooth's facial contour.

Anterior %crown is NOT USED as often today as it once was. Unsightly and unnecessary displays of
gold in poor examples of this restoration have made it less popular with the public and dentists.
However, the standard % crown on a maxillary anterior tooth does not need to show large quantities of
gold if prepared correctly.

A pin-modified %crown can preserve the facial surface and one proximal surface. This is preferred in
cases which require repairing of severe lingual abrasion on incisors and canines, avoiding other more
destructive options like full-veneer metal-ceramic restorations.

*
A reverse crown is most frequently fabricated for a MANDIBULAR MOLAR. This reverse design pre-
serves the lingual surface, and is indicated for restoring mandibular molars with damaged buccal sur-
faces and intact lingual surfaces. It is also indicated on teeth with severe lingual inclinations where
large quantities of tooth structure would be destroyed if a full veneer crown were to be used.

*
The standard crown is a partial veneer crown where the buccal surface is left covered. It is the
most commonly used type of partial veneer crown.

7/8 crown-is a %crown whose vertical distobuccal (DB) margin is positioned slightly MESIAL to the
middle of the buccal surface. A7/8 crown can be used on any posterior tooth. Advantages of a 7/8 crown:
• Esthetics is good since the veneered DB cusp is obscured by the MB cusp.
• DB finish line is easy to access, making tooth preparation easier, and makes patient cleaning of the
margins easier.
• A 7/8 crown provides more coverage than the standard % crown which improves its resistance.
• Extremely useful when the distal surface has caries or decalcification.
• Serves as an excellent abutment for a bridge.

Crown Margins:
1. Bevel (feather-edge) Margin-in theory, this margin design is the best finishing margin for CAST
FULL GOLD restorations, allowing burnishing and adaptation of the gold to the tooth . However,
in practice it is difficult to read on the impression and die, and may lead to inaccurate
extension and distortion of the wax pattern, and subsequent casting, as a result of the thin
wax. It also has the LEAST MARGINAL STRENGTH to the casting.
• An acute edge/angle with a nearby bulk of metal is the optimum margin for a casting
because it is easily burnished to improve crown fit.

2. Chamfer Margin-this is the PREFERRED FINISHING LINE for cast full gold restorations. The
resultant casting has sufficient marginal strength while allowing the sliding joint at its periphery
to minimize the gap between the tooth and preparation, thus reducing the thickness of the cement.
Awell-prepared chamfer margin combines the advantage of an easily definable margin on the
impression and die, with minimal tooth preparation.
328
 3. Shoulder Margin (Butt Joint)-this preparation is the finishing line of choice for porcelain jacket NOTES
and ALL CERAMIC crowns. The edge strength of porcelain is low, thus a BUn JOINT is required.
The shoulder provides resistance to occlusal forces and minimizes stresses in the porcelain.
The margin can be easily read on the impression and die. Main disadvantage is any
inaccuracies in the crown fit are reproduced at the margin, causing in increased thickness
of cement. The should margin (butt joint) is the POOREST type of finish line used with cast
metal restorations.
• Unlike the PFM restoration which accepts any marginal design (bevel, chamfer, shoulder),
marginal tooth preparation for the ALL-ceramic crown or porcelain jacket crown MUST BE
ASHOULDER.
• The main reason to use porcelain jacket crowns and all-ceramic crowns is superior esthetics.
These crowns can mimic the optical properties of a natural tooth. However, the guidelines for
usage, such as tooth preparation are more critical and more complicated than for PFM
restorations. It is advisable to use these more esthetic crowns only in the anterior region
where esthetics is critical.
• Used for metal-ceramic with porcelain extended to the marginal edge.

4. Shoulder with a Bevel-this margin allows a sliding fit to occur at the margin, thus may be used
on the proximal box of inlays and occlusal shoulder of the mandibular %crowns. It may also be
used for labial margins of PFM crowns (metal ceramic). If these margins are placed in the gingival
crevice (subgingival), little display of metal is seen . This margin can be used for metal-ceramic
(PFM) with metal collars.

Periodontium remains much healthier when crown margins are placed ABOVE THE GINGIVAL CREST
(SUPRAGINGIVAl), however, supragingival margins are often not possible due to esthetics or caries.
Subsequently, the margins must be placed subgingivally. If a margin must be placed subgingivally,
the major concern is NOT TO EXTEND the preparation into the tooth's attachment apparatus (invade
biologic width). If the margin extends into the biologic width, a constant gingival irritant occurs and
ultimately the crown will fail. In this case, the tooth should have crown lengthening performed PRIOR
to final crown preparation.

The most important criterion for a gingival margin on a crown preparation is that its position is
easily discernible (must be able to recognize it easily).

Most common cause of crown failure (regardless of which type) is lack of attention to tooth shape,
position, & contacts. For gingival health, the correct contour of interproximal gingival areas and gin-
gival third are most important.
...,
".,
The greatest potential for wear exists between porcelain and tooth. Gold is a more favorable material CI
en
for the occlusal surface because its wear characteristics are more in harmony with enamel. ......
::
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Porcelain causes accelerated wear of the opposing dentition. Gold is preferred for the restoration c
CI
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of occlusal surfaces in the presence of a tooth-grinding habit (bruxism). ::::!
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en

FULL GOLD CROWNS - the preparation involves circumferential and occlusal reduction between
O.5-1.0mm. This reduction is done to eliminate undercuts and create space for sufficient metal to
ensure adequate crown strength.

ALL-CERAMIC CROWNS - these crowns have a relative tendency to fracture at a minimum de-
formation . Microscopic surface defects, under load lead to crack propagation and eventual failure.
• All-ceramic crowns are known for their lOW flEXURAL STRENGTH (this inability to flex is the major
weakness of all-ceramic crowns). Their relative tendency to fracture at a minimum deformation.
Microscopic surface defects, under load lead to crack propagation and eventually to failure.

329
 Porcelain Flexural Strengths:
• In-Ceram Zirconia = 800 Mpa (has the strongest flexural strength of all porcelains)
• Procera = 687 Mpa
• In-Ceram = 450 Mpa
• In-Ceram Spinell = 350 Mpa
• OPC = 150 Mpa
• IPS Empress = 140-180 Mpa
• Vita blocs = 120 Mpa
• Dicor = 120 Mpa
• Aluminous = 100 Mpa
• Feldspathic = 60-90 Mpa

• Preparations for all-ceramic restorations must be well-rounded with NO SHARP ANGLES to avoid
porcelain fracture. Porcelain is much stronger under compressive forces than tensile forces from
opposing teeth. Porcelain fracture in all-ceramic restorations is avoided by keeping the preparation
angles ROUNDED.

• CAD-CAM-these ceramics are processed into an inlay, onlay, or crown shape via a computer-controlled
milling machine.

Porcelain Layers: restoration is bulked out (over-contoured) to compensate for 20% shrinkage that
occurs during firing.
1. Opaque Porcelain-the first layer of porcelain applied to the metal coping to create the chemical
bond of the porcelain to the metal alloy and MASK THE COLOR of the metal. The opaque layer is
applied first to mask the metal and give basic shade to the restoration.
• Opaque porcelain showing through the facial surface of a PFM crown may be caused by
inadequate tooth reduction (fault of the dentist), too thick of metal, too thick of opaque
porcelain, or inadequate thickness of body porcelain (all due to lab error).

2. Body Porcelain-added over the opaque porcelain to make up the bulk of the restoration and
provide most of the color shade.
3. Incisal Porcelain-a translucent layer of porcelain added to the incisal or cuspal1l3 of the
crown to give translucency.

METAMERISM - a phenomenon that causes teeth/porcelain to appear color matched under one
light source, but appear very different under another light source (appears different under different
lights). This property is important in matching the shade of a PFM crown to a natural tooth. Thus, if pos-
sible, color matching should be done under two or more different light sources, one of which should be
su nIight. Staining a porcelain restoration decreases value and increases metameric responses.
• Light source affects the perception of color because the light source must contain the wavelength
of the color to be matched in order to see that color.

flUORESCENCE - the optical property by which a material (Le. teeth) reflects UV radiation. The
energy the tooth absorbs is converted into light with longer wavelengths, in which the tooth actually
becomes a light source. Human teeth fluoresce mainly BLUE-WHITE HUES (400-450nm). Fluorescence
makes a definite contribution to the brightness and vital appearance of natural teeth.
• "Blue fatigue" accelerates "yellow sensitivity". This means if you look at blue color objects (i.e.
drapes, charts, wall-color) while selecting the shade, it helps accentuate the ability to discriminate
yellow shades.

The production of color sensation with a pigment is a physically different phenomenon from that ob-
tained by optical reflection, refraction, and dispersion. The color of a pigment is determined by se-
lective absorption and selective radiation (scattering).

330
SHADE of a ceramic crown is matched first based on the color's value, chroma, then hue.
1. Value-a color's brightness. The most critical characteristic that is matched first. Value is the
NOTES
relative amount of lightness or darkness in a color (intensity of a color). An evaluation of value
represents the most important aspect in shade selection (for the restoration to match an
existing dentition).
• In esthetics, the value of a denture tooth depends on the relative whiteness or blackness
of its color.
• Staining a porcelain restoration or using a complementary color will reduce the value. It is
almost impossible to increase the value.
• A 60-year old patient, compared to a 25-year old patient is most likely to have teeth with a
color that is lower in value and higher in chroma .

2. Chroma-a color's strength or saturation. The aspect of color that indicates the degree of
SATURATION of the hue. Chroma is the single most important factor in shade matching. Chroma
can be successfully increased by using stains (especially in the gingival area).

3. Hue-the basic color (color families) like red, blue, yellow, green, etc.
• Drastic changes of hue (color or shade) are often impossible. Orange stain is most often
used to change the hue.

COLOR - a 3-D quantity specified by values of three variables (hue, chroma, and value). Color is
LIGHT REFLECTED from an object.

Shade Selection Sequence:

1. use the same shade guide given by the manufacturer.
2. match the shade before preparing the tooth .
3. remove all distractions (i.e. lipstick, dark glasses, heavy make-up).
4. quick rubber cup and paste prophylaxis can make shade selection more accurate.
5. position yourself between the patient and light source.
6. when observing, do not gaze for more than 5 seconds. Prolonged gazing decreases the
ability to discriminate colors and shades.
7. proceed by process of elimination. First exclude shades that are too light or dark.
8. half-closed eyes can increase sensitivity of retinal rods to better select the color's "value".

Staining Porcelain:
• Stains-metallic oxides that fuse to porcelain during a predetermined firing cycle.
• Porcelain's surface characteristics or can affect the perceived form of the final restoration as follows:
a smooth porcelain surface gives the impression of a larger size, and changes in contour are used .....,
::o::r
to alter the apparent long axis inclination of a tooth. o
~
:z::
o
c
DENTAL PORCElAIN - a mixture of FELDSPAR (main constituent), QUARTZ, & metallic oxides o
:z:
(silica, alumina, potassium oxide), which are used to impart proper shade to the porcelain . When ..,
:::!
en
feldspar undergoes fusion, it forms a glassy material, which gives porcelain its translucency. It acts as
a matrix for the high-fusing quartz, which then forms a refractory skeleton for the other materials to
fuse around. The compressive strength of a porcelain restoration is GREATER than it's tensile or
shear strengths. Dental porcelain restorations are BRITTLE and are not capable of much plastic
deformation.
• Quartz-a strengthener.
• Aluminous Porcelain-uses alumina instead of quartz as a strengthener. This porcelain is considerably
stronger than conventional porcelains.
• Kaolin-a clay and sticky material that binds the particles together when the porcelain is "green" or
unfired .
• Dental porcelain used in fabricating restorations MUST have these properties: be low-fusing
temperature, high viscosity, and have resistance to devitrification (crystallization). When porcelain
is fired too many times it can devitrify (appearing as a "milky" state and makes glazing very difficult).
• Constituents of dental porcelain include: silicone dioxide (64-69%), aluminum oxide (8-19%),
potassium oxide (8%), and sodium oxide (2-5%).

331
 NOTES 3 Classes of Dental Porcelains:
1. High-fusing porcelains-used to manufacture DENTURE TEETH.

2. Medium-fusing porcelains-used for all-ceramic and porcelain jacket crowns. Medium fusing
porcelains also contain oxides of lithium, magnesium, and phosphate (in addition to silicone
dioxide, aluminum oxide, potassium oxide, and sodium oxide).

3. Low-fusing porcelains-used for metal-ceramic (PFM) crowns.

• Aluminum oxide-the agent that must be added to low-fusing porcelains during its
manufacture to increase its resistance to "slumping down" during firing.
• Calcium oxide-also added to low-fusing porcelains.
• Oxides of potassium, sodium, and chromium are modifiers that help reduce cross linkages
between oxygen and silicone to lower the porcelain's fusing temperature. However, this
also decreases the viscosity of the porcelain that may "slump down" during firing .

DEGASSING (HEAT TREATMENT) - the process by which a casting is heated in a porcelain fur-
nace to a temperature of 980°C to burn off any remaining impurities prior to adding porcelain. De-
gassing is necessary for all gold-porcelain systems. Degassing of the metal at too Iowa temperature
will effect the formation of the oxide layer, which is important in bonding of the porcelain. The number
of bubbles formed at the interface decreases as time and temperature of degassing are increased.
• After degassing the casting is ready for porcelain .addition. The metal framework must not be
contaminated by handling prior to porcelain addition. If it is, the bond of the opaque porcelain
becomes weakened .

Causes of porcelain fracture at the porcelain-metal interface:

• Poor metal framework design is the MAIN cause of fracture.
• Degassing of the metal at too Iowa temperature effects formation of the oxide layer, thus
decreasing the bond.
• Contamination of metal prior to applying the opaque porcelain.
• Fusing the opaque coat of porcelain at too Iowa temperature or for too short a time.

• Both the metal (alloy) and ceramic (porcelain) must have closely matched coefficients of thermal
expansion (alloy is usually slightly harder) to avoid undesirable tensile stresses at the PFM interface
(porcelain fracture). Alloys should have a high proportional limit & high modulus of elasticity to
reduce stress on the porcelain.

Ways to Classify All-Ceramic Crowns:

1. Composition:
• Feldspathic porcelain-used for conventional porcelain-jacket crowns.
• Aluminous porcelain-found in Vitadur, Hyceram , Cerestore, &Inceram systems. Alumina is
used to reinforce glass. Porcelain strength is determined by the amount of
alumina reinforcement.
• Mica glass-found in Dicor &Cerapearl systems .
• Crystalline-reinforced glass-used with Optec, Cerestore &Empress systems. This is a glass
in which a crystalline substance like leucite is dispersed to impart strength to the ceramic.

2. Fabrication Method:
• Refractory die technique-used with Optec, Hyceram, &Inceram systems.
• Casting-used with Dicor systems.
• Press technique-used with Cerestore &Empress systems.

3 Stages involved in firing dental porcelain: The temperature at which each occurs depends on
the type of porcelain.
1. low bisque firing.
2. medium bisque firing.
3. high bisque firing.

332
GLAZED PORCELAIN - is non-porous, resists abrasion, possesses esthetic ability, and is well N
tolerated by the gingiva. A natural glaze occurs when the porcelain restoration itself is glazed by a
separate firing ("glaze firing"). If the body porcelain previously fired as a high bisque is heated rapidly
(10-15 min) to its fusion temperature and maintained at that temperature for -5 minutes before it is
cooled, the glass grains flow over the surface to form a vitreous layer which is the "glaze". This type of
glaze is much more permanent than overglazes (applied glazes). Glazed porcelain is the LEAST IRRI-
TATING to the gingival tissues compared to polished cast gold, polished direct filling gold, and pol-
ished acrylic resin.
• Overglazes (Applied Glazes)-ceramic powders that may be added to a porcelain restoration after
it has been fired. A transparent, glossy layer forms over the porcelain restoration surface at a
maturing temperature lower than the body porcelain's temperature, resulting in a glossy or semi-
glossy non-porous surface. Erosion of this overglaze may occur in the mouth, leaving a rough and
sometimes porous surface.

Metal-Ceramic Restorations (PFMs):

• The absolute minimum required thickness of the porcelain is O.7mm and the metal coping
thickness can vary from O.3-0.5mm for high-noble gold alloys and O.2mm for base metal alloys.
This proper thickness is to prevent distortion during the firing of the porcelain. It should be reinforced
in load-bearing areas (i.e. interproximal space) and can be strengthened in areas where the metal
exists alone (i.e. lingual collar).

• In preparing a tooth for a metal-ceramic crown, it is required to create space for .5mm of metal +
at least 1.0mm of porcelain (preferably 1.5mm) to ensure adequate strength and optimum esthetics
of the ceramic material. Supporting cusps require 2mm reduction. The opposing walls should
converge no greater than 10°. A chamfer finish line and all margins should be placed
supragingivally when possible.

• The necessary thickness of metal substructure is 0.5mm . The minimal porcelain thickness is 1-
1.5mm. Thus, the tooth reduction required for a PFM crown is -1.5-2.0mm. The labial shoulder width
is ideally 1.5mm.

• APFM and an all-ceramic crown require THE SAME amount of overall tooth reduction (1.5-2.0mm).
• The metal and porcelain must have compatible melting temperatures coefficient of
thermal expansions.

• The metal coping (substructure) must have all of its surfaces smooth and rounded to prevent
porcelain shrinkage.

• The metal coping ensures proper crown fit and maximizes the strength of the porcelain veneer.

• The outer junction of porcelain to metal should be at a right angle (90°) to avoid burnishing the
metal and prevent subsequent porcelain fracture.

• All porcelain should be supported by metal.

• The melting temperature should be at least 300-500°F higher than the fusing temperature of
the porcelain.

• In function, glazed porcelain on the occlusal surface removes 40x as much of the opposing tooth
structure than gold.

• The most common cause of porosity in the porcelain is inadequate condensation of the porcelain. The
effectiveness of condensing porcelain powder to reduce shrinkage is determined by the shape and
size of the particle.

333
 • If all crown margins are closed at the metal try-in appointment, but return from the lab all open, check
the contacts as they are probably too tight (over-bulked porcelain).

• Porcelain baked onto a high-fusing gold alloy may exhibit a green discoloration most likely due to
metal contamination by copper traces.

• The best measure of the potential clinical performance of a casting alloy is its ADA certification.

• In metal-ceramic restorations, failure or fracture usually occurs IN THE PORCELAIN. One of the
major reasons for acceptance of the PFM restoration is its greater strength and resistance to fracture.
The combination of porcelain and metal fused together, is stronger than porcelain alone. Since true
chemical adhesion occurs, the bond strength is such that failure or fracture will occur in the porcelain,
rather than at the porcelain-metal interface.

• Repeated fracture of a porcelain-fused-to-metal restoration (PFM) is due primarily to an inadequately

designed framework.

PFM Alloys:
1. High-gold noble alloys: used to fabricate metal-ceramic restorations (PFMs) consist of 98%
gold, platinum, & palladium (with trace elements). These noble alloys (gold, platinum,
palladium) do not oxidize on casting. This feature is important in a metal substrate so that
oxidation at the metal-porcelain interface is controlled by adding trace elements to the metal
(silicon, indium, iridium). This is the BEST TO USE.
2. Palladium-Silver alloys: 50-60% palladium + 30-40% silver (not a noble metal, thus
oxidizes on casting).
3. Nickel-Chromium alloys (base metal alloys): 70-80% nickel + 15% chromium. These
base metal alloys readily oxidize and can create porcelain-to-metal interface problems.

SPRUE - a small diameter (10-12 gauge) PIN made of wax or plastic. The general rule for sprue pin
diameter when using a centrifugal type of casting machine is the sprue pin diameter should be equal
or greater than the THICKEST portion of the wax or plastic pattern.
• A1D-gauge sprue pin can be used on most patterns, while the 12-gauge is used on small premolar
patterns. The sprue is attached to the wax pattern (i.e. cast post-core impression) at its point of
greatest bulk at a 45° angle to allow the incoming gold to freely flow to all parts of the mold.

• Spruing at a thin area of the pattern can produce the same result as using a sprue that is too small
("shrink back" porosity) caused by turbulence in the flow of the molten metal which creates a
shrinkage void, or suck-back porosity. Low investment permeability and insufficient wind-up of the
casting machine can also cause shrink back porosity.

DENTAL INVESTMENT - a refractory material used to surround the wax pattern during the proce-
dure of fabricating the metallic permanent restoration. It forms the MOLD into which the alloy is cast
after the wax is eliminated. Classes of dental investment materials:
1. Gypsum-bonded investments: gypsum (calcium sulfate hemiydrate) is the "binder" used when
casting conventional GOLD alloys. Gypsum bonded investment material can be used for DOWEL
CROWNS to be cast in silver-palladium alloys. The strength of dental investments for GOLD
alloys is dependent on the amount of GYPSUM.
• Dowel cores do not require as much expansion as crowns. So while they are cast with Ag-Pd
alloys (alloys that require a high temperature for expansion), a gypsum bonded mold is used
and heated to only 1200°F. Type I, II, III gold alloys can also be cast in gypsum-bonded
investment material.
• Gypsum-bonded investment material CANNOT be used for titanium crowns/copings,
Type IV gold alloys, or the substructure for metal-ceramic crowns.

334
 2. Phosphate bonded investments: the "binder" is a metallic oxide and phosphate used when
casting base metal alloys for PFM crowns.
• Phosphate bonded investment material is chosen for silver-palladium, gold-platinum, and
nickel-chromium alloys. These alloys all have a higher melting temperature that can be
withstood by phosphate bonded investment materials.
• The substructures for PFM crowns and Type IV gold requires heating above 2l00°F, so these are
invested in phosphate-bonded material. Any alloy with a casting temperature> 21 OO°F
(1150°C) should be cast in an investment with a binder other than gypsum. High
temperatures cause decomposition of calcium sulfate in the gypsum binder with the resultant
release of contaminating sulfur into the mold .

3. Silica-bonded investments: the "binder" is a silica gel used when casting base metal alloys
for RPD fra meworks.
• Magnesium phosphate reacts with primary ammonium phosphate to produce magnesium
ammonium phosphate which gives the investment its strength at room temperature. At higher
temperatures, silicophosphates form, giving the investment its greatest strength.

QUARTZ OR CRISTOBALITE - refractory materials used for these investments to provide thermal
expansion for the investment.

The metal-ceramic alloys must have a high melting range so the metal is solid well above the porce-
lain baking temperatures to minimize distortion (sag) of the casting during porcelain procedures. A
high sag factor leads to distortion of the bridge spans when the porcelain is fired. Important: when
casting a certain alloy, use a crucible that has not been used for other alloys.

4 Mechanisms compensate for solidification shrinkage of the alloy during casting procedures:
These mechanisms playa role in producing an expanded mold, thus compensate for the solidification
shrinkage of the alloy.
1. Setting expansion of the investment-results from normal crystal growth. In air, it is 0.4%, but
is partially restricted by the metal investment ring.
2. Hygroscopic expansion of the investment-used to augment normal expansion by al lowing the
investment to set in the presence of water. This water replaces the water used by the hydration
process, thus maintains the space between the growing crystals. Allows continued expansion
outward rather than restricting them. This expansion ranges from 1.2-2.2% .
3. Thermal expansion of the investment-occurs when the investment is heated in the burn -out
oven . It also eliminates the wax pattern and prevents the alloy from solidifying before it
completely fills the mold .
4. Wax pattern expansion-the wax pattern is warmed while the investment is still fluid. The heat ."
;:JO
may come from the chemical reaction of the investment or water bath in which the casting ri ng C>
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is immersed . :z:
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Expansion of the investment provides a LARGER mold to compensate for the subsequent contraction .,.,
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of the alloy.

Porcelain adheres to metal primarily by a CHEMICAL BOND. A covalent bond is established by shar-
ing 02 with elements present in the porcelain (silicon dioxide (Si02) and metal alloy (oxidizing ele-
ments like silicon, indium, &iridium).

Retentive characteristics of a full crown may be enhanced by adding pinholes in the preparation,
adding vertical grooves parallel to the path of draw, and maximizing the parallelism of the axial walls.
The type of cement used does not affect crown retention .
Retention and resistance forms in full-coverage preparations on short molars are enhanced by plac-
ing several vertical grooves.

335
 N CEMENTS - cements do NOT increase crown retention. Atooth must be WIPED DRY before crown ce-
mentation, as opposed to drying the tooth with alcohol and warm air to decrease the possibility of pulp
damage. Also, ALWAYS apply cement to both the restoration and the tooth.
1. Composite Resin-the luting material of choice to cement a ceramic crown and can provide the
STRONGEST BOND. Ceramic crowns are bonded with composite resin after etching the internal
surface of the crown, and are shown to be better in bonding strength than other materials.
2. Zinc-Phosphate Cement-can also be used to cement ceramic crowns. It has good compressive
strength (14,000-16,000 psi). However its high pH is a problem because two layers of varnish
must be applied to protect the pulp.
3. Zinc polycarboxylate or ZOE-these biologically compatible cements are used on teeth with
preparations that possess adequate length and retentive features, or when the preparation depth
raises some concern regarding pulp vitality. Also, these cements exhibit better resistance to
solubility than zinc phosphate cement. Zinc polycarboxylate and glass ionomer cements adhere
to calcified dental tissue, and have superior biologic compatibility than zinc phosphate cements.

Prolonged sensitivity to heat, cold, and pressure after cementing a crown or fixed bridge is usually
related to OCCLUSAL TRAUMA. If CR occlusion is high, patient complain of cold sensitivity and pain on
biting down hard. All patients should have an appointment specifically to check the occlusion on all
crowns and bridges. Excursive movements should also be evaluated, since often patients complain of
pain on chewing soft foods (this indicates improper balancing or working contacts). The occlusion of
gold restorations is best checked with SILVER PLASTIC SHIM STOCK.
• Initial sensitivity can be caused by acid irritation accentuated by dehydrated dentin from prolonged
drying of the tooth before cementation or incorrect liquid/powder ratio of cement.
• Radiographic Signs of Occlusal Trauma: hypercementosis, root resorption, alteration of lamina dura
& widening of the periodontal ligament (POL) space. Periodontal pockets is NOT a radiographic
sign of occlusal trauma.
• Common Clinical Signs of Trauma from Occlusion: increased tooth mobility, thermal sensitivity (cold),
enamel attrition, and recession of facial gingival tissues.
• If a marginal ridge is left higher than an adjacent marginal ridge, a retrusive interference movement
may occur. So, whenever a restoration is done, the occlusion must be correct. The degree of contact
on the restoration should be to the same degree that teeth contact in that quadrant and on the
opposite side.
• Periapical Film-the radiograph of choice to evaluate root surfaces, supporting bone, and
the PDL.

Endodontically treated teeth restored with a cast post, core, and crown are subjected to the high inci-
dence of VERTICAL ROOT FRACTURE. The main symptom is almost always PAIN WHEN BITING, and the
.."
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radiograph usually appears normal.
o • Advantages of using a post & core, rather than a post crown when restoring endodontically
en
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::c treated teeth:
o
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:z: • marginal adaptation and fit of the restoration is independent on the fit of the post.
:::! • restoration can be replaced in the future if needed, without disturbing the post and core.
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• If the endodontically treated tooth is to serve as a bridge abutment, it is not necessary to make
the root canal preparation parallel with the line of draw of other preparations (it can be treated
as an independent abutment).

• The post and core is made separate from the final restoration. The crown is fabricated and cemented
over the core just as a restoration is placed over a preparation done on tooth structure.

• Apost & core can be used for teeth with little or no clinical crown, but with roots with adequate
length, bulk, and straightness. For posterior teeth with less extensive destruction of coronal tooth
structure, or teeth with less favorable root configurations, a pin-retained amalgam or composite core
can be used.

336
NON-RIGID CONNECTOR - a broken-stress mechanical union of the retainer + pontic, rather than NOTES
the usual rigid, solder joint. It is comprised of a KEY &KEYWAY. Its use is restricted to a SHORT-
SPAN BRIDGE that is replacing one tooth. It is indicated when retainers cannot be prepared to
draw together without excessive tooth reduction. Prosthesis with non-rigid connectors should NOT
be used if prospective abutment teeth have significant mobility.

• T-shaped key-the most commonly used non-rigid design that is attached to the pontic, with a
dovetail keyway placed within the retainer. The path of insertion of the key into the keyway should
be parallel to the pathway of the retainer, not involved with the keyway.

• When a non-rigid connector is used in a FPD, the path of insertion of the key into the keyway should
be parallel to the path(s) of insertion of the retainer NOT involved with the keyway.

• Solder joints-the connectors of choice when abutment teeth are in normal alignment and have good
bone support (canine and 1't molars).

• The strength of a soldered connector of a fixed partial denture is best enhanced by increasing its
height.

FIXED BRIDGES
If the dentist's clinical and technical skills do not math the case demands, then fixed bridgework
should not be done because a failed bridge is more detrimental to dental health than a failed RPD.

Unless specifically contraindicated, fixed restorations are ALWAYS the treatment of choice.

Fixed bridges can be used in conjunction with an RPD (i.e. a patient with a couple of missing anterior
teeth and no posterior teeth) . Treatment could be a fixed bridge in the anterior, and RPD in the poste-
rior region.

To maintain and protect the health of the gingival tissues and prevent recession, the correct contour of
the crown's gingival 1/3-1/5 and interproximal areas are most important in the final restoration.

Factors that Determine a Fixed Bridgework Design:

1. Root configuration: an important factor when assessing an abutment's suitability from a
periodontal standpoint. Roots that are broader labiolingually than mesiodistally are preferred to
roots that are round in cross-section.
• Multi-rooted posterior teeth with widely separated roots provide better periodontal support
than roots that converge, fuse, or present a conical configuration.
• Single-rooted teeth with an irregular configuration or some curvature in the root's apical third
are better abutments than teeth with a nearly perfect taper.
• Root surface area on a prospective abutment should also be evaluated.

2. Crown-to-root ratio: 1:2 is the ideal crown-to-root ratio of a tooth to be used as a bridge
ABUTMENT. This high a ratio is rarely achieved, but a ratio of 2:3 is more realistic. A 1: 1 ratio is
the minimum acceptable ratio for a prospective abutment under normal circumstances. Crown-
to-root ratio alone is NOT adequate criteria for evaluating a prospective abutment tooth .

3. Axial alignment of teeth: parallelism of abutment preparations is BEST determined by the

LONG AXIS of the prepa rations.

337
 NOTES 4. Length of the lever arm (span). REPLACING 3 TEETH IS THE MAXIMUM! The absolute MAXIMUM
number of posterior teeth that can be safely replaced with a fixed bridge is THREE, and only
under ideal conditions. Any bridge replacing more than two teeth is considered high risk.
• An edentulous space involving 4 adjacent teeth other than four incisors is usually best treated
with a RPO. If more than one edentulous space exists in the same arch, even though each of
them could be individually restored with a bridge, it may be desirable to restore them with a
RPO, especially if the spaces are bilateral and each space involves two or more missing teeth .
• 3'd molars can rarely be used as abutments since they often display incomplete eruption,
short-fused roots, and a marked mesial inclination in the absence of a 2nd molar.

Fixed Bridgework Indications or important considerations to consider when contemplating

fabricating a fixed bridge:
1. Limited number of edentulous areas that would not otherwise be more satisfactory
restored with a RPO.
2. Need to prevent the over eruption of opposing teeth and the drift of teeth neighboring
the edentulous space.
3. Suitable abutment teeth (favorable crown:root ratio, adequate alveolar support, and absence
of apical pathology).
4. Esthetics
5. Patient motivation and availability.
6. Clinical and technical ability.

Fixed Bridgework Contraindications:

• Poor oral hygiene, high caries rate.
• Multiple spaces in the arch or teeth likely to be lost in the near future.
• Space not detrimental to the maintenance of arch stability or dental health.
• Unacceptable occlusion.
• Bruxism.
• An anterior fixed bridge is contraindicated when considerable residual ridge resorption exists.
A RPO is indicated in this case.

Splinting:
• Splinting adjacent abutment teeth in a FPO (fixed bridge) is performed primarily to improve
distribution of the occlusal load.
• Adentist primarily splints adjacent abutment teeth in a FPO to improve the distribution of the
occlusal load.
• The most likely indication for splinting is tooth mobility with patient discomfort.
• Although controversial, do NOT splint natural teeth and implants in a FPD. Implants do not have
a POL, thus do not have the same ability to absorb shocks like natural teeth (they have different
mobilities). When this bridge is subject to occlusal loading, the difference is detrimental to the
natural teeth and causes bone loss around the implants.
• Horizontal loads/forces on natural or abutment teeth are MOST destructive to the periodontium .

PONTIC - the suspended member of a fixed bridge that replaces a missing tooth. The pontic is a
tooth substitute that MUST provide patient comfort, covenient contours for hygiene, and be esthetic.
1. Modified Ridge Lap Pontic-the design of choice for pontics used in the "appearance/esthetic
zone" for maxillary and mandibular bridges. This design uses a ridge lap for minimal ridge
contact. It gives the illusion of being a tooth, but has All convex surfaces for easy cleaning.
2. Sanitary Pontic-this design leaves a space between the pontic and ridge. Most commonly
used where esthetics are NOT important (non-appearance zone), and is convex in all
areas for easy cleaning.
• conical pontic-has a rounded top and conical bottom, used for thin mandibular ridge in a
non-appearance lone.
3. Saddle Pontic-this design looks most like a tooth, covering the ridge labiolingually with a
large concave contact. It is impossible to clean and is NOT USED.
• ovate pontic-a sanitary substitute for the saddle pontic design . Set in the concavity of the
ridge (which is either present or surgically made) that gives the appearance that it is growing
from the tooth.

338
In a posterior fixed bridge, a pontic should be: in contact in centric occlusion, mayor may not be in
contact in working-side movements, and should NOT be in contact in non-working side movements.
• Success or failure of a bridge depends mostly on the pontic design which is dictated by function,
esthetics, ease of cleaning, patient comfort, and the maintenance by the patient of healthy tissues
on the edentulous ridge.

• Proper pontic design is more important to cleanability and acceptable tissue well being, than the type
of material (porcelain, gold, etc.).

• Multiple adjacent pontics on an anterior fixed bridge have reduced facial embrasures to enhance
esthetics.

EXTREMLY IMPORTANT: All pontics must be properly designed to prevent an unhealthy response to
the underlying ridge mucosa, and must:
• Be non-porous, smooth, with a polished surface.
• Make passive pinpoint contact with the gingival tissue.
• Not be concave in two directions.
• Be readily cleanable by the patient.
• Be narrower at the expense of the lingual aspect of the ridge.
• Be on as straight a line as possible between the retainers to prevent any torquing of
reta iners or abutments.

• In constructing a FPO for a patient, the dentist will use a hygienic pontic. The position of the opposing
contact area will primarily determine the F-L dimension of the occlusal portion of this pontic.

• In adapting a pontic to the residual ridge, the dentist must maintain a proper biologic and hygienic
environment. Thus, the pontic must NOT be concave in two directions.

• The F-L dimension of the occlusal portion of pontics is determined by the F-L position of the opposing
centric holding contact areas.

• Pontic should be convex M-O, touch the residual ridge, and be concave F-L.

• The portion of the pontic approximating the ridge should be as convex as possible.

• With regard to ease of cleaning and good tissue health, proper pontic design is more important than
the choice of material used in fabricating the pontic.
-0
• The contour and nature of the pontic contact with the ridge is very important. "'"
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• The area of contact between the pontic and ridge should be small. CJ
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• The pontic should exert no pressure on the ridge, only passive contact with no blanching of tissue. en

• Excessive tissue contact is one of the major causes of failure of fixed bridges.

• Glazed porcelain, polished gold, unglazed porcelain, and polished acrylic are preferred in that order
for their acceptability to the soft tissue.

A FPO will be supported by both an osseointegrated implant and natural teeth. The most serious poten-
tial problem is the implant and natural teeth have different mobility (the implant has no POL, thus no
mobility).

339
 QUENCHING - a metal is rapidly COOLED from an elevated temperature to room temperature or
below. Quenching is usually done either to preserve at room temperature a phase ordinarily stable only
at elevated temperatures, or to rapidly terminate a process that only occurs at elevated temperatures.

• To achieve a softened condition for a Type III dental gold alloy, the casting should be quenched in
water within 30-40 seconds of being made.

• Quenching is rapid cooling by immersion in water of a dental casting from the high temperature
at which it has been shaped. Quenching is usually done to maintain mechanical properties
associated with a crystalline structure of phase distribution that would be lost upon slow cooling.

Advantages of Quenching:
1. Noble metal alloy is left in an "annealed" condition or burnishing, polishing, and
similar procedures (it maintains its malleability and ductility).
2. When water contacts the hot investment, a violent reaction ensues. The investment becomes
soft and granular, and the casting is more easily cleaned.

HEAT TREATMENT - occurs when a metal is elevated to a temperature above room temperature and
held at that temperature for a length of time.

BURNISHING - somewhat related to polishing in that the surface is drawn or moved. However, in-
stead of using many tiny particles, only one large point is used. If a round steel point is rubbed over
the margin of a gold inlay (made from Type I or II gold alloy), the metal can be moved so that any small
discrepancy between the inlay and tooth can be closed.

ANNEALING (DEGASSING) - softening a metal by controlled heating and cooling to make its ma-
nipulation easier. Annealing is the process of heating and cooling a metal to make the metal tougher
and less brittle. Annealing comprises 3 stages (recovery, recrystallization, and grain growth). The
higher the metal's melting point, the higher temperature required for annealing. During the annealing
process, the stresses in the metal are relieved.
• Gold foil is annealed (degassing) to remove volatile surface impurities prior to placement
in the cavity preparation.

FRITTING - a process of manufacturing low and medium fusing porcelains, and involves raw con-
stituents of porcelain to be fused, quenched, and ground back to an extremely fine powder. This "frit"
can be added over by other metallic substances to produce color in porcelain.

SOLDERING - process of joining two metals using a filler material (or solder) that has a substan -
tially lower fusion temperature than that of the metal parts being joined (the filler material or solder is
fused to each of the parts being joined). Soldering is used in dentistry to connect bridgework and in
fabricating orthodontic appliances. Gold solders are generally used for fixed bridgework and silver sol-
ders for orthodontic appliances. The solder MUST melt at least 150°F below the fusion temperatures of
the metals or alloys being soldered.
• To be biologically and mechanically acceptable, a solder joint should be circular in form and occupy
the region of the contact area. The strength of the solder joint is increased by increasing the height
of it (as opposed to width).

• Bonding of the solder is contingent on wetting the joined surfaces by the solder, and not upon melting
of the metal components.

• Cleanliness is the most important (prime) prerequisite of soldering, since the soldering process
depends on WETTING the surfaces to achieve bonding. Corrosion products like oxides and sulfides
that are present due to the casting process interfere with bonding. Flux is placed on the surfaces
to be soldered before they are heated. When it melts, the flux displaces gases and removes
corrosion products by either combining with them or reducing them. The flux is then displaced by
the solder, which can now form an interface with and bond to the surface being soldered.

340
• Fluxing-the oxidative cleaning of the area to be soldered. Fluxes (most commonly borax) are used to
dissolve surface impurities and to protect the surface from oxidation while heating. Fluxing is also
performed on molten metal alloys during the casting of a crown or RPD framework.
• Potassium fluoride-the agent most commonly added to the FLUX (used for soldering stainless
steel or cobalt-chromium alloys) with a specific purpose to dissolve the passivating film
(chromium oxide film) that may prevent wetting of the metal with the solder.
• Other constituents of the flux: sodium pyroborate (55%), boric acid (35%), and silica (10%).
• In addition to the usual reducing and cleaning agents incorporated in a flux, a flux used for
soldering stainless steel or cobalt-chromium alloys also contains a fluoride to dissolve the
passivating film supplied by the chromium (chromium oxide film) . The solder will not wet the
metal when such a film exists. Potassium fluoride is the most common agent.
• Anti-flux-a material used to outline the area to be soldered to restrict the flow of solder.
The most common anti-flux is a soft graphite pencil.

PICKLING - a process that involves careful heating of the casting which is placed in an acidic solu-
tion to reduce the surface oxides. The most effective pickling solution is 50% hydrochloric acid (HCL)
solution (HCL fumes are very corrosive and damage metal objects in the office). It is recommended to
use commercially available pickling agents that are acid salt solutions since (acid salts act slower,
but produce acceptable results). Frequently the surface of a gold casting is dark due to formation of a
surface oxide film. Pickling removes this surface oxide film on gold castings. 2 pickling methods:

1. Place the casting in pickling solution and gently heat the solution to produce a clear,
gold-colored casting.

2. Heat the casting until it emits a dull glow, then drop it in pickling solution. There is a risk of
distorting delicate margins with this method. A practitioner pickles gold alloy restorations by
heating them to redness and plunging them into an acid bath. This procedure can result in
WARPAGE of the restoration.
• The process of removing surface oxides from a casting prior to polishing is PICKLING. The
casting is placed in an acidic solution that reduces surface oxides. To prevent injury, safety
goggles are always worn when pickling.

COLD WORK {STRAIN HARDENING OR WORK HARDENING} - is HARDENING (deformation) of

a METAL at room temperature (in contrast to the effect of working at a higher temperature as in forg-
ing). An example of cold work is bending a wire back and forth rapidly between the fingers.
• In polycrystalline metal, dislocations (defects) tend to build up at the grain boundaries. Also, the
barrier action to slip at the grain boundaries causes the "slip" to occur on other intersecting slip
planes. Point defects increase, and the entire grain may eventually become distorted. Greater stress ."
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is required to produce further "slip" and the metal becomes stronger and harder. This process en
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is called "strain hardening" or "work hardening". CI
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• SLIP is a deformation process requiring the simultaneous displacement of an entire plane of atoms CI
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relative to the plane and below the plane. C">
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• Work hardening is derived from the fact that the process is a result of cold work (i.e. deformation at
room temperature, in contrast to the effect of working at a higher temperature like in "forging" .
• The ultimate result of strain hardening with further increase in cold work is FRACTURE.
• The phenomenon of "cold work" and "strain hardening" is familiar to everyone. For example, one way
to cut a wire is to bend it back and forth rapidly between the fingers. When all the slip possible has
occurred, the wire fractures.
• Under a microscope, elongated grains in the microstructure of a wrought wire indicate the wire has
been cold worked or strain hardened.
• The surface hardness, strength, and proportional limit of the metal are INCREASED with strain
hardening, while ductility and resistance are DECREASED. However, the elastic modulus is not
changed greatly.

341
 ELECTROSURGERY - while many consider this to be a more radical means of gingival tissue re-
traction, it is an acceptable method. It functions by passing small current of electricity through the
gingival tissues, causing cells to desiccate (scorch). Electrosurgery usually results in some delayed
healing because of the lack of proper clot formation, but is very good at stopping hemorrhage. Note:
too low of an electrical current in an electrosurgical electrode can be detected by tissue drag.
• Electrosurgery Objectives: coagulation, hemostasis, access to cavosurface margins, and to
reduce the inner wall of the gingival sulcus (removing a thin layer of crevicular gingival tissue).

• Indications:
• To remove hyperplastic gingival tissue where it has proliferated into preparations or
over crown margins.
• In place of gingival retraction cord where substantial attached gingiva is present.
• For crown-lengthening procedures prior to fabricating a provisional crown.

• Contraindications: areas of thin attached gingiva tissues, or where an underlying dehiscence is

suspected because gingival recession may be marked after using electrosurgery in such situations.
Electrosurgery is NOT used on or in the vicinity of patients with CARDIAC PACEMAKERS (major
contraindication).

• Great care must be used when performing electrosurgery due to potential serious damage to the PDl
and surrounding bone, resulting in loss of attachment.

OCCLUSION
TEMPOROMANDIBULAR JOINT (TMJ) - a combined hinge &gliding joint (a ginglymoarthrodial
joint) that permits both hinge-like rotation and gliding (sliding) movements. Ginglymus means "rota-
tion" and arthrodial means "freely movable".
• In the lower (condyle-disc) compartment, only a hinge-type (rotary motion) can occur. This
rotational or terminal hinge-axis opening of the mandible is possible only when the mandible is
retruded in CR with a conscious effort by the patient or by the dentist's control. A pure hinging
movement is possible only in the terminal hinge position .

• In the upper compartment (mandibular fossa-disc) only sliding movements (translation) can
occur. When the lateral pterygoid muscles contact simultaneously, the discs and condyles slide
forward down over the articular eminence (protrusion), or can move backwards together (retrusion)
,.,
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o Muscles Acting on the TMJ:
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• If the mandible fractures, UPWARD displacement of the fractured segment would be caused by
the elevator muscles (masseter, medial pterygoid, & temporalis).

• Depressor Muscles (Open) mandible/mouth: lateral pterygoid, anterior belly of digastric, & omohyoid.

• Protrusion Muscles: lateral pterygoids together (individually, lateral pterygoids cause lateral
excursion). lateral pterygoids are mainly responsible for positioning and translating the condyles.

CENTRIC RELATION ("RETRUDED CONTACT POSITION") - a "ligament-guided" position

that is the supero-anterior position of the condyle along the articular eminence of the condyle with
the articular disc interposed between the condyle and eminence. This position is an optimum rela-
tive position between all anatomic components, and is a REPEATABLE reference position to mount
casts on the articulator.
• CR is the most unstrained, retruded anatomic and functional position of the mandibular condyle
heads in the mandibular glenoid fossae of the TMJs. CR is a "bone-to-bone" relationship (bones
of the upper and lower jaws) independent of tooth contact. The presence or absence of teeth and
type of occlusion are not factors.

342
• The mandible cannot be forced into CR from the rest position because the patient's reflex
neuromuscular defense would resist the applied force. Rather, the mandible should be relaxed and
gently guided into CR.
• To place a patient in CR, have the patient swallow, turning the tongue upward towards the palate, relax
the jaw muscles, or protruding and retruding the mandible can be effective ways to help record CR.
• In fixed and removable prosthodontics, CR should be established PRIOR to designing the frameworks.
• When a CR record is taken in the natural dentition, imprints of the teeth should be confined to CUPS
TIPS and the registration material should not be perforated.
• CR is a "ligament-guided" position. CR is the closing end-point of the retruded border movement
(terminal-hinge movement).
• Transverse Horizontal Axis (Terminal Hinge Position)-the one relation of the condyles to the fossae
in which a pure hinging movement is possible.
• Recording CR is an essential starting point in the design of the artificial denture.
• In complete denture prosthodontics, the position of the planned MIC of the teeth in centric occlusion
is established to coincide with the patient's CR (CO = CR) .

Primary Requirements for making a CENTRIC RELATION record when fabricating a RPD:
• Record the correct horizontal relation of the mandible to the maxilla.
• Stabilize the lower record base with equalized vertical pressure.
• Retain the record in an undistorted condition until the casts have been accurately mounted
on the articulator or until a previous record can be verified.

Materials used to record jaw relationships have varied widely over the years. An ideal recording
medium is easy to handle, uniformly soft while the record is being made, rapid setting, and totally
rigid but not brittle when set. Rapid setting plaster zinc oxide & eugenol pastes, and modeling plas-
tic are ideal. Avoid soft waxes as a recording material because they never become rigid and are
likely to distort during the cast mounting procedure.

If sufficient natural posterior occlusion exists, the mandibular cast may be mounted in CO using a ZOE
reinforced wax bite. In the case of a distal extension RPD, base plates and occlusion rims should be
placed on the framework, and the patient closed into softened recording wax or zinc oxide-
eugenol paste (preferred). Whether this record will be in CO or CR depends on the case, and is dic-
tated by the presence or absence of any natural posterior occlusion in the patient.

A reliable method is to use a record of all remaining occluding surfaces in a wax wafer with the
mandible in the terminal hinge position and teeth just out of occlusion.

CENTRIC OCCLUSION (lNTERCUSPAL POSITION (lP) - a "tooth-guided" position defined as -c

::c
the maximum intercuspation of the teeth. When the teeth are in CO, the mandible's position in rela- o
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tion to the maxilla is determined by the intercuspation of teeth. During typical "empty mouth swal- ::c
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lowing" the mandible is braced in the intercuspal position. o
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• Empty mouth swallowing occurs frequently throughout the day and is an important function that rids c:;
en
the mouth of saliva, and helps moisten the oral structures. The hourly rate of non-masticatory
swallowing is related to the amount of salivary flow and is usually an involuntary reflex activity.
• Masseter muscles contract and the tongue tip touches the roof of the mouth during
normal swallowing.
• Tooth contacts are longer during swallowing than chewing, but this varies greatly in frequency
and duration among people.

When the mandible is in it's physiologic rest (postural position), TEETH DO NOT CONTACT. Physiologic
rest position occurs when the mandible and all of its supporting muscles (8 muscles of mastication +
suprahyoids &infrahyoids) are in their resting posture (there is muscular equilibrium). This lack of tooth
contact is the "freeway space" or "interocclusal distance" and averages 2-Gmm. This position is a
"muscle-guided" position and is the beginning and end point of most mandibular movements.
• Interocclusal Distance {"Freeway Space")-the vertical distance or space created when the
mandible is in its physiologic rest position between incisal and occluding surfaces of maxillary and
mandibular teeth or occlusion rims.
• The rest position of the mandible (postural position) is determined mostly by the musculature. The
usual reflex cited as the basis for the mandible's postural position is the tonic stretch reflex of the
mandibular elevator muscles (i.e. myotatic reflex). It is a "muscle-guided" position.
343
 VERTICAL DIMENSION OF OCCLUSION (VDO) - the vertical length of the face as measured be-
tween tow arbitrary selected points (one above and one below the mouth) when the teeth or any substi-
tute material (occlusal rims) are in contact in CR. Phonetics and esthetics help verify a patient's
vertical dimension of occlusion.
• Excessive vertical dimension (VDO): may result from trauma to underlying supporting tissues
(denture patient), straining of the elevator/closing muscles, and adversely affects interocclusal
clearance (decreased freeway space) causing loss of interocclusal distance in the rest position.
Excessive vertical dimension is the usual causes of CLICKING OF DENTURE TEETH (to treat remount
and fabricate a new complete denture).
• Clicking of dentures can also be caused by lack of retention of the maxillary &mandibular
dentures. To treat, if due to underextension, border mold and reline. If due to overextension,
reduce as indicated with PIP and disclosing wax.
• Porcelain teeth can also cause denture clicking. To treat, use acrylic resin teeth.

• Decreased vertical dimension (VDO): an occluding vertical dimension that causes

EXCESSIVE INTEROCCLUSAL DISTANCE (increased freeway space) when the mandible is
in the physiological rest position.
• Classic Example: people with no teeth or who have worn dentures for a long time present with
the lower portion of the face scrunched up, or do not show their lips anymore (poor facial profile).
To correct, make new dentures and increase the VDO. This decreases the interocclusal distance
(freeway space).
• Decreased VDO often results in CHEEK BITING.

Factors to consider when verifying VDO:

• Pre-extraction records
• Amount of interocclusal distance (freeway space) to which the patient was previously accustomed.
• Esthetics (facial harmony and facial expression are considered).
• Phonetics (speech sounds).
• Length of the lip in relation to the teeth.
• Condition and amount of shrinkage of the ridges.

VERTICAL DIMENSION OF REST (VDR) - the vertical length of the face measured between two
arbitrary points (1 point above & 1 below the mouth) when the mandible is in the rest position. In a
physiologically healthy individual, there will always be a vertical space between the teeth (freeway
space) when the mandible is in the rest position. This position is important in complete denture fabri-
cation because it provides a guide to the VDO.
• VDR = Vertical Dimension of Occlusion (VDO) + Interocclusal Distance
""0
::c • VDR is always greater than VDO.
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en
......
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c::> ARTICULATION - relationship of teeth during movements into and away from the eccentric position,
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en
CONDYLAR GUIDANCE - a factor TOTALLY dictated by the patient. It is the mechanical device on
an articulator intended to produce similar guidances in articulator movement that are produced by the
condyle paths during mandibular movements.
• Condylar guidance is completely dictated by the patient and cannot be varied or "adjusted" by
the dentist.

• The inclination of condylar guidance depends on: shape & size of the bony contour of the TMJ
(fossae and disc), action of the muscles attached to the mandible, limiting effects of the ligaments,
and the method used for registration.

• The incline (angulation) of the condylar element on the articulator is anatomically related to the
slope of the condylar articular eminences (condylar inclination).

• When adjusting the condylar guidance for protrusive relationship, the incisal guide pin on the
articulator should be raised out of contact with the incisal guide table. The protrusive record is
probably the LEAST reproducible maxillomandibular record.

344
• When restoring the entire mouth with crowns, the protrusive condylar path inclination influences the
mesial inclines of the mandibular cusps.

• A retrusive movement requires the condyles to move BACKWARD &UPWARD.

• In lateral movements, the working condyle moves down, forward, and laterally.

• In lateral movements, the non-working condyles moves down, forward, and medially.

• The inclination of the condylar path during protrusive movement varies from steep to shallow in
different patients. It forms an average angle of -30 0 with the horizontal reference plane. If the
protrusive inclination is steep, the cusp height may be obviously longer. If the inclination is shallow,
the cusp will be shorter. This factor is the MOST important aspect of condylar guidance that affects
the selection of posterior teeth with appropriate cusp height.

• In complete dentures, the condyle path during free mandibular movements is governed mainly by the
SHAPE of the fossa and meniscus (articular disc) and the muscular influence.

Determinants of Occlusion:
• Right & left TMJs
• Occlusal surfaces of teeth and the neuromuscular system. The concepts of occlusal arrangement
aim to place artificial teeth in harmony with the TMJ and neuromuscular system. If done properly, it
results in minimum stress on the teeth and requires minimal effort by the neuromuscular system when
performing mandibular movements. Optimal occlusion requires minimum adaptation by the patient.

4 Human Dentition Features that Directly Effect PDl Health &Hard Tissue Anchorage to
Resist Occlusal Force:
1. anterior teeth have slight or no contact in MICP (intercuspal position).
2. occlusal table is < 60% of the overall F-L width of the tooth .
3. occlusal table is at right angles to the tooth's long axis.
4. mandibular molar crowns are inclined 15-20 0 toward the lingual.

4 Theoretical Determinants Required to Restore a Complete &Functional Occlusal

Surface of a Tooth:
1. Amount of vertical overlap of anterior teeth. The anterior determinant of occlusion is
the horizontal and vertical overlap relationship of the anterior teeth .
2. Contour of the articular eminence.
3. Amount and direction of lateral shift in the working side condyle. ....,
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4. Tooth position in the arch. o
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However, the jaw relationship most commonly used in the ACTUAL design of restorations is the AC- o
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QUIRED centric occlusion. The height of the pulp horn of a particular tooth is NOT a required deter- :::!
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minant to restore a complete and functional occlusal surface. en

COMPENSATING CURVE - the anteroposterior and lateral curvature in the alignment of the oc-
cluding surfaces and incisal edges of artificial teeth which is used to develop a balanced occlusion.
• The form of the compensating curve is entirely under the dentist's control (i.e. if during a try-in
evaluation a dentist notes that a protrusive excursion movement results in the separation of posterior
teeth, the problem can be corrected by simply increasing the compensating curve).

• The compensating curve allows the dentist to alter the effective cusp angulation without changing
the form of the manufactured denture teeth. The function of this curve is to help provide a
balanced occlusion.

• A prominent compensating curve is required when there is a steep condylar path associated with a
low degree of incisal guidance.

345
 NOTES OCCLUSAL PLANE - an imaginary surface related anatomically to the cranium and theoretically
touches the incisal edges of the incisors and tips of the occluding surfaces of the posterior teeth. It is
not really a plane, but represents the mean curvature of the surface.
• The anterior point of the occlusal plane is determined by the position of the anterior teeth.
• The posterior determinants are anatomical landmarks (2/3 the heights of the retromolar pads).
Thus, it is debatable as to the extent of control the dentist may exercise over the orientation of
the occlusal plane.

CUSP INCLINATION - angle made by the slopes of a cusp with a perpendicular line bisecting the
cusp, measured mesiodistally or buccolingually. Cusp inclination is under the dentist's control (choos-
ing 30° teeth, monoplane teeth, etc.).

BALANCED OCCLUSION - an occlusion of the teeth which presents a harmonious relation of the
occluding surfaces in centric and eccentric positions within the functional range. Balanced occlusion
is the objective in COMPLETE DENTURES.

• When establishing balanced occlusion for a complete denture, the lingual cusps of maxillary
posterior teeth on the non-working side (balancing side) should contact the LINGUAL inclines of the
FACIAL cusps of the mandibular posterior teeth.

• 5 Factors Govern Establishing Balanced Articulation (some of these, if not all, are controlled
by the dentist):
1. inclination of the condylar guidance which is completely dictated by the PATIENT.
2. inclination of the incisal guidance (horizontal and vertical overlap).
3. inclination of the occlusal plane (plane of orientation).
4. convexities of the compensating curve.
5. angle and height of cusps.

Posterior Teeth Contacts in a Balanced Occlusion:

• There is cusp-to-fossa contact in centric occlusion (MICP) in an ideal Class I occlusion.
• During lateral excursions, opposing cusps contact on the working side.
• During lateral excursions, on the balancing side (non-working), the maxillary lingual cusps (lingual
inclines) contact the mandibular facial cusps (lingual inclines).

BALANCED CENTRIC OCCLUSION - in partial dentures is necessary for appliance stability. The
framework's design and relationship of the teeth to the ridges also influence RPD stability.

BILATERAL ECCENTRIC OCCLUSION - is NOT an objective in RPD construction, UNLESS the

partial prosthesis is opposed by a complete denture. The vertical relation for RPDs is usually deter-
mined by the remaining natural teeth (unlike complete dentures).
• Eccentric Occlusion-a protrusive and right &left lateral contacts of the teeth's INCLINED planes
when the mandible is NOT moving (stationary).

BILATERAL BALANCED OCCLUSIOn - dictates a MAXIMUM number of teeth should contact dur-
ing mandibular lateral excursive movements. This concept of occlusal arrangement is ideal, but is
very difficult to achieve.

GROUP FUNCTION OCCLUSION ("UNILATERAL BALANCED OCCLUSION") - characterized

by NO non-working side contacts in a natural dentition. In group function there are ONLY working
side contacts from anterior and posterior teeth .
• Group function is an occlusal relationship where All posterior teeth on a side contact evenly as
the jaw moves toward that side (working side). All teeth on the non-working side 00 NOT contact.
Only teeth on the working side contact during a lateral excursion.

• Non-working (balancing) interferences: occur on inner inclines of the FACIAL cusps of mandibular
molars.

346
• Working side (non-balancing) interferences: occur on inner aspects of the LINGUAL cusps of
maxillary molars.

• Protrusive interferences-generally occur between the DISTAL inclines of the FACIAL cusps of
maxillary posterior teeth and MESIAL inclines of FACIAL cusps of mandibular posterior teeth. The
proximity of the teeth to the muscles and oblique vector of the forces, makes contacts between
opposing posterior teeth during protrusion potentially destructive. The purpose of making a record
of protrusive relation is to register the condylar path and to adjust the condylar guides of the
articulator so they equal the patient's condylar paths.
• The "protruded contact position" is symmetrical, and the underside of the meniscus (articular
disc) moves distally relative to the superior surface of the mandibular condyle. The condyle moves
forward and carries the disc with it.
• Protrusive Movement-accomplished when the mandible is moved straight forward until the
maxillary and mandibular incisors contact "edge-to-edge". This movement is bilaterally
symmetrical in that both sides of the mandible move in the same direction. The mandible
can protrude -1 Dmm.
• In a protrusive condylar movement (protrusion), interferences can occur between DISTAL
inclines of maxillary posterior cusps and MESIAL inclines of mandibular posterior cusps.
• In a protrusive movement, the mandibular condyles move in a DOWNWARD &FORWARD direction.
• During protrusive movement, there are occlusal contacts occurring on the maxillary distal inclines
and mandibular mesial inclines. Anteriorly, the facial surface of the mandibular incisors will
contact the guiding inclines (lingual) of the maxillary incisors and canines.
• In any restorative case involving ALL teeth in the mouth, the protrusive condylar path inclination
will have its primary influence on the same inclines (distal of maxillary & mesial of mandibular) .
• The pathway followed by the anterior teeth during protrusion may not be smooth or straight
because of contact between the anterior teeth and sometimes the posterior teeth.

• Centric Interference (Forward Slide)-is corrected by grinding MESIAL INCLINES of maxillary teeth
and DISTAL INCLINES of mandibular teeth.

• This group function of teeth on the working side evenly distributes the occlusal load. While, the
lack of contact on the non-working side prevents those teeth from receiving destructive, obliquely
directed forces found in non-working interferences, and saves the centric holding cusps (i.e.
mandibular buccal cusps and maxillary cusps) from excessive wear. The advantage is the
maintenance of the occlusion.

MUTUALLY PROTECTED OCCLUSION ("CANINE GUIDED" OR ORGANIC OCCLUSION)-

the most widely accepted arrangement of occlusion. Achieved when the anterior teeth protect the pos-
terior teeth in all mandibular excursions.
• With Canine ("Cupsid Protected Occlusion") CANINES ideally provide the predominant guidance
through the full range of movement in lateral mandibular excursions.

• Canine Guidance is an occlusal relationship exists where the vertical overlap of maxillary &
mandibular canines causes disclusion (separation) of ALL posterior teeth when the mandible
moves to either side. All other teeth do not contact once they move from CR. If there is contact of
other teeth, "working side" or "non-working side" interferences occur depending on which side the
mandible moves towards.

• When placing a crown on a maxillary canine, if you change a canine protected occlusion to group
function, you increase the chance for "non-working side" interferences to occur.

ANTERIOR GUIDANCE (ANTERIOR COUPLING) -the result of horizontal & vertical overlap of
anterior teeth. It is a tightly overlapping relationship of opposing maxillary and mandibular incisors
and canines that produce DISCLUSION of the posterior teeth when the mandible protrudes and
moves in lateral excursion. Anterior guidance also affects the surface morphology of posterior teeth.
The greater the overlap, the longer the cusp height.

347
 INCISAL GUIDANCE - a measure of the amount of movement and the angle at which the lower inci-
sors and mandible must move from the overlapping position of centric occlusion to an edge-to-edge
relationship with the maxillary incisors. Incisal guidance is the second end-controlling factor in ar-
ticulator movement and is to some degree, under the dentist's control. Influencing factors are es-
thetics, phonetics, ridge relations, arch space, and inter-ridge space.

• Esthetics &phonetics are the main factors the LIMIT a dentist's control of incisal guidance.

• Incisal guidance on the articulator is the mechanical equivalent of horizontal and vertical overlap.

• Right and left condylar mechanisms are the other end-controlling factors in articulator movement.

SUPPORTING CUSPS ("STAMP CUSPS" OR "CENTRIC CUSPS") - these cusps contact the
opposing teeth in their corresponding F-L center on a marginal ridge or fossa. These cusps are more
robust and better suited to CRUSH food.

• When posterior teeth are in a normal ideal relationship, maxillary lingual cusps + mandibular buccal
cusps are considered the SUPPORTING CUSPS.

• Centric stops-areas of contact that a supporting cusp makes with opposing teeth (i.e. the ML cups
of the maxillary 1st molar (a supporting cusp) makes contact with the central fossae (centric stop)
of the mandibular 1st molar.

• 5 Characteristics of Supporting Cusps:

1. contact the opposing tooth in the intercuspal position .
2. support the vertical dimension of the face.
3. are closer to the F-L center of the tooth than non-supporting cusps.
4. their outer incline has a potential for contact.
5. have broader, more rounded cusp ridges than non-supporting cusps.

NON-SUPPORTING CUSPS ("GUIDING" OR "SHEARING" CUSPS) - maxillary buccal (fa-

cial) cusps + mandibular lingual cusps. These cusps overlap the opposing tooth without contacting
the tooth and have narrower and sharper cusp ridges that serve to SHEAR food as they pass close to
the supporting cusp ridges during chewing strokes.
• The inner occlusal inclines leading to the guiding cusps are "guiding inclines" because in contact
movements, they guide supporting cusps away from the midline. Thus, there are the bucco-occlusal
inclines (lingual inclines of buccal cusps) of the maxillary posterior teeth, and the linguo-occlusal
inclines (buccal inclines of lingual cusps) of the mandibular posterior teeth.

IMPORTANT: In a posterior cross-bite situation, supporting and guiding cusps are opposite. The
maxillary buccal and mandibular lingual cusps are now the supporting cusps and the maxillary lingual
and mandibular buccal are the guiding cusps.

SElECTIVE GRINDING - the reduction of occlusal interfences usually done BEFORE construct-
ing a fixed bridge or denture for a patient to PREVENT duplicating the deflective occlusal contacts
in the final restoration. The purpose of selective grinding is to remove all interferences without
destroying cusp height. Thus, when interferences exist in centric, but not in lateral excursions, the
fossa or marginal ridge opposing the premature cusp is deepened. It is important that whenever a pre-
maturity is found, the occlusion be checked in all centric positions before any adjustment is made. If
cusps interfere with each other in excursions, then only the non-holding cusps are ground to prevent a
decrease in VOO.

• Acommon case where it is preferable to selectively grind AFTER a fixed bridge or RPO is in place is
when a FPO or RPO is to be constructed for a space over which the opposing tooth has extruded
slightly. The bridge or partial is frequently constructed to the ideal plane of occlusion and the opposing
tooth is adjusted after insertion.

348
• The most common complaint after cementation of a fixed bridge is sensitivity to hot & cold and
indicates a deflective occlusal contact. The involved teeth may be sensitive to touch and when
brushing. In these cases, an immediate correction of occlusion must be made.

• Important: if you plan on changing a patient's vertical dimension using crowns, it is critical to mount
the casts on the true hinge axis (face bow).

With Selective Grinding in Complete Denture Fabrication in Centric Relation (CR):

• Secondary centric holding cusps are the mandibular buccal cusps. Grind these cusps only if there is
a balancing side interference.

• Primary centric holding cusps are the maxillary lingual cusps. Never grind these cusps.

• Ideally, selective grinding should result in harmonious cusp-fossa contacts of all upper and lower
fossa (and marginal ridges of premolars). Do NOT grind the upper lingual or lower buccal cusps.
Aforward slide from CR can be corrected by grinding the mesial inclines of maxillary teeth and distal
inclines of mandibular teeth.

• Selective grinding of inner inclines of secondary centric holding cusps is done if a balancing (non-
working) side interference exists.

• Only grind cusp tips on maxillary buccal &mandibular lingual (BUll) cusps if they are premature
in centric, lateral, or protrusive movements. Check before grinding.

• Selective Grinding in Working Side (non-balancing side) Relation: the rule for selective grinding
interferences during working side movements follows the rule of BUll (buccal cusp inner inclines of
upper teeth & lingual cusp inner inclines of lower teeth).

• Selective Grinding in Non-Working Side (balancing side) Relation: grind the inner inclines of
mandibular buccal cusps, and NEVER grind maxillary lingual cusps (primary centric holding cusps).
You can only reduce the maxillary lingual cusp if it is high in centric and other occlusal positions,
however in reality you should not.

FUNCTIONALLY GENERATED PATHWAY TECHNIQUE - a prerequisite for using this technique

to restore a single tooth is to have optimal occlusion. A major difficulty for the dental lab technician is
to determine the dentition's cuspal movements using hand-held casts or casts mounted on a simple
hinge articulator. Thus, this technique allows cuspal movements of the dentition to be recorded in
wax intra-orally then transferred to the articulator in the form of a static plastic cast ("functional
index"). By registering the pathways of the opposing tooth surfaces during mandibular movements, "c::>
::c
~
this technique enables the lab technician to provide a restoration with an occlusal surface that is less :::c
c::>
likely to incorporate occlusal interferences. ""
c::>
:z:

• The involved tooth should be immobile and the recording material (low-fusing hi-fi wax) retained on
...
:::!
(;)

the prepared tooth, not moving separately during the generation of the FGP wax record. The involved
tooth should have unprepared teeth anterior and posterior to it to serve as reference surfaces for
checking complete seating of the functional core of the working cast. There should be no pre-
operative occlusal interferences and opposing surfaces should be properly restored.

• The functional index becomes a static registration of all movements of the opposing cusps.

• An important consideration in generating this FGPT is that all mandibular motion must be directed
from an eccentric centric position (never the reverse).

• Full case articulation is more universally applicable to obtain occlusal relationships to fabricate a
wax pattern.

349
 N POSTERIOR OCCLUSION CONTACTS IN IDEAL
INTERCUSPAL POSITION (MICP)
Maxillary 1't Premolar:
• Buccal (facial) cusp tip opposes the facial embrasure between their class counterpart (mandibular
I't) and tooth distal to it (mandibular 2nd premolar).
• lingual cups occlude in the distal triangular fossa of the mandibular 1st premolar
• During lateral excursive movements, the facial cusp ridge of the maxillary 1st premolar on the working
side opposes the distal cusp ridge of the 1st premolar and mesial cusp ridge on the 2nd premolar.

Mandibular 1't Premolar:

• Buccal cusp tip occludes in the mesial triangular fossa of the maxillary 1st premolar and distal
marginal ridge of the canine.
• lingual cusp DOES NOT OCCLUDE WITH ANYTHING. It is a very small cusp not really acting
as a guiding cusp will oppose the lingual embrasure between the maxillary canine and
maxillary first premolar.

Maxillary 2nd Premolar:

• Buccal (facial) cusp occludes in the facial embrasure between the mandibular 2nd premolar &
mandibular I't molar.
• lingual cusp occludes in the distal triangular fossa of the mandibular 2nd premolar.

Mandibular 2nd Premolar:

• Buccal cusps occlude in the mesial marginal ridge area (mesial triangular fossa) of
maxillary 2nd premolar.
• lingual cusp opposes the lingual embrasure between the maxillary 1'1 & 2nd premolars.

Maxillary 1't Molar: (5 cusps)

• MB cusp: occludes in MB groove of mandibular 1st molar. MB cusp is the key reference point in the
definition of Class I occlusion.
• DB cusp: occludes in DB groove of the mandibular 1'1 molar. This DB groove serves as an
"escapeway" for the ML cusp of the maxillary 1st molar during non-working excursive movements.
• ML cusp: occludes with the central fossa of the mandibular 1st molar. During non-working, excursive
movements, the ML cups escapes through the DB groove of the mandibular 1't molar.
• DL cusp: occludes with the distal marginal ridge of mandibular 1't molar &mesial marginal ridge
of mandibular 2nd molar.
."
::a
c:>
• Cusp of Carabelli: found on the MESIOLINGUAL aspect of the 1sl molar crown.
~ • Oblique ridge: opposes the developmental groove between DB &0 cusps of the mandibular
::z:
c:> 1sl molar.
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:z:
..,
:::!
en Mandibular 1't Molar: (5 Cusps)
• MB cusp: occludes with the mesial marginal ridge of the maxillary I't molar & maxillary 2nd
premolar's distal marginal ridge .
• DB cusp: occludes in the central fossa of the maxillary 1sl molar.
• 0 cusp: occludes with the distal triangular fossa of the maxillary 1'1 molar.
• ML cusp: opposes the lingual embrasure between the maxillary 1'1 molar and 2nd premolar.
• DL cusp: opposes (fits into) the lingual groove of the maxillary 1st molar.

Maxillary 2nd Molar: (4 Cusps)

• MB cusp: occludes/opposes with the buccal (facial) groove of the mandibular 2nd molar.
• ML cusp: occludes in the central fossa of the mandibular 2nd molar.
• DL cusp: occludes on the distal marginal ridge of mandibular 2nd molar &mesial marginal ridge
of mandibular 3rd molar.

350
Mandibular 2nd Molar: (4 Cusps)
• MB cusp: occludes in the mesial marginal ridge of the maxillary 2nd molar & distal marginal ridge
of the maxillary 1" molar.
• DB cusp: occludes with the central fossa of the maxillary 2nd molar.
• ML cusp: occludes with the lingual embrasure between the maxillary 1st & 2nd molars.
• DL cusp: opposes the lingual groove of the maxillary 2nd molar.

Maxillary 3rd Molar:

• ML cusp: occludes in the central fossa of the mandibular 3'd molar.
• DL cusp: is usually missing.

Mandibular 3rd Molar: (3 Cusps)

• MB cusp: occludes on the distal marginal ridge of the maxillary second molar and on the mesial
marginal ridge of the maxillary third molar.
• DB cusp: occludes in the central fossa of the maxillary third molar.
• ML cusp: occludes in the lingual embrasure between the maxillary second and third molars.

In ideal intercuspation, ML cusps of permanent mandibular molars occlude with the LINGUAL EM-
BRASURE between their class counterpart and the tooth MESIAL to it.

In ideal intercuspation, buccal cusp tips of permanent maxillary premolars oppose the facial em-
brasure between their class counterpart and the tooth DISTAL to it.

All maxillary buccal cusps & mandibular lingual cusps are GUIDING CUSPS. The inner occlusal in-
clines leading to these cusps are called guiding inclines because in contact movements they guide the
supporting cusps away from the midline. Thus, there are bucco-occlusal inclines (lingual inclines of
the buccal cusps) of the maxillary posterior teeth and linguo-occlusal inclines (buccal inclines of the
lingual cusps) of the mandibular posterior teeth.

During mandibular movements (working or non-working), the outer aspects of the lingual cusps of
mandibular molars will NOT contact their maxillary antagonists. All other areas of buccal and lingual
cusps may contact during mandibular movements (assuming all occlusal relationships are normal).

Anterior Occlusion Contact in ideallntercuspal Position (MICP):

• Maxillary Central Incisor-overlaps vertically and horizontally with the mandibular central and lateral
incisors, and its lingual surface is in opposition to them.

• Mandibular Central Incisor-the labioincisal angles opposes the mesial marginal ridge of the
maxillary central incisor and maxillary central's lingual fossa.

• Maxillary Lateral Incisor-overlaps the mandibular lateral & canine, and lingual surface is in
opposition to them.

• Mandibular Lateral Incisor-the labioincisal angle opposes the distal marginal ridge of the maxillary
central, and the mesial marginal ridge of the maxillary lateral, and the lingual fossa.

• Maxillary Canine-cusp tip is in the facial embrasure between the mandibular canine and first
premolar. It's cusp tip does not contact any other tooth.

• Mandibular Canine-cusp tip is in the lingual embrasure between the maxillary canine & maxillary
lateral incisor. It's cusp tip does not contact any other tooth.

Basic Principles of Occlusal Adjustment:

1. The maximum distribution of occlusal stresses in centric relation (CR).
2. Forces of occlusion should be borne as much as possible by the long axis of teeth.
3. When surface-to-surface contact of flat cusps occurs, it should be changed to a "point-to-
surface" contact (the cusp tip of the tooth occludes with the flat surface of it's opposing
tooth's cusp).
4. When centric occlusion is established, NEVER take the teeth out of centric occlusion.

351
 N BENNETI MOVEMENT -lateral translation (sideshift) of the working condyle during lateral excur-
sions. In early stages of right lateral movements, Bennett movement of the condyle refers to the slight
right lateral movement of the right condyle.

• Bennett movement is also called "lateral shift" of the mandible or "immediate side shift" . This
movement influences the MESIODISTAL position of the posterior teeth cusps.

• During right mandibular movement (on the right side/working side), the condyle moves from the
centric position to right working; this is the Bennett movement.

Translation in a mandibular opening movement occurs in the upper compartment of the TMJ.
Muscles involved in closing (elevating) the mouth to centric position : medial pterygoid, masseter,
temporalis. Horizontal load is the most destructive load placed on the periodontium.

BITE REGISTRATION MATERIAl- used to make an accurate interocclusal record should offer a
MINIMUM RESISTANCE to the patient's jaw closure and have LOW FLOW at mixing.

• Recently, addition-reaction silicone impression materials have dominated the interocclusal

record (lOR) market since these materials have VERY LOW FLOW when mixed and become
rigid after setting.

• Historically, the interocclusal was made by placing the lOR material into the mouth and closing the
patient's jaws into the material at the desired relationship. Although this concept is acceptable and
may produce a relatively accurate lOR, the act of closing into any material, regardless of its lack of
viscosity, often causes a deviation of the mandible away from the desired contact position.

Amore desired method to obtain an accurate interocclusal record is:

• Close the jaws into CO (MICP). This is the most interdigitated position) .
• With the teeth tightly occluded, inject the addition-reaction silicone material between the
maxillary and mandibular teeth (only into areas where teeth have been prepared, and not around
the entire arch).
• Advise the patient to place the tongue forward (just short of going between the teeth), thus
making a matrix for the lingual aspect of silicone.
• Let silicone set for -2 minutes.
• Remove the lOR and trim with a sharp knife.
• Mount the casts with the lOR material present ONLY in the areas of tooth preparations.

IMPRESSION MATERIALS
Two types of polymerization (process of changing elastomeric materials from a paste into a rubber-
like material).
1. Addition Polymerization-the formation of polymer without forming any other chemical.
2. Condensation Polymerization-occurs when other chemicals or by-products are produced
that are not part of the polymer.

All impressions must be RINSED and DISINFECTED prior to pouring or sending it to the laboratory.
Soak or spray for at least 10 minutes. Always follow the manufacturer's recommendation for the
specific product.

352
HYOROCOLLOIDS (REVERSIBLE & IRREVERSIBLE) - have the advantage of WETTING NOTES
INTRAORAL SURFACES well, but have very limited dimensional stability because they are
composed of 85% water.
1. Reversible Hydrocolloid (Agar-Agar)-an impression material whose physical state can be
changed from a GEL SOL by applying heat and is reversed back by removing heat. Reversible
hydrocolloids are composed of 85% water, 12-15% agar, traces of borax, potassium sulfate, &
sodium tetra borate. Agar impression materials and dental compounds do not involve a chemical
reaction to set.
• Advantages: Easy to pour, no mixing is required (but a hydrocolloid-conditioning unit is
required). No custom tray is required. Moisture tolerant, clean &pleasant with acceptable
odor, excellent shelf-life, inexpensive.
• Disadvantages: must be poured immediately, finish line is difficult to read, weak in a deep
sulcus, and potentially injurious to the patient if not handled properly. Very limited
dimensional stability.

2. Irreversible Hydrocolloids (Alginate)-an elastic impression material with very limited

dimensional stability.
• Advantages: inexpensive, can use stock tray, easily mixed, and easy to pour.
• Disadvantages: unstable, fragile, may affect the cast surface, and must be
poured immediately.
• Sodium Phosphate-a component found in alginate powder that controls the SETTING TIME of
alginate. The setting time of alginate is controlled by the AMOUNT of sodium phosphate present.
Sodium phosphate acts as a retarder in this reaction (it slows down the process). As long
as sodium phosphate is present, it will react with soluble Ca+ ions. Once all the sodium
phosphate has reacted, then sodium alginate reacts with the remaining Ca+ ions to form
calcium alginate. Sodium alginate + Sodium phosphate + Ca ions calcium alginate. FAST
removal of impression from the mouth increases the compressive &tear strength of
the impression.
• Alginate sets via a chemical reaction. Alginate's setting reaction is a "double decomposition"
reaction between sodium alginate + calcium sulphate. Casts must be poured within 24hrs
and the impression must be kept damp.

GElATION - the setting process of alginate impression materials.

• An increase in the water temperature used in mixing alginate impression materials decreases the
setting time (sets faster). The best method to control the gelation time of alginate is to alter the
water tem perature used in the mix. The higher the temperature, the shorter the gelation time. The
lower the temperature, the longer the gelation time.

• Changing the water/powder ratio and the mixing time alters the gelation time, but these methods also
impair certain properties of the material. Too little or too much water weakens the gel. Undermixing
may prevent the chemical action from occurring evenly; overmixing may break up the gel.

• Calcium Sulfate-the "reactor" in alginate is not very soluble in water and is entirely consumed
before gelation is completed . Thus, the set mass becomes an entanglement of calcium alginate
fibrils around residual sodium alginate sol, fi ller, and water. The residual sodium alginate has the
nasty habit of readily giving up water (synersis) or gaining water (imbibition). For accurate results,
the cast should be poured immediately.

• The setting reaction of alginate is a "double decomposition" reaction. Calcium sulfate + Potassium
alginate are the constituents of alginate that take part in this reaction .

• All set impressions are rinsed with water thoroughly to remove residual saliva from the impression
surface (or rinse with a watery mix of dental stone before pouring up the impression).

• Inaccuracies in impressions can be caused by fracture of the fibrils during gelation .

353
 Alginate Constituents Action %
Diatomaceous Earth 50% (filler)
Potassium Alginate 20% (reactor)
Calcium Sulfate 16% (reactor)
Zinc Oxide 7% (plasticizer)
Potassium titanium fluoride 6% (hardens stone)
Tri-sodium phosphate 1% (retarder)

• When taking an alginate impression, if the impression material appears grainy, it is mostly likely
caused by improper mixing, prolonged mixing, or too low water-to-powder ratio.

• Under-mixing and over-mixing alginate can reduce the impression's strength.

• Alginate has a long 24-48 month shelf-life.

• After taking alginate impressions, if you place the impressions in a bowl of water for a few hours to
try and prevent them from drying up before pouring the casts, IMBIBITION can occur (the impressions
absorb water and expands). When imbibition occurs, the impression is no longer accurate.

• Shrinkage occurs in alginate impressions even when placed under 100% relative humidity =
SYNERESIS (occurs when exudate like droplets of the liquid medium forms on the impression surface).
Since shrinkage is undesirable (causes distortion of impressions), alginate impressions should not
be left in water (causes expansion) or exposed to air (causes shrinkage). Impressions should be
poured immediately to ensure accuracy. When immediate pouring is not possible, alginate
impressions can be stored only briefly in a moist paper towel.

Techniques to help prevent GAGGING while taking alginate impressions:

• Decrease the time to take an impression.
• Have the patient breathe through their nose.
• Seat the patient in an upright position.
• Seat the posterior part of the tray first. Mixing the alginate rapidly causes it to set more rapidly.
• Decreasing water-to-powder ratio causes alginate to set faster (affects mix consistency as the mix
is much thicker when less water is used).
• DO NOT use cold water to mix the alginate because it retards alginate's setting time.

Mandibular alginate impression is taken FIRST since gagging is more likely to occur while taking the
maxillary impression. For the maxillary impression, seat the posterior portion of the tray first, then
the anterior portion to help prevent alginate from being squeezed out of the tray back toward the pa-
tient's throat. Always remove alginate impressions in one quick movement with a snap to help de-
crease permanent deformation. Do not over-seat the tray (0.25 inch) minimum of alginate should
remain over all critical structures (especially occlusal surfaces).

When taking an alginate impression, it is advised that the tray be placed in the mouth after all critical
areas are wiped with alginate. Critical areas are buccal to the maxillary tuberosities and retromylohyoid
space. Rest seats and guide planes should be covered with alginate and any other soft tissue undercuts.

When taking alginate impression for a RPD, it is best to apply some alginate directly on the teeth to
eliminate bubbles and saliva from the rest seat preparations.

354
ElASTOMERS - impression materials with elastic or rubber-like qualities used for crown &
bridge, secondary impressions for dentures, and inlays/onlays. When removing elastomeric impres-
sions, use steady force (a snap is not required) to minimize permanent deformation. Elastomers set
via a chemical reaction. Elastomers are NON-AQEOUS polymer-based rubber impression materials
with good elasticity.
1. Polysulfides (Rubber Base, Mercaptan, Thiokoll-the base contains a liquid polysulfide polymer
(mercaptan polymer) mixed with an inert filler. The accelerator is usually lead dioxide. When these
two pastes are mixed, the polymer chains are lengthened and cross-linked through oxidized thiol
groups to form a rubber-like material.
• Atray for a polysulfide rubber impression that lacks occlusal stops may result in an
inaccurate final impression because of permanent distortion during polymerization.
• Permalastic (Kerr), Coe-Flex (Coe), & Omniflex (Coe).
• Polysulfide rubber base impression materials require a custom tray for impression making to
control polymerization shrinkage by using a uniform thickness of impression material.

Polysulfide Rubber Base Properties:

• Sets in 12-14 minutes (the longest setting time).
• Moisture tolerance in the mouth is acceptable.
• Wettability with gypsum is poor, and it has poor taste and odor.
• Polysulfide has an IS-month shelf-life.
• polysulfide polymerization of is exothermic and accelerated by an increase in temperature or humidity.
• Polysulfides have good flow properties and high flexibility and tear strength. Polysulfides have
the strongest resistance to tearing, but impressions can distort when removed from areas where
deep undercuts exist. Polysulfides have a long working time and relatively long polymerization time,
which may add to patient discomfort. They have a low resistance to deformation .
• Lead dioxide-the accelerator responsible for the brown color and difficulty in cleaning clothes that
contact this polysulfide impression material.

2. Silicones (Condensation Silcone or Convention Silicones}-the base is a liquid silicone polymer

(dimethyl siloxane) mixed with inert fillers. The reactor consists of cross-linking agent (ethyl
ortho-silicate) and activator (tin octoate). The materials are cross-linked by a reaction between
terminal hydroxyl (OH) groups on the polymer and ethyl ortho silicate. Ethyl alcohol is a by-product
of the setting reaction . The evaporation of this alcohol causes the shrinkage of the material and
resultant poor dimensional stability. Ex: Elasticon (Kerr) & Xantopren (Unitek).
• Condensation silicone has a very poor dimensional stability because the principal reaction
that occurs during setting is a condensation reaction via elimination (evaporation) of ethyl
or methyl alcohol. This evaporation is also responsible for shrinkage of the material and
resultant poor dimensional stability. .."
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• Advantages: no special equipment required, moderate strength in deep sulcus, finish line easy c
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so have poor moisture tolerance (no moisture allowed in sulcus), difficult to electroplate, and
requires special care when pouring.
• Low permanent deformation, fair tear-strength, lowest temperature rise (reaction is sensitive
to heat & moisture which reduces working and setting times), medium stiffness, very poor
wettability by gypsum.
• Mixing time (30-60 seconds); moderate working time (2-4 min); long setting time (6-10 min).
Do not mix initially by hand (allergic reaction to catalyst may occur).
• Silicone impression materials have a "putty/reline" form allowing delayed pouring of up to
6 hours. Silicones record surface detail well and have excellent elastic properties. Silicones
require being poured immediately after being removed from the mouth (except putty/reline
forms). They use a "heavy-bodied" putty for the first step of the impression, which becomes a
custom tray for the second step "wash" impression (a thin relining impression) developed
specifically to overcome the dimensional stability problems. 75% of its content is silica (filler)
which is twice the amount present in wash-impression material. This results in lower
dimensional change in the bulk of the material.
• The best reason for pouring a condensation impression material ASAP is because
evaporation of a volatile by-product causes shrinkage of the set material.

355
 NOTES 3. Polyvinyl Siloxanes (Additional Silicones or Vinyl Polysiloxanes}-one tube contains silicone with
terminal silane H+ groups and an inert filler. The other tube is a vinyl silicone with terminal vinyl
groups, chloroplatinic acid catalyst, and filler. Upon mixing, there is an addition of silane
hydrogen groups across vinyl double bonds and does not form by-products, resulting in a very
dimensionally stable material. PVS can be poured up to 1 week.
• Latex gloves should not be worn when mixing polyvinyl siloxanes because sulfur in the latex
retards the setting of addition silicone materials. Sulfur in ferric and aluminum sulfate
reaction solution may also inhibit polymerization of PVS. Some latex gloves might inhibit the
setting of polyvinyl siloxane.
• Mixing time (30-45 sec), Moderate working time (2-4 min); moderate setting time (6-8 min) .
• Excellent dimensional stability and very low permanent deformation.
• Poor tear strength, lowest temperature rise, very high stiffness, very poor wettability by gypsum .
Addition silicones are temperature sensitive (increases in temperature shorten working &
setting times).
• Easy to mix, easy to clean-up, and acceptable odor and taste.
• Polyvinyl siloxanes are the MOST WIDELY USED &MOST ACCURATE elastic impression
materials. They have less polymerization shrinkage, low distortion, fast recovery from
deformation, and moderately high tear strength. Most PVS can be poured up to 1 week after
impression making and are stable in most sterilizing solutions.
• Reprosil (Caulk), President (Coltene), &Permagum (Espe) are types of PVS.

4. Polyethers (Impregnum/Premier &Polygel (Caulk}-are two component materials. The rubber

base includes a polyether polymer with ethylene imine groups, silica filler, and plasticizer. The
accelerator contains a cross-linking agent (aromatic sulfonic acid ester) which produces
cross-linking by cationic polymerization. When mixed, a rubber forms by a cationic
polymerization process.
• Advantages: excellent dimensional stability (when dry), clean, pleasant taste & odor, FAST
SETTING, dimensionally stable if more than one cast is poured, stable even if poured 24hrs after
taking an impression (very low permanent deformation) as it can be poured up to 1 week, and
are truly hydrophilic which results in superior wettability by gypsum. Polyether impression
material tolerates moisture better than any other elastomer.
• Disadvantages: the most difficult material to remove from the mouth (the most rigid/stiff
materia!), tears easily (poor tear strength), may adhere to teeth, high water absorption
(dimensionally unstable in the presence of moisture), and fine margins may break. Compared
to other materials, the main disadvantage of using polyether elastomeric impression
materials is they are much stiffer. Has the highest temperature rise and highest stiffness.
• Polyethers have the SHORTEST WORKING &SETTING TIMES of the elastomeric impression
materials. Mixing time is 30-45 seconds (mixes easily); Working time is 2-3 minutes; Setting
time 6-7 minutes.
• All elastomeric impression materials CONTRACT SLIGHTLY during setting (they do not expand).
• Polyethers set in 5-6 minutes.
• For best results when using an elastomeric impression material, the prepared tooth should be
free of surface moisture.
• Compared to hydrocolloids, elastomeric impression materials are easier to prepare, more
resistant to tearing upon removal, and have a superior dimensional stability.
• Custom Trays are an important part of rubber base impression techniques since elastomers
are more accurate in uniform thin layers that are 2-4mm thick. With all elastomers, a
custom tray should be fabricated with a plastic material, should be rigid, have occlusal
stops to avoid permanent distortion during polymerization, and be coated with an adhesive
that should dry completely before taking the impression to prevent the impression material
from pulling away.
• With hydrocolloid impressions (alginate), a greater bulk of material produces greater accuracy,
however the thickness of rubber-like (elastomeric) materials should be less and be
evenly distributed.
• Custom trays are recommended because they require less impression material and facilitate
uniform concentration of the impression materials. Stock trays are usually short in the flange
area and the uneven bulk of the impression material is conducive to distortion.
• The accuracy and reliability of an elastic impression is controlled by the custom tray in which
it is taken. The best custom tray is custom -made for each patient. In most cases, it is best to
take a complete arch impression to provide maximum reliability.
356
ZINC OXIDE-EUGENOl- an impression paste whose setting time is accelerated by ADDING a
drop of water to the mix. To retard the setting of ZOE, add inert oils (olive or mineral oil) during mix-
ing. ZOE sets via a chemical reaction.
• Advantages: can record soft tissue at rest, sets hard in 5 minutes, stable, & less expensive than
polysulfides.

• Disadvantages: messy to mix, very sticky, tissue irritant, not elastic, difficult to manipulate, not
recommended for gagging patients.

• ZOE pastes differ from elastic impression materials because they SET HARD in the mouth, so do NOT
use it if there are deep undercuts of soft tissues).

• ZOE's dimensional stability is most likely affected by failing to use a custom impression tray.

• If the paste is too thin or lacks body prior to setting, a filler (wax or inert powder like lanolin or kaolin)
can be added to one or both of the original pastes.

• One of the dentally useful chemical reactions is between zinc oxide + eugenol. Under proper
conditions, a relatively hard mass forms that possesses certain medicinal advantages and
mechanical usefulness in certain dental operations.

• The basic composition of these materials (whether it be a cementing medium, surgical dressing,
temporary filling material, or impression paste) is the same (mainly zinc oxide, eugenol, & resin).
Plasticizers, fillers, accelerators, and other additives are incorporated as needed to provide the desired
properties for the particular use of the product.

• ZOE's setting reaction is a typical ACID-BASE REACTION to form a CHELATE. This reaction can occur
in a solution or at the surface of the zinc oxide particles. The chelate forms as an amorphous gel that
crystallizes to impart increased strength to the set mass.

Other ZOE Impression Paste Components:

1. Rosin-facilitates the speed of the reaction and a smoother, more homogenous product results.
2. Calcium Chloride (CaCI2)-the accelerator in ZOE that "accelerates" the setting time. Moisture
(H20) also accelerates ZOE's setting time.
3. Oil of Cloves-contains 70-85% eugenol and is sometimes used in preference to eugenol because
it reduces the burning sensation in the oral soft tissues.
4. Mineral Oil or Fixed Vegetable Oil-the PLASTICIZER in ZOE that helps mask the action of
eugenol as an irritant. "'tJ
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1. Grainy Material: caused by improper or prolonged mixing, undue gelation, or too Iowa -t
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water-powder ratio.
2. Tearing of Material: caused by inadequate bulk, moisture contamination, premature
removal from the mouth, or prolonged mixing.
3. Irregularly Shaped Voids: due to moisture or debris on tissue.
4. Rough or Chalky Stone Cast: caused by inadequate cleaning of the impression, excess water
left in the impression, premature removal of the cast, leaving the cast in the impression too long,
or improper manipulation of stone.
5. Oistortion: impression not poured immediately, movement of tray during gelation, premature or
improper removal from the mouth, or tray was held in the mouth too long (only with
certain brands).

357
 N GYPSUM
GYPSUM - sets via a chemical reaction.
• All gypsum products are weaker in tensile strength than compressive strength.
• AU gypsum products that are reacted with water form calcium sulfate dehydrate as a
reaction prod uct.
• All gypsum produces come from the mineral gypsum (the dihydrate form of calcium sulfate). During
heating (the gypsum manufacturing process), water is lost and gypsum is converted into the
hemihydrate form of calcium sulfate (powder) . When water is added to the powder, a chemical
reaction occurs and the hemihydrate is converted back into the dihydrate form of calcium sulfate.

Classification of Dental Gypsum Products

ADA Specification Traditional Name

Type I (Plaster Impression) 1m pression Plaster
Type II (Plaster, Model) Model or Lab Plaster
Type III (Dental Stone) Class I Dental Stone
Type IV (Dental Stone, High Strength) Class II Stone or improved stone (die stone)

Type I: rarely used today.

Type II: used to make casts when strength is not important (orthodontics).
• Dental Model Plaster (Type II)-heating gypsum in an open kettle. This process produces porous and
irregularly-shaped particles. Dental plaster is the WEAKEST GYPSUM PRODUCT.

Type III: used for preparing casts of an alginate impression upon which dentures are processed.
• Dental Stone (Type liD-produced by HEATING GYPSUM under pressure with water vapor in an
autoclave. This process produces uniform-shaped and less porous particles. Heating gypsum in a
30% solution of calcium chloride produces high strength (improved) die stone. This process
produces the least porous and strongest particles.

Type IV: used when making stone "dies" (reproductions of teeth with prepared cavities) used for crown
and bridge, and operative (inlays and onlays).

"'0 Dental plaster &stone is vibrated when poured after mixing to ELIMINATE AIR BUBBLES (trapped
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water + ground-up set gypsum particles to mix with plaster or stone all cause gypsum to set faster.
• Once the impression is poured, it should harden for 45min-l hr (or until cool to the touch) before
removing the cast from the impression . If nodules of stone appear in occlusal pits of a stone cast,
it is usually due to entrapment of air during the insertion and seating of the tray.

Dental Stone &Dental Plaster have a slightly different principal component (Calcium Sulfate Hemi-
hydrate). The main constituent of dental plasters and stones is Calcium Sulfate Hemihydrate.
• Depending on the method of calcination, different hemihydrate forms are obtained (alpha or beta) .
Dental stone has Alpha-hemihydrate, while dental plaster has Beta-hemihydrate (Plaster of Paris).

• Beta-hemihydrate (Plaster of Paris}-crystals characterized by their sponginess &irregular shape.

Requires more water to float its powder particles so they can be stirred, since the crystals are more
irregular-shaped &porous.

358
• Alpha-hemihydrate-prismatic-shaped dental stone crystals that are more dense than beta-
hemihydrate crystals. When alpha-hemihydrate is mixed with water, the dental stone/die product
obtained is much stronger and harder than beta-hemihydrate (plaster). The main difference in
strength is alpha-hemihydrate powder (stone) requires much less gauging water when mixed than
beta-hemihydrate.

Principal difference between dental plaster &dental stone powders is PARTICLE SIZE &SHAPE. As
stated above, dental gypsum products are made of hemihydrate particles whose size, shape, and
porosity differ for each material. These gypsum-based powders require different amounts of water
for mixing because the different particle shapes produce different packing efficiencies that affect the
amount of excess water required for making a suitable mixture. Mixing Factors:

• Water-Powder Ratio: this is an important factor in determining physical properties. When a high
proportion of water is used, the powder particles are farther apart, resulting in less expansion with
a retarded setting time and weaker product. Dental plaster requires 2x more water has a higher
setting expansion than dental stone.
• When mixing gypsum products always SPRINKLE the powder into the water to produce better
powder mixing and to reduce air bubbles.
• When gypsum products are mixed with water, heat is given off (exothermic reaction) .
• Exposure of a stone cast to tap water should be minimized to prevent eroding of the cast.

• Water Temperature: colder the water, the LONGER setting time.

• Spatulation: rapid spatulation for a time equal to normal hand mixing for 1 minute accelerates
setting time and produces the greatest strength. Do not spatulate to a point where the stone
thickens to prevent producing a much weaker cast.

• Accelerators & Retarders (Modifiers):

• Accelerators: potassium sulfate, sodium chloride (NaCI), & alum (aluminum potassium sulfate).
• Retarders: borax and sodium citrate.

When placing packing cord around a tooth prepared for a crown on a patient with HYPERTENSION,
it is recommended to use a cord impregnated with ALUM (aluminum potassium sulfate).
• EPI causes local vasoconstriction, resulting in transitory gingival shrinkage. EPI impregnated cord
produces minimal physiologic changes when placed in an intact gingival sulcus. However, evidence
of increased HR and BP when the cord is applied to the severely lacerated gingival sulcus. For those
patients with medical conditions (i.e. cardiovascular disease, hyperthyroidism, or known
hypersensitivity to EPI), a cord impregnated with ALUM should be substituted.

• Zinc Chloride-is caustic and causes delayed healing (necrosis of sulcular epithelium &adjacent
layer of C.l), thus, should not be used in impregnated retraction cord.

• Tissue retraction-necessary to control bleeding, retract gingival tissues slightly away from crown
margins, allow impression material to flow into the sulcus, and to expose all gingival margins.

359
 NOTES Temporary Restoration Requirements:
1. provides pulpal protection: restoration must be fabricated from a material that prevents
conduction of temperature extremes.

2. positional stability: the tooth should not extrude or drift.

3. occlusal function: the temporary's ability to function occlusally aids in patient comfort &
preventing tooth migration.

4. easily cleaned: the temporary must be made of a material and contour that the patient can
keep clean.

5. non-impinging margins: it is VERY importance that the temporary's gingival margins do not
impinge on the gingival tissues to prevent inflammation that can cause hypertrophy, gingival
recession, etc. The margins should be well polished.

6. strength and retention: temporary must withstand the forces it is subjected to without
breaking or coming off.

7. esthetics: if the temporary is on an anterior tooth, it must provide a good cosmetic result.

After preparing a tooth for a dowel core, it is difficult to fabricate a provisional restoration for a tooth
prepared for a dowel crown because there is so little intact supra-gingival tooth structure remaining.
To best serve the purpose of a provisional restoration, place a piece of paper clip or stiff wire into the
canal and put a resin-filled polycarbonate crown over it.

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360
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361
 NOTES CEMENTS (LUTING AGENTS)

Glass lonomer Cements {GIC} - are hybrids of silicate and polycarboxylate cements designed to
combine the fluoride releasing properties of silicate particles with the chemically adhesive and more
biocompatible characteristics of the polyacrylic acid matrix compared to the extremely acidic matrix of
silicate cement. GICs are mixed powder-liquid component systems. The powder (calcium-
aluminofluorosilicate glass) reacts with a liquid (polyacrylic acid) to form a cement of glass particles
surrounded by a matrix of fluoride elements.
• Advantages of GIC:
• Releases fluoride (anti-cariogenic). Upon setting, GICs can inhibit recurrent caries
development at its margins because it releases fluoride from its surface. GIC can also absorb
fluoride when local ionic concentrations are high, then slowly release fluoride when the
environment concentration decreases, thus acting as a FLUORIDE SPONGE.
• Chemical adhesion to the prepared tooth and certain materials. Micromechanical bond to
composite resins.
• High biocompatibility, thus with enough dentin remaining (.5-1mm) no pulpal protective agent
(calcium hydroxide) is required .
• Good thermal insulators (equal to natural dentin).Thermal expansion is similar to that of tooth
structure.
• After the initial setting period, GICs have low solubility in the mouth. It is the least soluble
cement (compared to zinc phosphate and zinc polycarboxylate cements).

• Disadvantage: has a higher cement film thickness than zinc phosphate cement.

• Only GIC is used as a cement (luting agent) and as a permanent restorative material. GIC are
often used for root surface carious lesions (Class Vrestorations) because of the potential advantage
of fluoride release to help control the spread of caries. GIC is used as a luting agent and for Class
V restorations with composite "sandwich technique".

1. Glass ionomer cements are composed of aluminosilicate powder and polycarboxylate liquid.

Classification of GICs:
1. Conventional GIC-used as a luting agent. Ex: Ketac-Cem.

2. Light-cured GIC-used as a liner or base (the liquid version has HEMA added to it). Advantages:
extended working time, short on-demand setting times, as a set mass it is stronger, more
adhesive, and more resistant to desiccation than self-cured glass ionomers. Ex: Vitrebond &
XR lonomer.

3. Resin-Modified (Hybrid) Light Cured GIC-used for any application where glass ionomers are
good choices (the liquid has HEMA added to it). Ex: Fuji-II LC.
• Advantages of hybrid light cured ionomers are esthetics, bond strength, and coefficient of
cc
,..., -c thermal expansion.
:z: ,...,
..... =
c;;:=
..... -
=<
-< ,...,
Glass lonomer Restorations: both self-cured and light cured versions of GI restorations are available .
Light-cured glass ionomers are preferred because of extended working time and their improved physical
properties. Due to their limited strength and wear resistance, GI restorations are indicated to restore
low stress areas where caries activity potential is a significant concern.
• Are moderately esthetic, but do not polish as well as composites.
• Material of choice for restoring root surface caries in patients with high caries activity.
• Best surface finish for a glass ionomer restoration is obtained against a surface matrix.
• Adheres to mineralized tooth tissue.
• Glass ionomers have a lower compressive strength, tensile strength, and hardness than resin
composites. They are very technique sensitive due to their high solubility when first mixed. However,
with newer hybrid or light-cured resin-modified glass ionomers, these properties have been improved .

362
Glass ionomers are considered the nearly ideal base or liner material because of these properties:
• Adhesive bond to tooth structure.
• Snap set in the light-cured form (i.e. Vitrebond) .
• Anti-cariogenic due to fluoride ion release.
• Bond to composite. They make excellent liners for Glass V root caries restorations or "sandwich
technique" which achieves all the benefits of the GIG plus high polishability, surface hardness, and
strong bond to enamel of the composite resin.

Zinc Oxide-Eugenol Cements (ZOE) - a soft, sedative type cement used as a SEDATIVE or
TEMPORARY filling material, as an insulative base, and in interim caries treatment. Eugenol has a
palliative effect on the pulp which is one of the main advantages of using ZOE cement.
• Powder is zinc oxide and the liquid is eugenol. A conventional mixture of zinc oxide + eugenol is
relatively weak. Recently, "reinforced" or "improved" ZOE cements have been introduced ("Reinforced
ZOE or ZOE-EBAJ. The particles of the zinc powder are surface treated to produce better bonding of
the particles to the matrix.

• ZOE is soluble in oral fluids and is difficult to remove from cavity preparations. ZOE is used as a
base, temporary restoration, and as a cement (luting agent).

• ZOE, "reinforced" ZOE, ZOE-EBA, silicate, & zinc silicophosphate cements are no longer routinely
used to permanently cement restorations.

• When considering ease of cementation, the reinforced ZOE cements are preferred to zinc phosphate
because they do not require use of a varnish for pulp protection (zinc phosphate is very acidic).

2. Properties of improved zinc oxide-eugenol materials: they provide excellent marginal seal,
have a palliative effect on the dental pulp, and are easily removed from the cavity preparation.
They do NOT have thermal insulation qualities that compare to dentin.

• ZOE Contraindications:
• On dentin or enamel prior to bonding because it compromises bonding.
• As a base or liner for composite resins as eugenol interferes with composite polymerization.
• Patient's allergic to eugenol or "oil of cloves" as this is fairly common .
• Direct pulp capping as eugenol is a pulpal irritant when in direct pulpal contact.
• Zinc oxide-eugenol cannot be used under composite materials.

4 Types of Zinc Oxide Eugenol (ZOE) Materials:

1. Type I ZOE: temporary cement.
2. Type II ZOE: permanent cement.
3. Type III ZOE (Reinforced ZOE): a temporary filling material (lRM) and thermal insulating base.
The powder is composed of zinc oxide and finely divided polymer particles (polymethyl-
methacrylate) in the amount of 20-40% by weight. The zinc oxide powder is surface treated by
an aliphatic monocarboxylic acid like propionic. Eugenol is the liquid. This combination of surface
treatment + polymer reinforcement results in a material that has good strength and toughness co
rn -a
which markedly improves abrasion resistance. Good for basing large and complex cavities as :z: rn
..... ::<I
it withstands the pressure of amalgam condensation, with minimal effect on the pulp. c;:;~
..... -
::<1<
4. Type IV ZOE: a cavity liner. -< rn

Basic composition of all ZOE materials (whether a cementing medium, surgical dressing, temporary
filling material, or impression paste) is zinc oxide, eugenol, &resin. Plasticizers, fillers, accelerators,
and other additives are incorporated as needed to provide desired properties for the particular use of the
product.

363
 N Zinc Phosphate Cement: the oldest luting cement with the longest "track record" serving as the
standard to which newer systems can be compared. It is a powder-liquid system. The powder is mainly
zinc oxide, while the liquid is orthophosphoric acid.
• Its primary use is as a cement (luting agent) for cast restorations. It is also used as a base when
high compressive strength is needed. The initial mixture of ZPC is very acidic (pH 3.5), thus it can
cause irreversible pulpal damage if a cavity varnish (2 coats) is not placed on the tooth prior to
cementing the crown.

• If a zinc phosphate cement base is used when restoring a tooth, the varnish is applied PRIOR to
placing the base. The use of a base in conjunction with amalgam or gold foil does not alleviate the
need for a varnish as an aid in sealing the cavity margins against leakage. However, the type of base
governs the order of applying the varnish and base. If a zinc phosphate cement base is used , then
the cavity varnish is applied to the cavity walls PRIOR to placing the base. However, if a biocompatible
agent (i.e. calcium hydroxide, ZOE, or polycarboxylate cement base is used, then these are placed
against dentin, and the varnish is not applied until the base material has hardened. The varnish
reduces the initial microleakage of an amalgam restoration .

• ZPC is used as a luting agent (cement) for gold restorations and orthodontic appliances, and as
a base under certain restorations.

• ZPC may also be used as a liner when a particularly strong one is needed. It should always be
preceded by at least 2 coats of cavity varnish to prevent pulpal irritation. Can be used under
composite materials.

• ZPC has been extensively replaced by polycarboxylate or GIC. These cements are based on ion-
cross linked polyacrylic acid matrices with the potential to react chemically with residual powder
particles and the tooth structure surface.

• ZPC has superior strength compared to other cements, and its retention depends on mechanical
interlocking (as opposed to GIC and polycarboxylate cements which adhere to tooth structure by the
polyacrylic acid in the liquid).

• ZPC liquid that has lost some of its water content causes the setting time of the mix to increase
(slows setting) . ZPC shrinks slightly upon setting. Mixing ZPC very rapidly decreases the cement's
final compressive strength.

• Clean zinc phosphate cement from crown margins after the cement is completely set.

• When mixing ZPC, a cool glass slab is used to increase the powder-liquid ratio. Acool mixing slab
should be used (caution: the slab's temperature should not be below the dew point of the room).
Mixing should be started by adding a small amount of powder to the liquid. This procedure, along
with the cool slab, increases the cement's working time. Advantages of using the cool slab
method: substantial increase in working time of the mix on the slab, and shorter setting time of
the mix after placement in the mouth.
....
CJ CJ
:z:
..."
....
..... ::c
Vi!!i
..... - • Small increments of powder are added - every 20 seconds with vigorous mixing until a creamy
::c -< consistency is achieved to promote a high powder-liquid ratio and superior cementation medium by
-< ....
providing a lower viscosity of the mix, stronger final set, and lower solubility of the set cement.

• Zinc phosphate cements provide good pulpal protection from thermal, electrical, and pressure
stimuli, but can damage the pulp due to its initial acidic/low pH. However, this can be beneficial
since it provides an anti-bacterial effect which reduces the number of viable microorganisms in the
cavity floor, thus decreases pulpal irritation.

3. Factors that govern setting rate of zinc phosphate cement: powder-liquid ratio, rate of powder
incorporation, powder particle size, manner of spatulation, and water content in the liquid.

364
 4. In mixing zinc phosphate cement the liquid-powder ratio is the clinical variable with the greatest
effect on the cement's strength .

5. Prolonged, vigorous mixing of zinc phosphate powder into the liquid on a cool glass slab promotes
a higher powder-liquid ratio and superior cementation medium by providing a lower viscosity of
the mix, stronger final set, and lower solubility of set cement.

Zinc Polycarboxylate Cement - first cement system developed with a potential for adhesion to
tooth structure. The polycarboxylate cements are powder/liquid systems. Its liquid (an aqueous solution
of polyacrylic acid + copolymers), and it powder (zinc oxide + magnesium oxide).
• Their compressive strength is slightly lower than zinc phosphate cements, but they have greater
tensile strength. Its final strength depends on the powder-liquid ratio (the more powder, the greater
strength). The strength of the set material is sufficient for amalgam condensation and its effect on
the pulp is mild enough to eliminate the need for sub-lining. Zinc polycarboxylate cement is used
strictly as a cement (luting agent).

• Thermal conductivity is low, so it provides good protection against thermal stimuli applied to metallic
restorations. When cementing a cast restoration, always apply cement to the restoration and the
tooth .

• When using polycarboxylate cement as a liner, it is not required to first place two coats of cavity
varnish since this cement does not irritate the pulp (apply varnish AFTER placing the polycarboxylate
cement liner).

• Advantage: it can bond to tooth structure due to the ability of carboxylate groups in the polymer
molecule to CHElATE TO CALCIUM in the tooth.

• Disadvantage: extremely short working time.

• Glass ionomer and polycarboxylate both contain polyarcylic acid .

• Polycarboxylate cements may form a chemical bond to enamel.
• Compared with zinc phosphate cement, polycarboxylate cement has lower compressive strength, has
equal tensile strength, elicits less pulp response, and can bond to tooth structure.

BASES

Bases - materials 1-2mm thick that function as barriers against pulpally irritating agents, provide
thermal insulation below a restoration, and provide adequate resistance to compressive forces of
mastication. In essence, bases serve as a replacement or substitute for the protective dentin
destroyed by caries and/or cavity preparation.
• Materials used as bases:
• Zinc phosphate cement: remember to seal dentinal tubules with varnish prior to application .

• Zinc polycarboxylate cement: provides adhesion and does not irritate the pulp.

• ZOE (Type III or Reinforced ZOE): not used under composite restorations since eugenol
inhibits composite's setting reaction .

• GIC: provides fluoride release and adhesion.

• Calcium Hydroxide ("hard setting") Oycal: thicker then when used as a liner. It is very
effective in promoting secondary dentin formation (an important aid in pulpal repair).

All of these materials are suitable bases under AMALGAM &COMPOSITE restorations. However, for
composites, ZOE cannot be used because eugenol inhibits the composite setting reaction.

365
 N Primary Bases - placed on dentin in close proximity to the pulp to provide protection from toxic and
thermal irritants.
• Under amalgam and composite restorations, calcium hydroxide is the primary base.
• Under gold restorations, the primary base is zinc phosphate or zinc polycarboxylate cement, or
GIC.
• Aprimary base is not needed under zinc polycarboxylate cements, since these cements do not irritate
the pulp.

Secondary Bases - the most common use is placing zinc phosphate cement over a calcium hydroxide
base that has been placed over a pulpal exposure (direct pulp cap).

Important: C,ments used as bases should be mechanically stronger than when used as luting agents
and are mixed with the maximum powder content possible. A low powder-liquid ratio produces a low
viscosity cement that is needed for luting agents.

Selecting a base to be used under a permanent restoration is governed by the cavity design, type of
permanent restorative material used, and the pulp's proximity in relation to the cavity wall. The most
important consideration for pulp protection in restorative techniques is the thickness of the remaining
dentin.
• Cements thicker than 2mm are bases and function to replace lost dentin structure under restorations.
A base can be used to provide thermal protection under metallic restorations, increase resistance to
forces of amalgam condensation, or to block out undercuts when taking impressions for cast
restorations. A base should not be used unnecessarily.

• The only difference between a base, cement, and a cavity liner is their final application thickness.
• Cements for luting have a desired final film thickness of 15-25 microns.
• Cavity liners (solution or suspension liners) have a desired final film thickness of 5 microns.
• Bases have a final application thickness of 1-2mm (they can be thicker depending on the
amount of dentin that was destroyed).

Selecting the appropriate base or liner to restore the axial wall of a Class II restoration depends on the
biological effect required, and thickness of remaining dentin.

CAVITY LINERS

Cavity liners - used to PROTECT THE PULP, placed as thin coatings over exposed dentin. Their main
purpose is to protect the pulp by creating a barrier between dentin and pulpally irritating agents (i.e. acids
from etchants or cements, restorative materials, etc.) by SEALING the dentinal tubules.
Two types of cavity liners:
1. Cavity Varnish (Solution Liner or Copalite)-a natural gum like copal, rosin, or synthetic resin
dissolved in an organic solvent like acetone, chloroform, or an ether. It seals dentinal tubules
cc
,." ."
:z: ,."
without adding bulk. Copalite is the most commonly used and reduces initial microleakage of
...... := a restoration. This liner is NOT used under composite because it inhibits the polymerization of
u;!!i
:= -
...... <:
the resin. Functions of cavity varnish (solution liner):
-< ,."
• Reduces marginal leakage to improve the marginal seal for the short term.
• Helps prevent acid penetration.
• Protects pulpal tissues from phosphoric acid in zinc phosphate cements.
• Prevents mercury penetration into the dentinal tubules from amalgam restorations, which
prevent dentin discoloration.
• Cavity varnish (copalite) does not act as a thermal barrier (does not provide thermal
protection), and should not be used with composite restorations because it inhibits
polymerization.
• With any restorative resin, cavity varnish or ZOE is NOT used because they can inhibit
polymerization. Using cavity varnish might prevent direct contact between the composite and
tooth structure, preventing bonding.

366
 2. Suspension Liner (Zinc Oxide Eugenol & Calcium Hydroxide}-a liquid where calcium hydroxide NOTES
& sometimes zinc oxide are suspended in a solution of natural or synthetic resins. Suspension
liners are thicker (15 microns) than solution liners (1-5 microns). Suspension Liner Functions:
• prevents penetration of acids and thermal shock and has adequate strength for use under
permanent restorations.

• ZOE is a very good liner since it has a palliative (soothing) effect on the pulp, thus is
commonly used for temporary fillings.

• Calcium Hydroxide (Dycal}-the most commonly used suspension liner that prevents thermal
shock, prevents passage of acid from restorative materials, and has enough strength to resist
forces used in placing restorations. Calcium hydroxide can stimulate secondary dentin
formation when placed near or in direct contact with pulp. When viewed radiographically, it
can be easily confused with caries as both are radiolucent.

• Cavity liners (solution and suspension) are being replaced by new dentin bonding agents.

• Cavity varnish functions in an amalgam restoration: to improve marginal seal, prevent

dentin discoloration, and prevent acid penetration to the pulp from cements.
I
• When both a cavity varnish and polycarboxylate cement base are being considered for use in
conjunction with an amalgam restoration, the cavity varnish should be applied to the cavity
preparation after placing the base.

• Leakage after insertion of an amalgam is reduced when a cavity varnish is used .

• Cavity varnish is indicated for use under amalgam restorations to improve the marginal seal
of the restoration.

• Cavity varnish is indicated under amalgam restorations because it improves the marginal seal
of the restoration (it does not prevent galvanic currents from reaching the pulp nor does it
completely seal the dentinal tubules).

6. Calcium hydroxide, U.S.P. is the dental material easily confused with caries when viewed
rad iogra ph ica Ily.
7. When using the acid-etch technique to restore a Class IV fracture, exposed dentin should first
be covered with a calcium hydroxide liner.
8. The copal resin varnish that is placed in the cavity preparation before the amalgam is
condensed provides short-term sealing of the margins.

Bleaching Teeth: the most conservative way to lighten VITAL teeth is bleaching. There are two bleaching
methods:
1. Office Bleaching: most use a light-activated solution of 35% H202 in 4-10 minute cycles. Other
methods to lighten vital teeth:
• Direct composites which are useful for gray tetracycline-stained teeth. ,...,
CI CI
.."
:z: ,...,
-t :::a
• Porcelain Veneers which are useful when the shape, size, and arrangement of teeth are v;~
-t _
esthetically poor. -< <
:::a ,...,
• Full-Coverage Crowns are the most invasive and costly using all-ceramic or a PFM.

2. Home Bleaching: the active ingredient contained in all home tooth whiteners that has ADA
approval is a 10% carbamide peroxide concentration. The active ingredient in most OTC home
bleaching products is NOT carbamide peroxide, but H202.

Bleaching can affect the color of dentin and enamel. Extrinsic stains respond best to vital bleaching.
Yellow stains respond best (then brown and orange stains). The worst response to vital bleaching is gray
stains (tetracycline staining).

367
 CARIES

Dental Caries - an infectious microbiological disease process that causes localized dissolution and
destruction of tooth structure (calcified tissues). For caries to occur there are essential factors required
to initiate a carious lesion:
1. Susceptible host (tooth). Fluoride and occlusal sealants modify the susceptible host (tooth).
2. Microflora with cariogenic potential (plaque) .
3. Asuitable substrate (dietary carbohydrates).

These three factors interact to promote the disease severity. The greatest percentage of tooth loss in the
first 20 years of life (except from natural loss of deciduous teeth) is due to untreated dental caries. The
rate at which carious destruction of dentin progresses is slower in adults than in young people due
to generalized dentinal sclerosis which occurs with aging.

Dental caries is initiated at the tooth surface by the growth of Streptococci (S. mutans, S. mitis, S.
sanguis-the most frequently isolated Streptococcus in the oral cavity, & S. salivarius). These bacteria
produce DEXTRAN SUCRASE (Glucosyltransferase), which catalyzes formation of extracellular glucans
from dietary sucrose. Glucan production contributes to dental plaque formation which then holds
the lactic acid produced by Streptococci against the tooth. The lactic acid then eats through enamel,
creating caries. /

Predominant Bacteria Found in Plaque:

• Streptococcus sanguis (found the earliest).
• Actinomyces viscosus & naeslundii .
• Streptococcus mutans, mitis, salivarius.
• Veillonella, Lactobacilli casei, & Fusobacterium.

Dental Plaque - the soft, white film of organized bacterial colonies (main component), salivary
glycoproteins, and inorganic material that readily forms on teeth surfaces. *The strong correlation
between the presence of dental plaque and appearance of dental caries and periodontal disease
has been recognized for many years.

Cariogenic Bacteria: the evidence of bacteria's role in the genesis of dental caries is overwhelming.
Organisms that cause caries are "cariogenic". Mutans Streptococci: Streptococcus mutans & sobrinus
are the two most common cariogenic bacteria found in man.

• Properties of Cariogenic Bacteria:

• Acidogenic (produce acid) and aciduric (able to tolerate an acidic environment). Lactic acid is
formed in large quantities after the degradation of sucrose by mutans streptococci. Lactic
acid produced by acidogenic bacteria is the main cause of enamel decalcification.

• The ability to attach to the root surface. *Streptococci species have special receptors for
C CI
,..., "'1:1
:z: ,...,
adhesion to the surface and produces a sticky matrix that allows them to cohere to each other.
-I ::c
- I l>
"'-I
- _
::c <
-< ,..., • The ability to form a protective matrix. Streptococci species produce an extracellular insoluble
dextran that protects them from being removed from the teeth by saliva, liquids, foods, and
masticatory forces. *Glucans occur as dextrans or mutans, and are synthesized from sucrose
by plaque bacteria as extracellular polymers of glucose. Levans are polymers of fructose.

S. sanguis is etiologically related to caries. but is NOT a primary etiological agent in caries.

Main cause or etiology of caries is bacteria or plaque formation. There is abundant evidence that the
initiation of dental caries requires a high proportion of Streptococcus mutans within dental plaque.

368
The first in caries development is the deposit of plaque on teeth. Dental plaque is a highly organized
gelatinous mass of bacteria that adheres to the tooth surface. Streptococcus mutans produce large
amounts of lactic acid (acidogenic), are tolerant of acidic environments (aciduric), are vigorously
stimulated by sucrose, and are the primary organisms associated with dental caries. However, other
organisms are required to initiate caries. Other mutans streptococci species in humans can also do this
(i .e. S. sobrinus).

Factors the tooth surface is directly exposed to and that contribute to caries development:
1. Amount of plaque: large amounts of plaque on teeth (many bacteria that can produce acids)
create a low pH or acidic environment to cause tooth demineralization.

2. Type of Bacteria: large proportions of "cariogenic" bacteria cause a lower pH, sticky plaque, and
prolonged acid production.

3. Type of Diet: high amount and frequency of carbohydrates, and sucrose. A "sticky" diet leads to
a low pH for a longer time period. High sugar frequency results in longer timer per day with a low pH.

4. Saliva Secretion: reduced saliva flow leads to prolonged sugar clearance time and a reduced
amount of other saliva protective systems.

5. Saliva Buffer Capacity: low saliva buffer capacity results in prolonged time with a low pH.

6. Fluorides: if too low or absent results in reduced remineralization.

9. Saliva helps prevent caries by diluting acid, acting as a reservoir for Ca and P04 ions for
remineralization, and acts as a reservoir for Ca, P04, fluoride, and other ions for
hypermineralization of the enamel surface.

Developmental pits &fissures are the most susceptible areas on a tooth for plaque retention. Pit
and fissure caries has the highest prevalence of all caries. Smooth surface areas (especially proximal
enamel surfaces) immediately gingival to the contact area are the 2nd most susceptible areas to caries.
Streptococci and lactobacilli species are common in this area. Facial and lingual root surfaces may have
plaque-containing filamentous actinomyces species which can cause root surface caries.

Fluoride treatments dramatically reduce smooth surface caries, although they are not as effective
in preventing pit and fissure caries. Sealing pits and fissures after tooth eruption may be the single most
important procedure to help protect these areas from caries destruction.

Changes of pulp and dentin depend on the rate of carious progression. The pulp's response to carious
attack or trauma from operative procedures depends on the pulp's blood supply &cellular activity.
Pulp defense mechanisms to protect it from irritation include:
• sclerotic dentin (peritubular dentin) formation (pulp's initial defense mechanism).
• reparative dentin (irritation dentin) formation (pulp's 2nd line of defense).
• vascularity (inflammation).
,...,
CJ C
.."
:z: ,...,
..... ::c
Acute Caries {Rampant Caries)-characterized by rapidly progressing, little or no staining, often multiple, c:;;~
.....
::c
-
<
soft-to-touch lesions, & most common in children. The lesion entrance is small , but the lesion is deep -< ,...,
and narrow in large lesions. Pain may be feature.

Chronic Caries {Slow or Arrested Caries)-common in adults, progresses slowly, and the lesion entrance
is wide. Characterized by dark pigmentation with leathery dentin, shallow lesion {small lesion), and pain
is uncommon . Chronic caries should be completely removed when found in enamel and close to the DEJ.

Root Surface {Senile Caries)-often found in older patients and attacks cementum & radicular (root)
dentin. The rising incidence of root caries is attributed to the aging population and most adults are
retaining more teeth . In this population, there is increased gingival recession with exposure of root
surfaces, leading to root surface caries which generally spreads more on the surface, rather than in
depth. In older patients, rampant caries can be caused by poor oral hygiene, decreased salivary flow,
and medication side effects. Bacterial Etiology: the same as for coronal caries (S. mutans, S. sanguis,
A. viscosus, A. naeslundii, lactobacillus, and Veillonella).
369
 NOTES • Best way to prevent root caries is to maintain the periodontal attachment.

• Gingival recession is most related to the initiation of caries in the elderly.

• Microorganism most commonly associated with root surface caries is Actinomyces viscosus.

• Most current research suggests the microbial etiology of root caries is very similar to coronal caries
(in the past it was thought Actinomyces species (viscosus and naeslundiil were most commonly
associated with root surface caries.

Residual Caries-caries that remains in a completed preparation either by the dentist's intention or
accident.

Secondary (Recurrent) Caries-decay appearing at and under restoration margins.

Zones of Carious Dentin (Innermost Zone Outermost Zone):

1. Zone I (Normal Dentin)-the innermost zone of normal dentin with no bacteria in the tubules.

2. Zone II Carious Dentin (Sub-transparent Dentin)-zone of demineralization created by acid from

caries. Damage to the odontoblastic process is evident, but this zone does not contain bacteria.
Capable of remineranzation.

3. Zone III (Transparent Dentin)-softer than normal dentin and show further demineralization . No
bacteria are present. Capable or remineralization.

4. Zone IV (Turbid Dentin)-the zone of bacterial invasion as the dentinal tubules are filled with
bacteria. This dentin cannot remineralize and must be removed prior to restoration.

5. Zone V(Infected Dentin)-the outermost zone consisting of decomposed dentin filled with bacteria.
This dentin must be completely removed prior to restoration.

4 Zones of an Incipient Carious Lesion in Enamel:

1. Translucent Zone-the deepest zone that represents the advancing front of the enamel lesion.
2. Dark Zone-does not transmit polarized light. Areas of demineralization and remineralization.
3. Body of the Lesion-the largest portion of the incipient lesion that has areas of demineralization.
4. Surface Zone-relatively unaffected by the ca ries attack.

Saliva helps prevent caries by diluting acid and acting as a reservoir for Ca, P04, fluoride, and other
ions for remineralization and hypermineralization of enamel. It also affects caries through its anti-
microbial properties.

Enamel demineralization occurs at pH 5.5. Remineralization of damaged tooth structure occurs as pH

rises above 5.5.
CI CI
..., -0
:z: ..., • Prevalence of caries is decreasing children. However, a decline in adult caries is not as evident.
..... ;:g
c;;~ Fluoridation has received the most credit for the decline in caries development.
.....
;:g -<
-
-< ...,
• Pregnant patients, compared to similar non-pregnant patients, are likely to have the same degree
of caries, but more inflamed gingival tissues.

10. In radiographs of an incipient carious lesion limited to the enamel on proximal surfaces of a
posterior tooth , the lesion appears a radiolucent area that is smaller in the radiograph than
actually exists clinically.

11. An incipient carious lesion on an interproximal surface is usually located gingival to the
contact area.

12. Three essential factors for the initiation of a carious lesion: bacteria, suitable substrate, and
susceptible tooth.

370
 ......

13. A radiograph of a first molar shows a very extensive carious lesion that may involve a horn of
the dental pulp. The treatment of choice is to remove a major portion of the decayed tooth
tissue and place an interim sedative dressing.

14. Atooth elicits a sharp stabbing pain caused by mastication of sweets or application of cold .
Pain is relived by warmth and frequently by direct pressure. The cause of the pain is a moderate
carious lesion with resu ltant pulpal inflammation.

15. Dental caries incidence is higher in children and adolescents because their dietary habits are
erratic, there are more unrestored surfaces in patients of this age range, their teeth have not
had the advantage of fluoride's cumulative effect, and their oral hygiene is erratic and inefficient.

16. Streptococcus mutans is considered to be a principal etiologic agent of caries because it

produces organic acids and forms a gelatinous matrix material.

17. The rate at which carious destruction of dentin progresses tends to be slower in older adults
than in young persons is because of the generalized dentinal sclerosis with aging.

18. Maxillary first molar is the tooth most likely to benefit from occlusal sealant placement.
/
19. A large carious lesion on the distal surface of a maxillary central incisor involving the incisal
angle is a smooth surface lesion.

GOLD
Component Major Effect on a Gold Casting Alloy
-----------------------------------------------------------
Gold (Au) Corrosion resistance.
*THE MOST DUCTILE & MALLEABLE METAL

Copper (Cu) Solution hardening, orange color.

Ranks 3rd in malleability.

Silver (Ag) *Silver offsets the color contributions of copper

in a gold casting alloy.
Silver is the 2nd most ductile & malleable metal (after gold)

Zinc (Zn) Scavenger of oxygen during processing.

Palladium (Pd) Increases hardness, elevates melting range, strong

whitening effect on the color.
,...,
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:z: ,...,
Platinum (Pt) Elevates the melti ng ra nge. ..... ::0:>
c:;;~
Platinum ranks 3rd in ductility ..... -
::0:><
-< ,...,

Ductility - a metal's ability to easily be worked into desired shapes (i.e. ability to form a wire from
a metal). These materials undergo extensive plastic deformation prior to fracture (in tension). Ductility
depends on plasticity &tensile strength.
• Ductility is usually expressed in terms of the percent elongation (the higher the value, the more
ductile the alloy). Ductility decreases as temperature increases.

371
 N Malleability - a metal's ability to be hammered (compression) into a thin sheet without rupture.
Malleability depends on plasticity, but is not as dependent on tensile strength as ductility. Malleability
increases as temperature increases.

20. Pure gold can be contaminated when it comes in contact with moisture, sulfur or eugenol
vapors, or an oxygen-rich flame.

Alloy - a mixture of two or more materials mutually soluble in the liquid state. A pure metal solidifies
at a constant temperature, while alloys solidify through a range of temperatures. Alloys are used in
dentistry for cast restorations.
1. Base Metal Alloys (non-precious metals)-are based on active metallic elements that corrode,
but which develop corrosion resistance via surface oxidation that produces a thin , tightly
adherent film that inhibits further corrosion (i.e. cobalt-chromium alloys form a Cr203 oxide
film that passivates the surface).
• Base metals are LESS resistant to corrosion than noble metals. Their advantages are mainly
based on their strength and low density. They are stronger and less dense than noble metal
alloys. Base metal alloys are also harder to cast and finish than noble metals.

2. Noble Metals (Precious Metals)-are very resistant to corrosion and do not oxidize on casting.
Noble metals used in ctentistry are based on the noble or precious metal elements of gold, silver,
palladium, and platinum.

3. Solid Solution Alloys-the metals freeze without segregation of the individual constituents. These
are generally used in dentistry because they have a very homogenous structure and provide
maximum strength.

4. Eutectic Alloys-separate into individual grains of the respective constituents. Exhibit complete
liquid solubility, but limited solid solubility (i.e. silver-copper system).

Karat - the number of "pure gold" parts of a gold alloy, based on 24 parts as a unit (24 karat is 100%
gold, 18 karat 75% gold) .

Fineness - measured based on the parts of pure gold per 1,000 (1 ,000 fineness is 100% gold ; 500
fineness is 50% gold). Pure gold is only used in the gold foil restoration.

4 Types of High-Gold Alloys: High-gold alloys used for cast restorations are> 75% gold or other
noble metals.
1. ADA Type I: highest gold content (83% noble metals) . Used for small inlays and easily
burnished due to high ductility.

2. ADA Type II: > 78% noble metals. Used for larger inlays & onlays, and can also be burnished .

3. ADA Type III: > 75% noble metals. Used for onlays &crowns. Capable of being heat-treated.
eo
.., c>
:z:
.."
..,
• When a Type III dental casting gold alloy is heated to a cherry red color and quenched
-0 ,.,
-:z,.
In-o
immediately, malleability and ductility are increased (surface hardness and strength
-0 _
,., <:
-< .., are decreased).

4. ADA Type IV: > 75% noble metals. Used for bridges and RPDs (hardest high-gold alloy).
Can be heat-treated.

Medium-Gold Alloys-contain 25-75% gold or other noble metals.

Low-Gold Alloys-contain < 25% gold or other noble metals.

Gold Substitute Alloys-do not contain gold , but a called "passive" because they form a protective
surface oxide film layer that provides maximum corrosion resistance (i.e. palladium-silver alloys and
cobalt-chromium alloys).

372
Advantages of Cast Gold Restorations: strong and able to withstand mastication forces, ideal for occlusal N
rehabilitation, and are kind to gingival tissue.
• Gold alloy against gold alloy is the combination that most likely results in the LEAST occlusal wear.

Disadvantages of Cast Gold Restorations: gold has a high thermal conductivity, is expensive and non-
esthetic, time consuming, technique sensitive, and the need to use cement which is the weakest point
in the cast gold restoration.

For maximum retention of cast gold restorations, the axial walls should be as parallel and as long as
possible. Retention is directly proportional to the area of the axial walls and their parallelism. Axial
walls should converge slightly from the gingival walls to the pulpal wall.
• Cement's main function in a cast gold restoration is to seal the cavity (not for retention). Retention
is designed within the preparation and results from friction between the cavity wall and the casting.

ONLAYS: main advantage is it can permanently restore and reinforce a tooth by a conservative
technique. While conserving tooth structure is desirable, it is offset by a lack of retention. Conservative
onlays have inferior retention than full crowns due to the crown's greater axial surface area. Cast Gold
Onlay Indications:
• Restore large lesions that involve more than 1/3 intercuspal dimension, extensive loss of supporting
structure where at least 50% of the clinical crown remains, or loss of cuspts) with at least 1mm of
dentin supporting the remaining cusps.
• Restore ideal occlusion in cases of drifting, hypoeruption, & hypereruption.
• Restore optimal contour and proximal contact.
• Restore brittle teeth (RCT treated teeth).
• Restore an abutment tooth for an RPD to create ideal guiding planes, rest seats, and undercuts.
• Restore teeth to meet patient preference for gold.

Parallelism of vertical surface (axial walls) is the primary retentive feature in an onlay preparation.
Sharp point and line angles increase onlay retention. Auxiliary retentive features include a box or groove
(indicated where inadequate surface area of vertical walls is present). A box offers a greater increase in
surface area, thus greater retention than a groove, but is also more costly in terms of lost tooth structure.

The location of the gingival margin when preparing proximal surfaces is influenced by the amount of
retention required, need to extend gingivally to clear the contact area, and convenience form .

With respect to ONLAY preparations, "shoeing" a functional cusp is NEVER INDICATED (shoeing is
never indicated on functional cusps). There are two types of cuspal protection for onlay preparations to
achieve proper resistance form :
1. Cap-complete coverage of the cusp. Except in situations demanding a minimal display of gold
(primarily facial cusps of maxillary molars and premolars) , capping is always preferred
over shoeing.

2. Shoe-minimal or partial cusp coverage via a finishing bevel on the cusp crest.

• Axial walls in an MOD cavity preparation for a cast gold onlay should converge from the gingival
walls to the pulpal wall.

21. When preparing a tooth for an MOD onlay, occlusal reduction is influenced by ideal location
of subsequent centric contacts, amount of clearance existing before reduction, minimal
thickness needed to satisfy physical requirements of the restorative material (it is not
influenced by the thickness of enamel present on the occlusal surface).

22. Always bevel or plane the cavosurface margins or wall junctions of an onlay cavity.

23. Near parallel axial walls is the factor that contributes the greatest amount of retention to an
onlay restoration .

24. For an onlay preparation, the most effective means for verifying adequate occlusal clearance
is a wax bite chew-in.

373
 25. When placing temporary restorations for several onlays in a quadrant, acrylic resin is an
acceptable interim material if cemented with ZOE.

26. When making an acrylic resin temporary restoration for a large MOD onlay preparation,
necessary precautions to take are to avoid open margins, remove overextended resin, and
polymerization should not go to completion in the mouth.

27. In preparing a tooth to receive an onlay, a gingival bevel is used to remove unsupported enamel
and compensate for casting inaccuracy.

28. The dentist bevels the gingival margins of a gold onlay preparation. Beveling removes loose
enamel rods, facilitates finishing, and minimizes marginal opening. Beveling does not serve
to minimize the need for gingival extension.

GOLD INLAYS:
• Lack of undercuts (avoid undercuts) is the characteristic common to all Class II gold inlay
preparations. The restoration will not seat if undercuts exists. This is true for all cast metal
restorations.

• When designing a Class II inlay preparation, an occlusal lock (dovetail) should be established to
prevent proximal dislodgement. Also, marginal ridges of posterior teeth restored with cast gold
should be rounded to help form the occlusal embrasures and be in contact with opposing tooth
cusps. Marginal ridges should be the same height as the adjacent tooth's marginal ridge (to prevent
/ an interference in retrusive movement).

• When removing a Class II inlay, the best method is to cut through the isthmus to remove the occlusal
and proximal pieces one at a time.

Class II Gold Inlay Advantages or Indications:

• Desire for permanency, low caries index, and for moderate size lesions with conservative outlines.
• Esthetics (posteriorly where amalgam staining is to be avoided) .
• Tooth contours (where optimum contour and surface finish is desired to maintain periodontal health).
• Rest seat retainers on abutment teeth.

Class II Gold Inlay Disadvantages or Contraindications:

• Expensive (gold is 6-7x more expensive than amalgam).
• Time (at least two visits are required).
• Minimal lesions (best restored with gold foil).
• Large lesions (if the cavity width exceeds 1/3 the intercuspal width, the tooth should receive cuspal
coverage).

3 Types of Inlay Casting Waxes that differ in melting point and flow:
1. Type A: hard or low-flow wax rarely used except in some indirect techniques.
2. Type B: medium-flow wax used in some direct techniques.
3. Type C: soft or high-flow wax (the softest dental inlay casting wax) used in indirect techniques
to construct inlays, onlays, and full crowns.

Essential ingredients of a successful inlay wax: paraffin wax, gum dammar, and carnauba wax with
some coloring material.
• Paraffin wax-the main ingredient (usually 40-60% concentration).
• Gum dammar-added to paraffin to improve smoothness in the molding and increases the wax
toughness.
• Carnauba wax-hard and decreases wax flow.

However the wax pattern is prepared, it should be an accurate reproduction of the missing tooth structure.
The casting cannot be more accurate than the wax pattern. The inlay wax pattern should be invested
ASAP after fabrication to minimize changes in shape caused by relaxation of internal stresses in the wax.

374
 29. First step in fitting a gold inlay casting in the mouth is to ADJUST PROXIMAL CONTACT AREAS. NOTES
30. When preparing an MO cavity for an inlay on a maxillary first molar, the oblique ridge should
be crossed when the ridge has a defective fissure, is undermined by a carious lesion, and
extension into the distal pit is necessary for retention of the mesial restoration (not if there is
an incipient caries in the distal pit).

31. Forces for seating an inlay should be applied with a sustained heavy force with an instrument
and with properly directing occluding forces of the patient prior to initial set of the cement.

Cavosurface Angle Configurations used when preparing a tooth for a Cast Gold Restoration:
1. Bevel-a diagonal cut across the cavosurface margin that is flat in one dimension only, and is
curved in its other dimensions. It involves the external ends of enamel prisms, and follows a
continuous curved outline. It can be a short bevel (cuts only the externall/3 of enamel prisms),
a full bevel (involving the entire thickness of enamel) , or wide bevel (involving full thickness of
enamel and some dentin).

2. Chamfer-essentially a hollow ground bevel (not a flat diagonal cut across the cavosurface
margin). The chamfer is "scooped-out" to create more bulk of restorative material near the
margin and provide a greater cavosurface angle.
/
3. Plane-a diagonal cut across the cavosurface margin that is flat in all dimensions, and may
involve the entire enamel thickness (which is usually does) or most of it, but cannot be curved in
any direction.

A cavosurface bevel is used when preparing a tooth for a cast gold inlay or onlay mainly to improve
marginal adaptation . The cavosurface margin bevel permits closer adaptation of the gold margin
because the thinner margin of gold overlying the bevel is more ductile and can be burnished. During
cementation, the finishing (burnishing) of the margins of a cast gold restoration is started as soon as
the restoration is well-seated into the preparation .
• While preparing an inlay or onlay, a gingival bevel is used to remove unsupported enamel and
compensate for casting inaccuracies. Gingival margin trimmers, carbide finishing burs, or fine
tapered diamonds can place the cavosurface bevel. This gingival margin is always placed gingival
to the contact area.

• When preparing teeth with short clinical crowns, facial and lingual walls should have a minimal
gingival to occlusal divergence angle for maximum retention.

• From facial to lingual, the axiopulpalline angle of an onlay preparation is longer than the axiogingival
line angle (if it were not, the preparation would be undercut and the onlay would not seat). For an
MOD onlay preparation, axial walls must converge from the gingival walls to the pulpal wall (for the
same reason the onlay would not seat if the axial walls diverged).

Crystalline Gold (Mat Gold) - formed by electrolytic precipitation yielding a crystalline structure CJ CJ
,.., -0
resembling trees or links of chain. Mat gold is used for bulk filling of cavities. The flow and adaptation :z: ,..,
-< ::c
of mat gold is not as good as gold foil or powdered gold. c:;;~
-< -
::c<
-< ,..,

Powdered Gold - gold formed by atomizing. Most of the granules in this material have an overall
spherical shape. Advantages: Powdered gold can be placed in a very short time period and a gold foil
veneer is not required. Also, it is denser than foil, thus easier to manipulate and condense, which saves
time.
• Cohesion of direct gold at room temperature is an example of "atomic attraction".

375
 Gold Foil- the traditional and oldest type of gold formed by rolling and beating gold into thin sheets.
This process causes elongation of grains which give a fibrous appearance. Gold foil is available in sheets,
cylinders, and pellets, and is used for bulk filling and as a finishing veneer for mat gold .
e There are always microscopic voids in any compacted gold, no matter which type is used. The cause
of porosities or pits in a gold foil restoration is related to improper condensing technique and using
oversized pellets.

e The most important factor in securing adaptation of gold foil to all parts of the preparation is the
direction that the force is applied (and using a small condenser point).

32. During condensation, surface hardness of gold foil is always increased.

Direct Filling Gold: MAIN indication for using a direct filling gold is a small initial Class III lesion.
Reconciling permanency and esthetics are the key limitations and challenges to this classification.
Lesions on the distal surfaces of all anterior teeth are relatively invisible and are less of an esthetic
concern than mesial lesions. In most cases, the distal restoration in a canine is not visible.
e Has a high tensile strength (edge strength).
e Is the most nearly permanent of all restorative materials.
e Provides good adaptation to cavity walls.
e Its coefficient of thermal expansion is close to that of tooth structure.
e It will not corrode.

e Direct filling gold is considered by many operative dentists to be the finest and most desirable
restorative material. However, the additional skill required, demand for close attention to detail ,
and the limitation in versatility are disadvantages of the technique which have lowered it popularity,
resulting in a utilization rate much lower than what the material deserves. Disadvantages of direct
filling gold: poor esthetics, demanding technique, high cost, high coefficient of thermal conductivity
(12x that of amalgam).

e The amount of force needed to compact direct gold is influenced mainly by the surface area of the
condenser. A decrease in diameter of a condenser point produces a proportional increase in energy
concentration. For this reason, good concentration will less force and trauma is accomplished with
a SMALL POINT. During condensation, the surface hardness, tensile strength, and yield strength
of direct filling gold increase.

e Direct filling gold is heated prior to condensation to drive off moisture and volatile compounds that
have been placed on its surface.

e Direct Filling Gold Indications:

eldeallesion: no greater than 1-2mm into dentin, and of minimal outline form.
e Ideal pulp: at least 2mm of dentin between the restoration and pulp. Pulp should be vital with
no history of trauma or tooth sensitivity.
e Ideal periodontium: no tooth mobility, no inflammation or degenerative processes are present.
C C>
.,., -c
:z .,.,
...... = Class III Cavity Preparation for Direct Gilling Gold:
cn:=
...... - e Outline form is a horizontal slot. The incipient lesion and subsequent preparation are usually
=
-< <
.,., positioned gingival to the contact area. The preparation has a flat labial wall and straight, parallel
incisal and gingival walls. The axial wall is flat and there is no lingual wall.

e Retention form is attained by a sharp internal anatomy with well-defined line and point angles.
Retentive grooves are placed along the inciso-axial and gingivo-axialline angles.

e Resistance form is provided by flat walls and a flat well-supported labial wall.
33. A 26-year old woman has a Class III lesion on the distal aspect of a canine. The restorative
material of choice is amalgam or direct filling gold.

34. Mechanical separators used in Class III direct filling gold procedures should routinely be
stabilized to minimize trauma to the gingival tissues, provide more rigid resistance to
condensation forces, and provide uniform support during instrumentation .

376
Class VCavity Preparation for Direct Filling Gold: NOTES
• Sharp internal line angles and small retentive undercuts placed in the axio-occlusal and axio-gingival
line angles.

• Mesial & distal walls flair and meet the cavosurface at a 90° angle. M & 0 walls are placed at the
tooth line angles.

• A convex axial wall that follows the tooth's external contour and is placed .5mm into dentin (this
makes the occlusal wall slightly deeper than the gingival wall because there is a thicker layer of
enamel making up the occlusal wall). The axial wall is convex in a M-O direction to conserve tooth
structure and minimize pulpal irritation .

• Trapezoidal (most popular) or kidney-shaped outline form. For any Class Vpreparation (amalgam,
composite, or direct filling gold), the outline form is determined by the extension of the carious lesion.

• Retention form is attained by sharp internal line and point angles (axio-gingival &axio-occlusal).
• Proper retention form in a Class Vcavity prepared for direct filling gold is dependent upon the
angulation of gingivoaxial and occlusoaxialline angles.

• Retention placed in a Class Vcavity preparation for direct filling gold should be at occlusoaxial
& gingivoaxialline angles.

• Resistance form is provided by flat mesial &distal walls, and a convex axial wall that parallels the
external tooth surface.

35. In the standard Class Vcavity preparation for direct filling gold, the mesial and distal walls
diverge facially and are placed at the tooth's line angles.

36. Placing the axial walls of a Class Vcavity preparation for dental amalgam or gold too far
axially could result in pulp exposure, sensitivity from thermal conduction, or sensitivity owing
to damage of odontoblastic cells.

37. Proper retention form in a Class Vcavity prepared for direct gold filling is dependent upon the
degrees of the axiogingival &axio-occlusalline angles.

38. The position of mesial and distal cavity margins in a Ferrier Class V direct filling gold
restoration should be at the respective line angles of the tooth.

INVESTING - process of surrounding a wax pattern with a material that can accurately duplicate its
shape & anatomical features.
• Dental Investment Functions: a detailed reproduction of anatomical form , enough strength to
withstand the heat of burnout and the actual casting of the molten metal, and compensation
expansion equal to the alloy solidification shrinkage.
co
,.., ..."
Gypsum Bonded Investments - used with Types I,ll, III gold alloys. Main Components of Gypsum :z ,..,
..... :::c
c;;~
Bonded Investments: ..... -
:::cc::
-< ,..,
1. Refractory Filler-a form of silicon dioxide (Si02) like quartz or cristobalite that comprises 60-
65% of the investment. These two compounds have different crystal structures, thus have
different thermal expansion coefficients. This refractory filler regulates and provides thermal
expansion for the investment.

2. Binder-a gypsum matrix of a-calcium hemihydrate that comprises 30-35% of the investment.
This material hardens after being mixed with the liquid, thus holds the investment together (adds
strength). The actual or effective setting expansion depends on the gypsum content and water-
powder ratio. Using a thinner mix that contains more water of a gypsum-bonded investment
will decrease the setting expansion, increase setting time, increase porosity of the set
material, and ultimately weaken the set material.

377
 3. Modifiers-are added to modify various physical properties of the investment. Ex: magnesium
oxide, NaGI, boric acid, graphite, or potassium sulfate.

• The strength of dental investments for gold alloys is dependent on the amount of gypsum.

Gold alloys used for cast gold restorations shrink upon solidification . Thus, it is necessary to com pensate
for solidification shrinkage of the specific alloy used by expanding the mold enough to equal the shrinkage.
The dimensional compensation necessary is accomplished by 2 methods of expansion:
1. Setting expansion-occurs as a result of normal crystal growth, but can be enhanced by
allowing the investment to set in the presence of water, producing hygroscopic expansion.

2. Thermal expansion-achieved through normal expansion that occurs upon heating silica (quartz
or cristobalite) . The amount of expansion depends on the type of refractory material used
(cristobalite produces greater expansion than quartz). Thermal expansion is the main cause of
mold expansion.

Variables that Influence Expansion:

• Older the investment, the less it will expand.
• Increasing the water-powder ratio decreases expansion.
• Longer spatulation time, the greater expansion.
• Longer time between mixing and immersion in a water bath, the less expansion.

During solidification of an alloy, the number of grains forming depends on the rate of cooling & presence
of nucleating agents.

SPRUE: the best angle to attach the sprue pin to the proximal wall of a wax pattern is 45°. The purpose
of the sprue former (sprue pin) is to provide an ingate or sprue in the investment through which the
molten alloy can reach the model after the wax has been eliminated.
• The size of the sprue former depends on the type & size of the pattern, type of casting machine used ,
and dimensions of the flask or ring in which the casting is made. Generally, for the average size
pattern, sprue formers smaller than 1.5mm diameters are contraindicated. If a sprue is too small ,
the molten metal freezes completely in this area first, and localized shrinkage porosity results. The
general rule for sprue pin diameter when using a centrifugal type casting machine is the sprue pin
diameter should be equal to or greater than the thickest portion of the pattern.

• It is desirable to attach the sprue at the point of greatest bulk in the pattern as there is less chance
of distortion upon attaching the spure, and the molten metal is more apt to remain liquid in this
area until the entire mold is filled. The direction of the sprue former is also important, as it is never
attached at a right angle to a broad, flat surface of the mold because the entering hot metal impinges
the mold surface at this point causing turbulence of the metal, which creates shrinkage void or suck-
back porosity. When the same pattern is sprued 45° to the proximal wall, a satisfactory casting
is obtained.

• Placement of the sprue is most related to turbulence of molten gold in the casting process.
"" c:::>
J'T'I '"'CI
=J'T'I
.... :::0
cn!!i • Primary reason for using a casting-ring liner is it allows uniform setting expansion of the investment.
.... -
:::0<
-< J'T'I
Vacuum Investing - a method of investing that is more dependable in preventing surface
nodules/defects on a casting. Nodules are caused by the collection of air bubbles during investing. The
best way to eliminate these nodular defects is to subject the water-investment mixture to a vacuum
during the investing procedure to remove the air bubbles.

• Porosity of the investment is reduced by vacuum investing due to the increased density obtained. As
a result, the casting's surface texture is smoother, with better reproduction of fine detail. The
investment's compressive strength is increased slightly by the vacuum investment (the investment
does not fracture as easy).

378
• Not all of the air is removed by the vacuum treatment. The amount removed depends somewhat on
the consistency of the mix. The more viscous the mix, the more air bubbles remain in the investment.
However, a thick mix is usually necessary because of the desired shrinkage compensation, and
because of the poor surface texture obtained with a thin mix.

Parts of a Flame Obtained from a Gas-Air Blowtorch used to Melt Alloys:

1. Mixing zone-1st zone that is cool &colorless. The air and gas are mixed before combustion in
this zone.

2. Combustion zone-2nd zone that is greenish-blue and surrounds the inner cone. This is an
oxidizing zone where partial combustion occurs.

3. Reducing zone-3rd zone which has a dim blue tip and is the hottest area in the flame and is
the only part of the flame that should be used to heat the alloy. When this zone contacts, the
alloy surface is bright and mirror-like.
• The proper zone of a gas-air blowpipe flame used for melting casting gold alloys is the
reducing zone.

4. Oxidizing zone-outer zone where final combustion between the gas and surrounding air occurs.
When the oxidizing part of the flame contacts metal, a dull film of "dross" (scum on molten
metal) develops over the metal surface.

The proper zone in contact with the metal can be readily detected by the condition of the metal surface.

If a casting fails to completely seat in a cavity preparation, you should first check for residual temporary
cement or other debris in the cavity. Once all temporary cement and debris are removed, the first step in
fitting the casting is to adjust proximal contact areas.
1. When seating a casting, the initial interferences are usually proximal contacts. Complete
seating of the restoration is verified by an x-ray and sharp explorer used at the gold tooth margin.

2. When seating cast gold restorations, the restoration's occlusion should be to the same degree
that teeth contact in that quadrant and on the opposite side (use shim stock to check occlusion).

3. Initially, if a cast restoration is in hyperocclusion, the patient complains of cold sensitivity

and pressure in the tooth. If the restoration is not adjusted, the tooth becomes very cold sensitive,
show signs of mobility, and there might be recession on the facial gingival tissue.

MINIMAL reduction of working cusps (functional cusps) for protection from forces of mastication is
2.5-3mm for amalgam, and 1.5mm for cast gold restorations. Working cusps are lingual cusps on
maxillary teeth, and buccal cusps on mandibular teeth.

MINIMAL reduction for non-working cusps (non-supporting cusps) for amalgam is 2mm while forming
a flattened surface (this provides resistance form), and 1mm for cast gold. Non-working cusps are
buccal cusps of maxillary teeth and lingual cusps of mandibular teeth .
,..,
ee
:z ,..,
..."

..... :::c
For metal-ceramic (PFM) restorations: occlusal clearance is 1.5-2mm, and 1.5mm facial and lingual c:;:;~
..... -
:::c<
reduction. The difference between tooth preparation for a PFM restoration and porcelain jacket crown is -< ,..,
mainly related to the configuration of the finishing line (margin). Chamfer or bevel for PFM restorations,
and a butt joint (shoulder) for porcelain jacket crowns.

The most effective way to verify adequate occlusal clearance is a WAX BITE CHEW-IN.

Cavity Classification (Class I through VI): developed by Dr. G.V. Black in 1908 as a standardized method
of recording the need for restoration exist to facilitate communication among clinicians, researchers ,
and dental educators. The most commonly accepted way to classify cavities is by naming the surfaces
(anatomical areas) involved. Cavity classification relates to the cavity location (not cavity size). Class I,
V, &IV can involve any teeth (anterior or posterior).

379
 • Class I-involves pits and fissures (all other classifications involve smooth surfaces of teeth) .

• Class II-involve proximal and occlusal surfaces of premolars and molars.

• Class III-involve proximal surfaces of incisors and canines that do not involve the incisal angle.

• Class IV-located on the proximal surface of incisors and canines and do not involve the incisal angle.

• Class V-located on the facial or lingual surface of all teeth, and do not involve a pit or fissure.

• Class VI-located on the incisal edges of anterior teeth or occlusal cusp heights of posterior teeth.

*The best method to definitively detect incipient carious lesions on the interproximal surfaces of
posterior teeth (distal surfaces of canines through molars) is by BITE-WING RADIOGRAPHS.

COMPOSITES

Enamel is etched with PHOSPHORIC ACID (37%) to roughen the enamel surface which forms little tags
-10-25 micrometers long to provide mechanical retention. Enamel rods are most effectively etched
at the enamel rod ends. When using the acid etch technique, all enamel cavosurface margins should be
chamfered/beveled (to form obtuse angles to afford more surface area for etching and to enhance the seal
and retention to reduce microleakage). Also, the bevel improves esthetics and exposes enamel rod ends
for acid attack.

Aproperly acid-etched enamel surface appears DULL WHITE &CHALKY. One of the most effective ways
to improve marginal seal and mechanical bonding of composite resins to tooth structure is to
condition/pre-treat enamel with acid prior to inserting the composite resin. This procedure is the "acid-
etch" technique.
• The acid cleans the surface of debris left after cavity preparation to provide an opportunity for
better wetting of the enamel by the resin. More important, a selective dissolution of the enamel
occurs during etching. While enamel is usually porous, acid removes calcium salts to increase the
size and number of microspaces present. This "acid-etch" technique conserves tooth structure,
reduces microleakage, improves esthetics, and provides micro-mechanical retention.

• Studies show acid-etched composite resin restorations have the best initial seal (microleakage) .
However, over time this seal weakens (amalgam has the best seal over time) .

• Once the tooth is etched, it cannot be contaminated with saliva oryou must repeat the entire etching
procedure.

• The reduction of microleakage represents the most signigicant advantage of the acid-etch
technique.

• The specific purposes of acid etching enamel before insertion of a composite restoration or a sealant
are to provide more surface area and a roughened surface.

• According to microleakage studies, acid-etched composite resin is the restorative material that shows
the best initial seal when placed in a cavity preparation, thus protects the pulp from the effects of
microleakage.

• Enamel is etched usually with buffered phosphoric acid prior to placing a resin restoration to allow
increased retention of the resin restoration, allow better sealing of margins of the resin restoration,
and produce enamel irregularities ranging from 5-30 micrometers in depth.

• Acid etching enamel increases retention and adaptation of resin restorations by increasing surface
area, conditioning the surface for better wetting, and creating surface irregularities for better
mechanical locking.

380
• The correct technique of enamel etching prior to placing a composite resin restoration is etching NOTES
with 30-50% phosphoric acid and rinsing thoroughly with water and drying with air only.

• 37% phosphoric acid in water is the solution used to etch enamel when using the acid etch technique
with composite resins.

Dentin Bonding Systems - complex and multi-step systems that consists of:
1. Etchant-used to roughen the enamel surface to help provide mechanical retention.

2. Dentin Conditioner-the component of a dentin bonding system that functions primarily to

remove the smear layer of dentin and etch the intertubular dentin to prod uce microspaces
within the dentin surface. Conditioner is placed after the enamel is etched .

3. Primer-a wetting agent applied after conditioning that provides micromechanical and chemical
bonding to the microspaces created by the conditioner.

4. Unfilled Resin Adhesive (Bonding AgenU-a restorative material applied after the primer. The
resin is then cured (light, self, or dual-cured) . This layer can now bond to composite or amalgam.
• Unfilled resin has the lowest thermal conductivity and diffusivity (compared to amalgam,
gold, and filled resin). This characteristic offsets the undesirable effects of the relatively high
coefficient of thermal expansion (7-8x that of the tooth). Due to its low thermal conductivity
and diffusivity, the unfilled resin restoration changes temperature quite slowly. Thus, it takes
considerably longer for an unfilled resin restoration to become hot or cold com pared to metallic
restorations, which have a high thermal conductivity and diffusivity. Remember: A low
coefficient of thermal conductivity is most characteristic of currently available cement bases.

• Unfilled resin's compressive strength is low, and its yield and tensile strengths are
even lower.

• Unfilled resins have a higher coefficient of thermal expansion, but lower modulus of elasticity
than filled resins.

• Unfilled resins are the softest of all restorative materials.

• Compared to amalgam, filled resin, direct gold, and silicates, unfilled resins have the
greatest extent of marginal leakage related to temperature change.

• Marginal leakage related to temperature change occurs to the greatest extent with
unfilled resin.

3rd generation dentin-bonding agents can produce bonding strengths nearly comparable to that of
resin to etched enamel. These depend on difunctional coupling agents being able to bond to inorganic
or organic compounds in dentin.

Unfilled Resins (Acrylic) temporaries fabricated for inlays and onlays should restore and maintain ,...,
CI C)
.."
:z: ,...,
- t ::c
proximal contacts, occlusion, and tooth contours. Margins should be closed and flush with the tooth. c;;;~
- t _
::c <:
Most importantly, methyl methacrylate maintains the occlusal and interproximal contact relationships. -< ,...,
• For inlays &onlays, plastic (acrylic) provisional restorations are fabricated prior to the final restoration
being cemented. Their physical properties enable them to withstand occlusal forces and the adverse
oral environment for short time periods.

• Methyl methacrylate, ethyl methacrylate, and ethylene imine resins have been used to produce
provisional restorations. However, methyl methacrylate (MMA) is the most common (the liquid
monomer that is mixed with the polymer polymethyl methacrylate (the powder) . The MMA monomer
partially dissolves the polymer to form a plastic dough. The monomer is polymerized by the action of
an initiator (benzoyl peroxide).

381
 • Polymerization should not go to completion in the mouth for fear that the provisional will not be able
to be removed from the tooth. Provisionals are usually cemented with a ZOE cement.

• Main disadvantage of using methyl methacrylate as a permanent restorative material are its low
resistance to abrasion and high coefficient of thermal expansion.

Filled Resins (Composite Resins) - replaced unfilled acrylic resins. Afilled resin has inorganic
inert filler (silica or quartz) added to its resin matrix. Filled resins are harder, stronger, more resistant
to abrasion, with a lower coefficient of thermal expansion than unfilled resins.
• The first materials used as esthetic materials were based on silicate cements. Due to solubility
problems, silicate cements were replaced by unfilled acrylic resins which contracted excessively
during polymerization creating subsequent marginal leakage, and were not strong enough to support
occlusal loads.

• Filled resins are harder, and have higher compressive and tensile strengths than unfilled resins.

• Most current composite resins are based on BIS-GMA as the primary monomer (a difunctional
monomer) or UDMA (urethane dimethacrylate) difunctional monomer. Since both monomers are very
viscous, they are diluted with another difunctional monomer (TEGDMA) to reduce the overall viscosity.

• The high filler content and BIS-GMA resin matrix greatly reduce the coefficient of thermal expansion
(compared to unfilled acrylic resins) . The filler also reduces polymerization shrinkage and increases
hardness.

• Bisphenol A-glycidyl methacrylate-the component common to most composite resins, sealants,

bonding and glazing agents, and resin cements for orthodontic bands.

• An unfilled BIS-GMA glazing resin may be used on the surface of a polymerized composite restoration
because unfilled BIS-GMA glazing resin seals the margins and smoothes the restoration surface.

• Dental sea lants generally are comprised of Bis-GMA.

LOW WEAR RESISTANCE is the property of filled resins that is primarily to blame for the failure of
Class II composite restorations. Ideally, composite resins should only be used to restore minimal cavities
in posterior teeth (instances where it will not be subjected to excessive occlusal forces and when teeth
are in occlusion, there is cusp-to-cusp contact (not cusp to restoration).
• Posterior composite restorations are often indicated to treat occlusal lesions which allow conservative
preparations.

• Posterior composite restorations are contraindicated patients with heavy occlusion or parafunctional
habits (bruxism).

• Posterior composite restorations may be indicated to restore Class II cavities in premolars where
CJ CJ
esthetics is important, the cavity margins are in enamel, and the occlusal contacts are on the enamel.
,..., ""t>
:z: ,...,
..... ::c
c:;;:=
..... <- • The major indication for posterior composites is a demand for esthetics by the dentist and patient.
::c
-< ,..., Other criteria are non-involvement of cusps, minimal occlusal contact, no excessive wear, and the
isthmus must be no wider than 1/3 of the intercuspal distance.

• Composite is the material of choice if the patient has a documented allergy to mercury.

• In the past, posterior composite restorations were contraindicated in patients with a caries-active
mouth. New thinking says you should manage the disease (dental caries) before or while you are
treating the consequence of the disease (Le. by placing restorations). Thus, current literature
does not see a problem for these restorations in caries-active patients. These have as bad a prognosis
as any other restorative treatment if the disease is not managed simultaneously.

382
Although the ADA does not endorse composite resin as a substitute for amalgam in posterior teeth,
composite restorations can be excellent if strict guidelines are followed for tooth selection and if done
properly. However, composite resin restorations are inferior to amalgam in compressive strength and
abrasion/wear resistance, and they do not provide any anti-cariogenic effects as do freshly placed
glass ionomer or resin-modified glass ionomers.

Composites are classified based on filler particle size (diameter in microns) &polymerization method.
Composite resins are dimethacrylate monomers and polymerize by an addition mechanism initiated by
free radicals that are produced by chemical activation or external energy (heat or light).
• Chemically-activated (self-cured) composites: a two-paste system (benzoyl peroxide initiator &
tertiary amine activator).

• light-activated composites: visible light replaced UV light. A one-paste system that contains a
photoinitiator molecule (camphor Quinone) and amine activator.

The most common classification method for composite resins is based on filler content, filler particle
size, and method of filler addition. Almost all important properties of composite resins are improved by
using higher filler levels. However, as the filler level is increased, fluidity decreases.

Composite (Filled Resin) Composition:

1. Resin Filler Particles: colloidal silica, crystalline silica (Quartz), or silicate glasses (non-
crystalline). Ions are now added to the filler to produce desirable physical changes. Lithium and
aluminum ions make the glass easier to crush to produce small particles. Barium, zinc, boron ,
zirconium, and yttrium ions produce radiopacity in the filler particle.
• Macrofillers/traditional composite (10-100 microns dia meter), Midfillers (1-10 microns
diameter), Minifillers (0.1-1 micron diameter), and Microfillers/fine particles (0.01-0.1
micron diameter) that develop the smoothest finish.

• Small size filler particles in composite resins results in better finishing and greater resistance
to occlusal wear.

• Highly filled resins contain larger filler particles, but this composition results in a rough
finished surface. Smaller filler particles are used to produce a resin with a relatively smooth
finished surface.

• The first composite resins developed contained large filler particles (10-100 microns diameter)
= macrofill material. However, larger size filler particles reduce surface smoothness and
resistance to wear. Thus, manufacturers continue to produce smaller and smaller particles
that yield better finishing characteristics and greater wear resistance. Newer microfilled and
hybrid resins are 40-60% filler by weight, compared to the 70-80% filler of macrofill materials.

• Hybrid Resins-contain a mixture of particles (usually midfill or minifill with microfill) with
different diameters that allow higher filler levels while permitting good finishing. The principal
particle size is in the 0.1-1 micron range (minifiller).

• Hybrid and microfill resins use colloidal silica fillers to increase hardness and wear
resistance of the base resin material while maintaining high polishability and esthetics.

• New resins with nanofillers that range from .005-0.01 micron are being developed . These
particles are so small that very high filler levels are achieved while maintaining workable
consistencies.

• Composite Filler Particle Functions: Decrease coefficient of thermal expansion &

polymerization shrinkage. Increase tensile and compressive strengths, hardness, and
improve wear resistance .

• As the overall filler content increases, the physical, chemical, and mechanical properties
generally improve. However, there is a limit as to the amount of filler that can be added to a
resin because as the filler level increases, fluidity decreases. *Restorative composites have
higher filler content, while flowable composites have a low filler content.
383
 2. Matrix: difunctional monomers (BIS-GMA) or recently UDM (urethane dimethacrylate). Both of
these monomers are diluted with another difunctional monomer (TEGDMA) to reduce viscosity.
• Once proper finishing is complete, a thin layer of unfilled resin can be applied as a glaze to
seal the margins and smooth the surface. Difficulty in finishing composite resin restorations
is mainly due to the softness of the resin matrix and hardness of the filler particles. The
most desirable finished surface for composites is obtained with aluminum oxide disks.

3. Coupling Agent (Silane): acts as an adhesive between the inert filler and organic matrix.

The normal wear mechanism of composite resins occurs by abrasion of the matrix which then exposes the
filler particles causing subsequent dislodgement of the filler particles.

The most popular way to polymerize matrix monomers is VISIBLE LIGHT-CURED (VLC unit).
• Visible light-curing involves light energy in the range of 41 0-500nm with a peak intensity of
470nm. The curing light is used at wavelengths 400-500nm for adequate composite curing.

• Hold the light as close to the resin as possible (within 2mm to be effective).

• Place a shield between the light tip and operator's eyes. Patients who have had recent cataract
removal should also have eye protection . Studies show visible light used in polymerization of photo-
activated materials can cause RETINAL DAMAGE, so always use a shield and eyeglasses for protection.
Light from visible-light polymerization units can cause retinal damage (VLC units are most
hazardous to the retina) .

• For deep restorations, cure the composite in increments to ensure that deeper areas are cured.

• The most serious limitation of visible light-cured posterior composite restorations is

polymerization shrinkage which can cause internal stresses and gap formations at butt-joint
interfaces (seen at the gingival floor of Class II &V restorations).

• Ensure the bulb in the light is still powerful enough (there are commercially available products to test
the bulb).

• With darker resin shades, cure a little longer.

• For large restorations (those wider than the light tip's diameter), cure each area for the full required
time. Do not back off the light tip until it lights up the entire restoration surface.

• Advantages of visible light curing systems compared to old ultraviolet light curing systems:
• Greater depth of resin can be cured by visible light.
• Resin can be polymerized through enamel (especially advantageous in Class III restorations).
• Intensity of visible lights remains relatively constant until the bulb fails completely.

Visible light curing systems have totally displaced the UV light systems, and are now much more widely
CI CI
...... ""CI
z ...... used than the chemically activated systems (self-cured). An advantage of light curing systems as a
..... ;:a
c;;~
.....
-
whole is the dentist has complete control over the working time and is not confined to the built-in curing
;:a <
-< ...... cycle of the self-cure (this is especially beneficial when large restorations are placed).

To deal with problems of incomplete curing with VLC due to the thickness of restorations and filler particles
scattering light, manufacturers have developed composite resins that are dual-cured (combines self-
curing and visible light-curing) . Another polymerization method is "staged curing" (a two-staged cure).
However, VLC composites remain the most popular today.

Visible light cured composites are single component pastes, and the polymerization process is
activated by an external energy source. The alpha-diketone initiator (camphor quinone) absorbs
energy from a visible (470nm blue light) light source. The ketone absorbs energy and reacts with an
amine (added to the system to enhance the effect of the light-sensitive catalyst) to produce free radicals.

384
• When using a light to cure light-activated composite resin the light should be held as close to the NOTES
resin surface as possible, a shield should be placed between the light tip and operator's eyes, and
the curing time is increased with darker shade resins.

D-L of canines is a Class III lesion that should NOT be filled with composite resin. Composite resin is
not recommended for Class II I lesions on the D-L aspect of canines (use amalgam or direct gold) .
Composite material will not maintain the M-D dimension of the tooth (this may not be entirely true today
since there are much better wear-resistant resins). Alingual approach is made when preparing a Class
III dental amalgam preparation for the distal of a canine to preserve the esthetic value of the facial
surface.

When two adjacent teeth to each other have Class III lesions, the dentist should prepare the larger
lesion first and fill the smaller lesion first. Access to the preparations and shade matching are easier
when you do both at the same time.

In a Class III composite preparation, retention points should be placed entirely in dentin. The retentive
grooves are placed along the gingivo-axial & inciso-axial line angles (entirely in dentin) to provide
mechanical lock in the preparation . Small, rounded retentive areas are preferred (not sharp angles) since
it is difficult to insert viscous composite material into the sharp angles.

When placing composite material in a Class III preparation, the wooden wedge is placed to provide
some separation of teeth for contact, stabilize the mylar strip, and avoid creating excess gingival flash .
Restoring the contact area must be done properly and diligently. Adiagnostic aid used as a last resort
to confirm caries on the proximal surface of an anterior tooth is mechanical separation with a wedge.

After the dentist completed acid etching a Class III composite preparation, the preparation becomes
contaminated with saliva . In response , the dentist should rinse away the saliva with water, dry the
preparation with air, then repeat the etching procedure.

For Class III preparations using resins, the rule of "extension for prevention" into embrasures is
DISREGARDED for Class III esthetic restorations. This compromise is for esthetic reasons and the
unnecessary removal of tooth structure which will often involve the incisal edge. If possible, the outline
form should place the gingival margin incisally from the crest of the gingiva.

The outline form of a Class Vcomposite preparation resembles a Class Vamalgam preparation except
that the internal line angles are much more ROUNDED. When restoring with composite resin , it is much
easier to compress the material into rounded line angles.
• The outline form of a Class V restoration is not always uniform and varies depending on the
location and amount of caries or decalcification (the size and location of the carious lesion
determines the outline form of the cavity preparation). When carious tissue is removed and the
margins are on sound enamel or dentin , the outline is usually rectangular with the corners round ,
ovoid, or kidney-shaped, very much resembling an amalgam Class V preparation except that the
internal line angles are much more rounded .

• The cavosurface margin for a composite restoration is chamfered when placed on enamel (a "" -c
.... CI
:z: ....
-t :=
major difference between composite &amalgam preparations). This chamfer is etched and cn~
-t _
provides retention for the restorative material, improves marginal seal, and maintains the resin's := -<
-< ....
strength with sufficient bulk. Retentive grooves supplement the etched enamel retention (these
grooves are placed in both incisal and gingival axial line angles). Whenever possible, use a composite
syringe to place composite resin in the restoration to minimize trapping air in the final restoration .

• The most important factor in preparing and restoring a Class II lesion with composite resin is
moisture control.

• Resin cements are the cement of choice for composite inlays.

• With a composite inlay preparation there should be divergent internal walls and all margins should
be finished in sound enamel.

385
 N • Beveling the enamel margin of a composite resin preparation is accomplished to improve esthetics
and expose the ends of enamel rods for acid attack.

• Compared with self-cured resins, light cured composite resins provide denser restorations because
no mixing is required that introduces air bubble porosity.

• Composite resin is the material most likely to cause an adverse pulpal reaction when placed directly
in a deep cavity preparation.

• The cavosurface angle of a cavity preparation for an acid-etched composite is beveled to afford more
surface area for etching to enhance seal and retention.

• Retention in a cavity prepared for composite resin usually is gained by undercuts in dentin and acid
etching.

• The normal wear mechanism of the composite resins is best explained by abrasion of matrix, exposure
of filler, and dislodgement of filler particles.

• The use of composite resin for Class II restorations is not generally recommended because its clinical
performance is inferior to amalgam with respect to occlusal wear.

• Whenever possible, a syringe should be used for placing composite resin because the possibility of
trapping air in a restoration is minimized.

• In preparing a cavity for restoration with composite resin combined with an acid etch technique, all
enamel cavosurface angles should be obtuse angles.

• Difficulty in finishing composite resin restorations is due primarily to the softness of the resin matrix
and hardness of the filler particles.

• Composite resins are not generally recommended for restoration of Class II cavities because of
excessive occlusal wear.

• A patient presents with numerous carious lesions. To restore these lesions, the dentist will place
composite resins and use a visible-light curing unit. The patient's history of cataract removal will
necessitate that the dentist take extra precautions when using this unit.

AMALGAM
Outline Form - the part of a cavity preparation that is the shape or form of the cavity on the surface
of the tooth. Important: margins are placed in areas of lessened caries susceptibility (extension for
00
...... "'0
prevention which can be restricted in patients with very low caries susceptibility). Also, all undermined
:z: ......
.....
en:!:;"'" enamel (enamel not supported by sound dentin) should always be removed. These important points are
..... - influenced by: lateral spread of decay at the DEJ, type of restorative material to be used, and the
""'<
-< ......
tooth and its relative position in the arch.

When establishing "ideal outline form" caries remains on any of the preparation walls, the next step is
to extend the outline form before excavating any caries.

Convenience Form - the form the cavity preparation takes to aid the operator in preparing, placing,
or finishing the restoration.

386
Retention Form - that form the cavity preparation takes to resist dislodgement or displacement of
the restoration
• Ex: buccal and lingual walls of a Class II amalgam preparation converge occlusaly to prevent
amalgam dislodgement.

• For Class II restorations, this resistance to dislodgement is provided by the occlusal dovetail and
retention grooves in the proximoaxialline angles.

• Retention grooves are placed in axiobuccal and axiolingualline angles, and extend to the height of
the axial wall (resistance to dislodgement) .

• Resistance to proximal displacement in the ideal Class II restoration is provided by occlusal dovetail
and retention grooves in proximoaxialline angles.

Resistance Form -that form the cavity walls take to resist forces of mastication to prevent fracture
of the restoration and tooth.
• Ex: severely undermined cusps should be reduced to prevent fracture. The axiopulpalline angle in a
Class II amalgam preparation is rounded or beveled to reduce concentration of stresses which
prevents fracture of brittle amalgam.

• Ex: proper angulation of cavity walls (converging) and pulpal and gingival walls that are prepared
perpendicular to occlusal forces (flat walls at right angles to the tooth's long axis) help achieve
resistance form .

• Most common cause of fracture at the isthmus of a Class II amalgam restoration is inadequate
depth at the isthmus area (must be adequate depth to obtain resistance form) . Most detrimental
to the strength of a posterior tooth in a cavity preparation is an increase in F-l width.

• Axiopulpalline angle is rounded or beveled to reduce concentration of stresses (resistance form) .

• Fracture of a Class II amalgam restoration at the junction between the occlusal and proximal portions
is the result of inadequate resistance form.

Trituration: increasing trituration time, reduces the setting expansion of amalgam (the longer the
trituration time, the smaller the setting expansion). If the trituration is carried to the extent that the
amalgam is shiny and wet, the strength will be maximal and the smooth, carved surface will retain its
luster long after polishing. Aproperly triturated amalgam is shiny, wet, smooth, and homogenous. An
overtriturated amalgam mix is better than an undertriturated mix.
• Inadequate trituration creates a low strength amalgam mix and rough surface that accelerates
corrosion. An undertriturated amalgam mixture appears dry and grainy. Condensing this mixture
results in poor adaptation to the preparation walls, lacrimation between condensed increments, and
reduced strength .

• The discolored, corroded, superficial layer often seen on the surface of an amalgam restoration is CI CI
,..., ""CI
most likely a sulfide. :z: ,...,
-< ::c
c;;;~
-< -
::c <
-< ,...,
• When carving an amalgam restoration , trim the margins with a sharp instrument that rests on tooth
structure to prevent "ditching" the margins. If an amalgam chips during carving, it is because the
amalgam was condensed AFTER its working time had elapsed.

The principal purpose of trituration is to coat the alloy particles with mercury. The object of trituration
is to bring about an amalgamation of the mercury and alloy. Each individual alloy particle is coated
with a slight oxide film that prevents mercury penetration. During trituration, this oxide film is rubbed
off and the clean metal is then readily attacked by the mercury.
• Once amalgamation occurs, no free (unreacted) mercury is associated with the amalgam restoration
(it now has no toxic properties). However, if the amalgam is heated above 80°C, liquid mercury can
form on the amalgam surface, and its vapors can present a health hazard.

387
 Pins: function to retain the restorative material. It does not increase the strength of the restorative
material. The retention of a pin increases as the pin diameter increases. The largest pin that can
safely be placed should be selected in any situation. As a rule, one pin per missing axial line angle is used.
Optimal pin placement is at the line angles (corners) of the tooth where the tooth-to-root mass is greatest
and the risks of perforation into the pulp of furcation are minimal.

Pin Indications:
• Class II amalgam preparation where one or more cusps have been lost, or where the outline form
otherwise far exceeds that which is considered normal.
• Avery large Class III amalgam preparation.
• Class Vamalgam preparation that far exceeds minimal dimensions (especially in the gingivo-incisal area).
• A preparation for an amalgam buildup over which a cast restoration will be fabricated.
The main advantage of pins is to improve retention of large restorations.

Pin Disadvantages: placement can cause pulpal exposure, perforation, or tooth fracture. When placing
pins in endodontically treated teeth, use only self-threaded pins or cemented pins (not friction-locked
pins) . Pins can weaken the restorative material into which they are placed. If placed by force, pins can
create stresses that cause crazing of tooth structure. Pins may provide an additional deep path for
microleakage. If placed in close proximity to the pulp, they may aggravate an existing pulp problem or
create one.

• Pins may be contraindicated in young teeth with very large pulps and teeth with reversible pulp
pathology, which might be aggravated by instrumentation. Placement is always influenced by the
limitations of access and vision .

• If when attempting to drill a pin hole the drill enters a vital pulp chamber, the proper treatment is to
allow the bleeding to stop, dry with a sterile paper point, and place calcium hydroxide into the hole.
Proceed with a better pin hole location. If a pin channel perforates the tooth's external surface and
all factors are favorable, a pin can be placed if there is no extension beyond the tooth surface. When
preparing a pin hole for a pin-retained amalgam restoration, the spiral drill tip enters a vital pulp
chamber. The next step is to apply calcium hydroxide in the pin channel and proceed.

• Pins should be inserted into DENTIN ONLY. Ideally, pin are placed 1-1.5mm inside the cavosurface
margin and at least .5mm inside the dentinoenamel junction (DEJ), if present. Placement of the pin
channel at least .5mm away from the DEJ helps prevent crazing or complete fracture of remaining
enamel. The optimal depth of the pinhole into dentin is 2mm.

• Pins should be 2mm into dentin, 2mm within amalgam, and Imm from the DEJ (to be safe) with no
bends in the pins.

• Cusps restored with dental amalgam should be reduced 2mm while forming a flat surface
perpendicular to occlusal forces.

• The twist drill used to prepare the pin channels must be angled so it remains in dentin only. The
...,
CI c:::>
:z:
."
..., channel should be prepared parallel to the external surface of the tooth .
-I ::c
c:;;~
- I _
::c <:
-< ..., • After restoring a tooth, check occlusion very carefully. If a restoration is left in hyperocclusion, the
patient will return complaining of discomfort when biting, usually with no other symptoms.

• The mostfrequently used pins are SELF-THREADED PIN SYSTEMS (TMS, Whaledent) which use holes
sized just under the screw diameter. The elasticity (resiliency) of the dentin function to retain the
screwed pin. This system comes with a self-limiting drill of optimal 2mm depth and self-shearing
pins that guard against overtightening. This type of pin system is the most retentive of the 3 types
of pins. TMS system has 4 pin sizes (regular, minim, minikin, & minuta) which are available in
titanium or stainless steel plated with gold .

• Threaded pins used in a dental amalgam restoration should be placed -2mm in depth at a position
axial to the DEJ and parallel to the external surface between the pulp and tooth surface.

• Cemented pins-serrated stainless steel pins cemented into pinholes that are larger than the pin diameter.
388
• Friction-locked pins-are tapped into pinholes that are smaller than the pin diameter. They are
retained by dentin's elasticity.

• New state-of-the-art systems are now available for bonding amalgam to dentin and enamel. These
systems may make the use of pins obsolete. Ex: Amalgambond (Parkell), All Bond 2 (Bisco), &
Dentastic (Pulpdent). These systems allow adhesion to preconditioned substrate with the added
benefits of retention and sealing of the restoration, and a stronger total cohesive mass to support
all remaining cuspal segments of the tooth .

• Inclusion of pins in an amalgam restoration results in an increase in retention only.

Class I Amalgam Preparation: Preparation's MESIAL &DISTAL walls must DIVERGE slightly towards to
the occlusal surface to provide support for mesial and distal marginal ridges. This divergence also
applies to Class I preparations involving direct filling gold and gold inlays.

Class II Amalgam Preparation Features:

• Class II amalgam preparations have independent retention and resistance form for the proximal box and
occlusal portion of the preparation. Occlusal dovetail provides resistance to proximal displacement.

• Pulpal floor is flat (same as with a Class I preparation).

• Lingually, it is often necessary to create a reverse curve in the outline (a reverse "s" curve is a curve
put into the buccal or lingual wall so the wall meets the external tooth surface at a 90° angle. All walls
should meet the tooth surface at a 90° angle (butt joint). A conservative Class II amalgam
preparation has a proximal cavosurface margin that forms a 90° angle with the external surface.

• Buccal and lingual walls of the proximal section should converge occlusally (the extension of these
walls is determined primarily by the position of the adjacent teeth in relation to the tooth being restored).

• Buccal, lingual, and gingival walls are extended into embrasures enough to allow easy cleaning (to
decrease caries susceptibility).

• Mandibular 1st premolar (bicuspid) requires special attention when preparing the occlusal aspect
for a restoration. Bur is tilted lingually to prevent encroachment on the facial pulp horn and to
maintain dentinal support of the lingual cusp. The pulpal floor should be parallel to the occlusal
plane F-L and should slope to coincide with the slope (height) of the cusps.

• The most sensitive area of the tooth during cavity preparation is the DEl

• In a Class II cavity prepared for dental amalgam, the facial and lingual proximal walls should be
formed slightly diverging as the wall approach the proximal surface.

• A conservative Class II preparation for dental amalgam should have independent retention and
resistance form for both the proximal and occlusal portions.
'" <=>
.... -c
:z: ....
..... ::0:>
Comparison of Cavosurface Margins for a cn~
..... -
::0:><
Conservative Class II Amalgam vs. Inlay Preparation -< ....

Cavosurface Margin Class II Amalgam Class II Inlay

Occlusal cavosurface 90° with external surface Beveled to result in 40°
margin marginal metal

Proximal cavosurface 90° angle with external Outer planes carried into
margins tooth surface cleansable area to provide
access for finishing
margins. Beveled to result
in 40° marginal metal

Gingival cavosurface margin 90° angle with Beveled to result in 40°

external surface marginal metal
389
 Gingival cavosurface margin of the proximal box and occlusal cavosurface margin are the only ones
beveled when preparing a Class II amalgam preparation .

• The gingival cavosurface margin is beveled only if it is placed in enamel. It should be beveled to
remove any unsupported enamel, and is usually placed with a gingival margin trimmer (beveling is
not necessary if the gingival margin is within cementum). This gingival margin must be below any
existing contact with the adjacent tooth to allow proper finishing of the gingival margin .

• The bevel is no steeper than necessary to ensure full-length enamel rods forming the gingival
margin, and is no wider than the enamel. *Enamel rods in the gingival third of primary teeth extend
occlusallyfrom the DEJ which eliminates the need in Class II preparations forthe gingival bevel that
is required in permanent teeth.

• Primary molar teeth have marked cervical constriction. Thus, when preparing the proximal portion
of a Class II cavity preparation, a satisfactory gingival seat may be difficult to obtain if the
preparation extends too deeply gingivally.

• The position of the gingival margin of a Class II amalgam restoration is dictated primarily by the
extent of the carious lesion. The gingival margin should clear the contact area to allow for adequate
finishing of the enamel margins and matrix band placement.

• Instruments used for placing gingival bevels on inlay preparations: margin trimmers, carbide
finishing burs, and fine, tapered diamond stones.

• Gingival cavosurface margin of a Class II inlay in a patient with gingival recession should ideally
terminate gingival to the contact area and gingival to the lesion.

• A deficient margin at a proximogingival cavosurface angle of a freshly packed Class II amalgam

restoration may have been caused by poor condensation of the amalgam, using too large an initial
increment of amalgam, or debris in the corner of the proximal box.

Matrix Band: is removed from the tooth prior to final carving of the restoration. The reason for placing
the matrix for a Class II amalgam restoration to protrude above the cavity preparation is to allow for
overfilling to enhance adequate cavosurface coverage.
• Contact areas are always carefully restored in all restorations to protect the gingival tissue. The
matrix band is burnished into contact with adjacent teeth to help ensure contact.

• One of the most difficult teeth to adapt the matrix band to is the mesial of a maxillary 1st premolar
due to its developmental depression/groove.

• The larger circumference of the matrix band is always placed toward the tooth's occlusal surface. This
accommodates the larger tooth circumference at the contact level. Also, the diagonal slot opening
on the Tofflemire matrix retainer ("Universal Matrix System"), is always placed facing the gingiva to
permit easy separation of the retainer from the band in an occlusal direction.
..,
CJ CJ
:z:
..."
..,
..... :::c
~~
..... - • Wedges are inserted from facial or lingual embrasure (whichever is larger), slightly gingival to the
:::Co<
-< .., gingival margin. The wedging action between the teeth should provide enough separation to
compensate for the thickness of the matrix band.
• The thickness of a good Class II matrix should be approximately 0.002 inches.

Matrix Function for Placing Class II Amalgam Restorations: establish proximal contour, limit moisture
contamination during condensation, and aid in preventing gingival overextension of the amalgam.

• Primary function of the matrix is to RESTORE anatomical contours and contact areas.

• Other Matrix Functions: provide a rigid wall to condense filling material against, prevent excess
filling material from going subgingivally, and to limit moisture contamination during condensation .
Aproperly placed wedge also protects the gingival tissue and helps reduce moisture leakage into the
cavity preparation.

390
• Before inserting amalgam into an MOD cavity preparation, a matrix is placed around the tooth. The
procedures that should be performed next are the band should be burnished into contact with
adjacent teeth and tapered wedges should be placed interproximally to obtain close adaptation of
the matrix band at gingival margins.

• A matrix for a Class II dental amalgam restoration is extended occlusally to the cavity preparation
to allow for overfilling the amalgam.

Comparison of Conservative Class II Amalgam vs. Inlay Preparation

Feature Class II Inlay Class II Amalgam

Occlusal isthmus width 113 intercuspal (max) 113 intercuspal (max)

Inclination of walls with Diverge 2-5 0 occlusally Buccal & lingual walls
respect to the occlusal surface converge para lIel to the
external tooth surface

Depth into dentin O.5mm O.5mm

Internal line angles Sharp Slightly rounded

Axio-pulpalline angle Blunt or rounded Blunt or rounded

Proximal retention form Rectangular box Retentive grooves

& reverse bevel

Gingival wall Form a reverse bevel at Gingivo-axialline angle

the axial-gingival line angle slightly rounded
into the gingival wall

Outline Form of a Class V Amalgam Preparation is a deformed trapezoid ("kidney-shaped"). This

outline form is determined mainly by the location and size of the carious lesion/area.
• The Class V amalgam restoration is used to restore lesions from caries, erosion, and abrasion.

• The non-parallel mesial &distal walls of the preparation are also straight and parallel, but never
extend beyond the transitional line angles. The direction of these walls is determ ined by the direction
of the enamel walls (as is the decay pattern).

• Mesial, distal, gingival, and incisal walls of the cavity preparation DIVERGE outward.

• Retention form is provided by the gingival retention groove along the gingivoaxialline angle and
an incisal retention groove along the incisoaxialline angle.
c
,.,., c
-c
• A cervical clamp is usually necessary to retreact gingival tissues. :z: ,.,.,
--t :::c
cn:!:t
--t _
:::cc::
• Occlusal and gingival walls of the preparation should be gently curved arcs as determined by the -< ,.,.,
contour of the free margin of the gingival tissue. These arcs should be as parallel to each other as
possible. The occlusal arc will normally be the longer of the two arcs. The gingival margin will
normally be at or slightly below the margin of the free gingiva.

• For incipient lesions, the axial wall should be uniformly deep into dentin.

• Be careful not to "ditch" cementum when finishing and polishing. Occasionally, you will notice the
gingival tissues have receded apically from the gingival margin that was previously polished due to
irreversible tissue changes caused by inadvertently traumatizing the tissue when the restoration was
being polished, so be careful.

391
 • In a Class Vamalgam preparation for an incipient lesion, the ideal internal form of the preparation
has the axial wall uniformly deep into dentin.

DELAYED EXPANSION of amalgam restorations is associated with insufficient trituration &

condensation, and amalgam contamination by moisture during trituration and condensation (MAIN
cause of failures).
• If moisture is incorporated into an alloy that contains zinc, the water reacts with the zinc to produce
hydrogen gas. The resulting pressure from the liberated gas produces severe expansion of the
amalgam, causing amalgam to protrude from the cavity preparation, post-operative pain, and
excessive corrosion.

• Amalgam's compressive strength is greatly reduced when contaminated with moisture.

• Amalgam has a coefficient of thermal expansion -2x that of tooth structure, thus percolation
occurs during temperature changes.

• Amalgam's tensile strength is 1/5-1/8 of its compressive strength (this is why enamel is needed
to support amalgam at the restoration margins). Amalgam is more abrasion-resistant than composite
resin or unfilled resin.

High mercury content is manifested in the clinical amalgam restoration by SEVERE MARGINAL
BREAKDOWN. The most important consideration in amalgam's strength is its mercury content. If the
mercury content exceeds 55%, a dramatic loss in strength occurs. Amalgam restoration that contains
mercury levels of -55% exhibits a high incidence of marginal breakdown, fracture, corrosion, and the
surface finish of the restoration is not good .
• Factors that influence the final mercury content of a restoration: original mercury-alloy ratio,
amount of trituration, and condensation pressure and time involved in carrying out condensation.

• Removing the mercury-rich matrix by proper condensation and carving produces a stronger and
more corrosion-resistant amalgam because it minimizes formation of the matrix phases of amalgam
(the least desirable parts of the set material).

• The strongest phase of set amalgam is GAMMA phase (the original silver-tin particles unreacted
powder). Gamm-two is the weakest phase and the most susceptible to corrosion in the mouth.

• The reaction that occurs between the alloy particles and mercury is:

Silver-tin alloy (Ag3Sn) + Mercury (Hg) Silver-tin alloy (Ag3Sn) + Silver-mercury (Ag2Hg3) + Tin-mercury (SnaHg)
Gamma Gamma Gamma-l Gamma-2
(*Strongest Phase) (*Weakest Phase)

Amalgam Facts:
• Smaller particle size results in higher strength, lower flow, and better carvability.
• Spherical amalgams high in copper have the best tensile and compressive strengths.
,...,
CI CI
." • Amalgam has a coefficient of thermal expansion 2x that of natural tooth structure.
:z: ,...,
- I ::c • Amalgam's tensile strength is 118 of its compressive strength.
c;:;~
- I _
::c -<
-< ,...,
• Weakest phase of the set amalgam is Gamma-2.

Dental Amalgam Composition:

1. Silver (Ag): 40-70%. Decreases setting time, increases setting expansion and strength.

2. Tin (Sn): 25-27%. Increases setting time, and decreases setting expansion (tin influences
amalgam opposite of silver). Tin (Sn)-the component in amalgam that causes contraction.

3. Copper (Cu): < 6%. Increases hardness, strength, and resistance of amalgam to corrosion .
Low Copper alloys have 6% or less (this is traditional alloy) . Comminuted (irregular, filing,
or lathe-cut) or spherical particles.

392
 4. Zinc (Zn): < 1%. Prevents oxidation of the other metals while the alloy is being prepared by the NOTES
manufacturer. Moisture contaminated zinc-containing amalgam manifests grossly delayed
expansion &reduced compressive strength.

5. Mercury (Hg): 3% maximum. Reacts with the other alloy particles to produce different phases.
• Most amalgam restorations show slight setting expansion, but not of clinical significance.
The more free mercury, the more setting expansion (and vice versa).

• Amalgam's Strength: amalgam is BRITTLE, but possesses good compressive strength. The
most important consideration in amalgam's strength is its mercury content. Mercury content
> 55% greatly decreased strength (should be within 45-53% by weight).
• Higher condensation pressure, smaller particle size, longer trituration time, and
fewer voids all increase amalgam's strength .

• Brittle describes a material with high compressive strength, but low tensile strength.

• Brittleness is the property of amalgam that makes it undesirable to bevel occlusal

margins of an amalgam cavity preparation.

The amount of MERCURY remaining in dental amalgam after condensation directly affects: restoration
porosity, compressive strength, corrosive resistance, and surface finish of the restoration.
• The amount of mercury remaining in a set amalgam restoration is related to how much of the mercury-
rich matrix is left in the amalgam after condensation . The key is to minimize the amount of
mercury-rich matrix that forms during the reaction. By condensing the amalgam mixture in the
cavity preparation , the mercury-rich matrix rises to the surface and is removed by subsequent
condensing and carving. The final amalgam restoration will be composed of mostly residual alloy and
very little of the mercury-rich matrix.

• Mercury is used to initiate the reaction with the alloy. Although an amalgam restoration is non-
toxic, mercury is poisonous. Free mercury, in the form of vapor or liquid droplets, is a significant
health hazard in the dental office. The greatest potential hazard of chronic mercury toxicity comes
from inha ling mercury vapor. The vaporization is most likely to occur during amalgam condensation
(always use high speed suction). Mercury hypersensitivity (allergy) is very rare (1 in 100 million).

• The area of the condenser point and force exerted on it by the operator determine the
condensation pressure. The smaller the condenser point, the greater pressure exerted on the
amalgam. By doubling the diameter of the condenser and doubling the hand pressure applied to the
instrument, the operator actually exerts less condensation pressure.

• Mercury vaporization in an amalgam restorative procedure utilizing well-sealed pre-measured

capsules is most likely to occur during condensation.

High Copper Amalgam Alloys: newer alloys that contain 10-30% copper in their composition. The main
purpose of adding copper to an amalgam alloy is to decrease the gamma-2 phase (tin-mercury). The
copper reacts with tin to prevent the formation of gamma-2 phase. High copper alloys have less marginal ,..,
CJ CJ
."
:z: ,..,
..... ;:g
breakdown and are less likely to corrode. c:;;~
..... -<:
;:g
• Spherical: sets faster and attains final mechanical properties more rapidly. -< ,..,

• Comminuted: can have zinc or be zinc-free, and can be fine cut or microcut.

• Combination (Admix): a mixture of spherical and comminuted particles.

• Dispersed phase alloy: the original admix alloy (a mixture of communited traditional silver
alloy and spherical particles of silver-copper eutectic alloy (made of elements that when solid
are insoluble and form a layered structure). Most commonly used alloy today.

• Copper contents over 6% ("high-copper" alloys) eliminate gamma-2 phase by forming a copper-tin
phase with superior properties.

393
 • High copper dental amalgams are superior to other amalgams because high copper dental amalgams
are less likely to corrode and have less marginal breakdown.

• High copper content of amalgams are superior to conventional amalgams because high copper dental
amalgams are less likely to corrode and have less marginal breakdown.

Amalgam Setting Expansion:

• Increasing amalgam's trituration time increases compressive strength and decreases setting
expansion (less expansion).
• Increased condensation pressure increases compressive strength, and decreases setting expansion
(less expansion).
• A decrease in particles size increases compressive strength and decreases setting expansion (less
expansion).

Creep (time-dependent deformation or strain relaxation)-deformation with time in response to a

constant stress. Creep is one of the main causes for margin fractures on amalgam restorations. Creep
is time-dependent.
• High copper and low mercury content of an amalgam restoration DECREASE CREEP. Increasing
condensation pressure also decreases creep rate AND the restoration's final mercury content.

• Altering the trituration time and condensation pressure can change the creep rate of an amalgam
restoration. Undertrituration and overtrituration increase the creep rate. If a delay between
trituration and condensation occurs, creep rate increases.

• Higher the creep, the greater marginal deterioration.

• Creep of a metal indicates that the metal will deform under a static load.

• Creep is a property of dental materials that is time-dependent.

Marginal leakage of an amalgam restoration DECREASES as the restoration ages. Corrosion products
are helpful to reduce marginal leakage around amalgam restorations. These corrosion products (tin oxide
&tin sulfide) accumulate in the gap between the restoration and tooth to provide an excellent seal.
The proper amount of time to wait until an amalgam restoration can be finished and polished is 24-
48 hours. The final finish of the amalgam restoration should not be done until after the amalgam is fully
set. It should be delayed for at least 24hrs after condensation and preferably longer. By waiting, you
ensure the reactions between the alloy and mercury is complete, creating a more corrosion-resistant
surface.
• Amalgam restorations should be finished and polished to reduce marginal discrepancies, create
a more hygienic restoration. reduce marginal breakdown which reduces the chance of recurrent
decay, to prevent tarnishing, and improve the restoration's appearance.

• Heat generation during polishing must be avoided. Using dry polishing powders and discs can
easily raise the surface temperature above 60°C (140°F) danger point. Thus, a wet abrasive powder
00
,..., ""CI
z: ,..., in a paste form is the agent of choice. Heat damages the pulp and draws mercury to the restoration
..... ::a
cn~ surface to create an inferior restoration.
..... -
::a <
-< ,...,
• When checking occlusion on a newly condensed amalgam restoration, the marks left by the
articulating paper should be the same intensity as other markings in the same quadrant.

Amalgam's thermal insulation properties explains why cold sensitivity is the most common problem
encountered after placing a dental amalgam restoration. Amalgam is a POOR THERMAL INSULATOR
(this is why a base of calcium hydroxide or ZOE is placed under most amalgam restorations to provide
thermal protection).

394
 Comparison of Materials

Characteristic Direct Gold Amalgam Composite

Close adaptation to cavity walls Very good Good Good

Coefficient of thermal expansion Very good Good Poor

similar to tooth structure

Chemically acceptable to Very good Good Poor

hard/soft tissues

Absence of irritation of gingiva Very good Good Poor

High edge strength Very good Poor Poor

Non-corroding in oral fluids Very good Fair N/A

Insolubility in oral fluids Excellent Excellent Good

Clinical longevity Very good Good Fair

High abrasion resistance Good Good Fair

Permanently restores M-O dimension Good Very good Fair

Withstands masticatory forces Fair Good Poor

Versatility in use Fair Good Poor

Imitates natural tooth color Fair Poor Very Good

Ease of manipulation and placement Poor Good Very Good

Thermal and electrical insulator Very good Poor Good

• In preparing a Class I cavity for dental amalgam , the dentist will diverge the mesial &distal walls
toward the occlusal surface to prevent undermining of the marginal ridges.

• The margins of a dental amalgam restoration are trimmed by carving along the margins with a sharp
instrument that rests on the tooth surface.
co
,..., .."
:z: ,...,
...... :=
• Apatient presents with an amalgam restoration fractured at the isthmus six months after placement. c:;;~
...... -
<
The most likely cause is inadequate preparation depth. :=
-< ,...,

• Proper proximal contour is given to an amalgam restoration placed in a Class II cavity preparation
by carving the restoration and adapting a contoured matrix (not by the matrix retainer, or overfilling
the cavity preparation with amalgam, or heavy condensation of the amalgam) .

• Restoring a cusp with dental amalgam requires at least 2mm of the cusp be removed to provide
resistance form.

• An MO amalgam restoration is more resistant to fracture if the axiopulpalline angle is beveled or

rounded.

395
 • Adeficient margin at a proximogingival cavosurface angle of a freshly condensed Class II amalgam
restoration may have been caused by poor condensation of the amalgam, use of too large an initial
increment of amalgam, or debris in the corner of the proximal box (not from neglecting to wedge the
matrix band) .

• Direction of mesial & distal walls of a Class V amalgam cavity preparation is determined by the
direction of enamel rods.

• Use of water spray and high volume evacuation is recommended when removing old amalgam or
polishing dental amalgam restorations because mercury vapor is released during these procedures.

• When attempting to place a self-threaded pin to retain an amalgam restoration, the spiral drill enters
a vital pulp chamber. The next step should be to cover the pin channel with calcium hydroxide and
proceed .

• When comparing the pulpal depth of a standard Class II inlay cavity preparation with a Class II
dental amalgam cavity preparation, the pulpal wall should be the same depth for both restorations.

• Cusps to be restored with dental amalgam (MOD) should be reduced by 2mm while forming a flat
surface (perpendicular to the occlusal forces).

• Self-threading pins offer the greatest degree of retention into the dentin.

• Threaded pins are used in large dental amalgam restorations to provide retention form.

• Threaded pins used to retain amalgam should NOT be parallel to each other only and should not be
parallel to each other and parallel to the long axis of the crown.

• When pins are included in an amalgam cavity preparation, the strength of amalgam is decreased.

• If the proximal box is too wide to allow facioaxial & linguoaxial grooves to oppose one another, pins
or slots on the gingival floor should be used.

• When pins are included in an amalgam cavity preparation, the strength of the amalgam is decreased.

• A patient has sensitivity in a mandibular premolar. Awell-condensed Class V amalgam restoration

was placed five months prior with no discomfort for the first four months. Since then, it has become
painful. The problem probably relates to irreversible pulpal damage.

• A newly condensed amalgam restoration seems to chip away when being carved. The likely cause of
this problem is the amalgam was condensed after its working time elapsed.

Rubber Dam Functions: the best method to use when attempting to isolate an operating field in the
oral cavity.
00
I'T'I . "
:z: I'T'I 1. Retracts soft tissue (lips, cheeks, tongue) and provides a clean, dry field. "Woodbury" rubber
..... XI
~~ dam frame provides more retraction of the soft tissues. However, the Young's frame is the most
XI
-<
<
I'T'I popular (U-shaped metal frame).

2. Protects the patient by eliminating the possibility of swallowing debris or instruments. It protects the
dentist by isolating him/her from possible infectious conditions in the patient's mouth.

3. Provides for maximum physical properties of materials (i.e. it provides a dry field which is
essential for placing amalgam and cements. *Cements placed under dry conditions have
maximum strengths. A dry field prevents delayed expansion of amalgam.

4. Saves time because the operator can work more efficiently in a clean, dry field where visibility is
not impaired.

5. The use of a rubber dam is the STANDARD OF CARE when performing endodontics.

396
Rubber Dam Advantages: dry clean field, access and visibility, improved properties of dental materials,
protection for the patient and operator, and operating efficiency.

Rubber Dam Disadvantages: time consumption &patient objection. However, if you become proficient
in placing the rubber dame and explain to patients the advantages of using it, you can eliminate these
disadvantages.

Conditions that preclude the use of Rubber Dam: severely tilted teeth, some 3rd molars, partially erupted
teeth, some respiratory problems (asthma or severe colds) where breathing through the nose is difficult.

Important Points About the Rubber Dam:

• Apply lubricant to the lips and corners of the patient's mouth.

• Plot the hole on the rubber dam. Always isolate at least 3 teeth. Punch the appropriate size hole for
a particular tooth. For a tooth bearing a clamp, the hole should be one size larger than the holes over
teeth without a clamp.

• An appropriate clamp is selected that will fit the most distal tooth to be isolated. The dam can either
be stretched over the clamp with the clamp in place on the tooth or may be carried with the dam and
placed on the tooth in one step.

• Once the dam is placed, it is secured with either a Woodbury or Young's holder (frame).

• The rubber dam is INVERTED into the gingival sulcus with floss and/or a blast of air and a plastic
instrument to prevent seepage of saliva.

• When removing the rubber dam, the removal process is the reverse of placing the dam, except
all ligatures (interdental septum of the dam) must be CUT and removed before the dam is
removed.

For a rubber dam clamp to be stable, all four points of the clamp jaws must contact the tooth gingival
to the height of contour. They should not extend beyond the line angles to prevent impingement of
interdental papilla and possible interference with wedge placement. In order for a rubber dam clamp to
be stable on the anchor tooth, all four points of the clamp jaws must contact the anchor tooth and the
clamp must contact the anchor tooth gingival to the tooth's height of contour.

Wrinkling the rubber dam between the teeth isolated means the holes were punched too far apart.
Punching holes too close together in the rubber dam may cause damage to the gingival papilla.

Arubber dam is essential to prevent contamination of the gold with saliva. Acervical clamp is usually
necessary to retract the gingiva (#212 ivory clamp). The hole to be punched in the rubber dam for the
tooth being restored should be facial to the normal alignment with the adjacent teeth.

• The application of a rubber dam for a Class V facial preparation to include #212 clamp on a
mandibular 2nd premolar requires the hole for the 2nd premolar punched larger than usual and slightly ..,
CI
:z:
c::>
~
..,
..... ::c
to the facial of the other holes in the arch . cn!:t
..... -
::c <:
-< ..,
• When punching holes in a rubber dam for a facial Class Vcavity, the hole for the tooth in which the
restoration is to be placed should be located facial to the normal tooth alignment.

• Jaws of a rubber dam retainer should NOT extend beyond the line angles of the anchor tooth to prevent
impingement on the interdental papilla and possible interference with wedge placement.

• When removing a rubber dam, the first step should be to cut the interseptal rubber with scissors.

• In addition to maintaining a dry field, the rubber dam functions to retract soft tissue, protect the
patient and operator, save time, and improve access.

397
 Embrasures-triangular-shaped spaces located between the proximal surfaces of adjacent teeth.
There are 4 embrasures for each contact area (buccal/facial, lingual, occlusal/incisal, cervical/gingival) .
In posterior teeth, gingival tissues fill the cervical embrasure. It is normally "col " shaped from a F-L
cross section view.
• Embrasure Functions: make a spillway for food during mastication, make teeth more self-cleansing,
and protect gingival tissue from undue frictional trauma while providing the proper degree of tissue
stimulation.

• Contact Area-an area where the mesial and distal surfaces of adjacent teeth in the same arch
contact.
• Height of Contour-the thickest portion or point of greatest circumference of the tooth when
viewed from the incisal/occlusal surface. Its functions to form the contact area on the mesial
and distal surfaces and protects the gingiva surrounding the tooth.

• Proximal contact area functions: to support neighboring teeth (stabilize the dental arch),
prevent food particles from entering interproximal areas, protect the periodontium, and form
embrasures.

• Loss of proximal contact between teeth can cause periodontal disease, malocclusion, food
impaction, or drifting of teeth. Thus, it is important to restore proper proximal contact when
restoring teeth to:
1. minimize periodontal pocket formation & food impaction.
2. maintain proper height of interproximal papillae & maintain the tooth 's M-D dimension of
the tooth.

• Contact Point-a point where teeth of opposing arches meet or touch in occlusion or closure.

From the facial view, all premolars have their contacts at the junction of the occlusal and middle
third. From this same view, molars have a proximal contact in the middle third.

From an occlusal view, all posterior teeth have contacts located slightly buccal to the middle third
(mesial & distal). This creates a wide lingual and narrow facial embrasure.

BIOMATERIALS

ADHESION - the attraction of unlike molecules. Adhesive potential is predicted by measuring the
spreading or wetting of the adhesive over a substrate surface. This is done by determining the contact
angle of the drop of adhesive as it spreads out. The smaller the angle, the greater wetting & potential
for adhesion. 2 types of adhesion:
• physical forces (van der Waals forces) .
• chemical forces (chemisorption).
00
J'T'I '"1:1
:z: J'T'I
- I XI
cn~
- I _
Cohesion - the attraction of similar molecules.
XI <
-< J'T'I
Strain -the actual change in shape or deformation that accompanies any stress. 3 Types of Stresses:
1. Compression-the squeezing of material by external forces. If the wire were a thin metal rod on
a firm (hard) surface with a weight on the top, it would spread the weight (stress) across the
entire rod. Here the rod 's atoms are being pushed together.

2. Tension-the pulling of a member or part of a member, resulting in an increase in length. If a

long metal wire were hung from the ceiling with a weight on one end, the weight would place a
force on the wire. Inside the wire, the force spreads evenly through the whole wire. If enough force
or weight were put on the end of the wire, it could cause the wire to stretch . The wire's atoms are
being pulled apart by the weight or force on the wire.

398
 3. Shear-the sliding of one layer of a material relative to another layer of material. Ex: two blocks
of wood nailed together. If one block was pushed to the right, and the other block pushed to the
left, the nails experience a shear stress at the point where the two blocks of wood meet. If pushed
hard enough, the nails could bend or break.

Toughness - the total energy absorbed to the point of fracture (the property of being difficult to
break). It is affected by yield strength, percent elongation, and modulus of elasticity.
The mechanical property of toughness is affected by yield strength, tensile strength, percent elongation,
and modulus of elasticity.

Brittleness - the opposite of toughness. A brittle material is vulnerable to fracture at or near its
proportional limit. A brittle material has a high compressive strength, but low tensile strength (i .e.
amalgam). This is why amalgam preparations doe NOT have beveled margins (they need butt ioints).

Modulus of Elasticity - a measure of a material 's stiffness or rigidity (the ratio of stress to strain
below the elastic limit).
The higher the modulus of elasticity, the stiffer (more rigid) the material.

Resilience - the energy that a material can absorb before the onset of any plastic deformation.

Galvanic Shock - a clinical phenomenon where an electrical charge is created when two dissimilar
metals come into contact. Ex: a dental patient may experience a sharp pain when two restorations
constructed of different materials in opposing arches contact in the wet environment of the oral cavity.
• Ex: an amalgam restoration is placed on the occlusal surface of a lower tooth directly opposing a gold
inlay of a maxillary tooth . Because both restorations are wet with saliva, an electric couple exists, with
a difference in potential between the dissimilar restorations. When the two fillings contact, the
potential is short-circuited through the two alloys, resulting in sharp pain. Such post-operative pain
usually occurs immediately after inserting a new restoration and it gradually subsides and disappears
in a few days.

• Within an hour after cementation of a cast gold onlay on an unanesthetized tooth, the patient
complains of a "shooting pain" every time the teeth come together. The most probable explanation
is a galvanic current caused by the gold onlay occluding with a large amalgam restoration.

Coefficient of Thermal Expansion - a measure of the tendency of a material to change shape

when subjected to temperature changes (i.e. eating or drinking hot or cold items). Apossible break in the
marginal seal of any restoration becomes imminent when there is a marked difference in the CTE between
the tooth and restorative material. The closer the CTE to the tooth , the better (direct gold is the best).

A consequence of thermal expansion and contraction differences between a restorative material and
adjacent tooth structure is percolation (the cyclic ingress and egress of fluids at restoration margins).
The possibility of recurrent decay at the margins increases with increased percolation.
,..,
CI CI
."
:z: ,..,
-I ::c
Material Coefficient of Thermal Expansion (ppm/c x 10) u;~
- I _
::c <
-< ,..,

Tooth 11.4 (lowest)

Direct Gold (the best) 14.4

Amalgam 22-28

Composite 28-35

Unfilled Resin (the worst) 81-92 (highest)

399
 N Elastic limit - the greatest stress a material can be subjected to and still return to it original
dimensions when the forces are released.
• Ex: if a small tensile stress is induced in a wire, the resulting strain might be such that the wire
returns to its original length when the load is removed. If the load is increased progressively in sma ll
increments then released after each additional stress, a stress value finally is found at wh ich the wire
does not return to its original length after the load is removed . In this case, the wire is stressed
beyond its elastic limit.

• The elastic limit (proportional limit) on a stress-strain diagram, the modulus of elasticity is the
ratio of stress to strain.

• Elastic limit and proportional limit are properties so equal in magnitude that they may be used
interchangeably even though they are defined differently.

Proportional limit - the greatest stress produced in a material such that the stress is directly
proportional to the strain. Amaterial with a high proportional limit has more resistance to permanent
deformation than a material with a lower proportional limit.
• While elastic limit & proportional limit are defined differently, their magnitudes are so identical that
these two terms are used interchangeably.

Yield Strength - a stress slightly higher than the proportional limit.

• Before adhesion can occur between a liquid and solid, it is essential that the solid surface be wetted
by the liquid .

• When a liquid wets a solid completely, the contact angle between the liquid and solid is 0°.

• A percentage elongation of a metal is a measure of ductility and is related to the permanent strain
at fracture.

• The property that most closely describes the ability of a cast gold inlay to be burnished is percentage
elongation.

HAND INSTRUMENTS

Modified Pen Grasp - the most common grasp used with hand instruments to allow the greatest
intricacy or delicacy of touch. With this grasp, the middle finger. index finger. and thumb all rest on
the handle close to the junction of the handle and shank. The middle finger rests on the shank, and
thumb and index finger are opposite each other on the handle.

,...,
"",0
..., Inverted Pen Grasp - very seldom used, but is sometimes used for cavity preparations using the
:z ,...,
..... :::a lingual approach on anterior teeth.
~~
:::a<
-< ,...,
Palm & Thumb Grasp - the most powerful grasp, and is most effective on the maxillary arch. It is
similar to the grasp used for holding a knife while peeling the skin of an apple.

Modified Palm &Thumb Grasp - allows much of the power of the palm and thumb grasp, but also
permits more delicate control. It works best when you can rest the thumb on the tooth being restored, or
on the adjacent tooth. Also works best on the maxillary arch.

Excavators - designed to remove caries and refine the internal parts of a preparation. There are 4
types of excavators:
1. Hatchet excavator-has the cutting edge of the blade directed in the same plane of the handle
and is bi-beveled. Used primarily on anterior teeth for preparing retentive areas.

400
 2. Hoe excavator-has the cutting edge of the blade perpendicular to the axis of the handle. NOTES
Commonly used in Class III and V preparations for direct gold.

3. Angle Former-has the cutting edge at an angle (other than 90°) to the blade. Used for sharpening
line angles and is useful to form convenience points for gold foil preparations.

4. Spoon excavator-has a curved blade with a rounded cutting edge. Used to remove carious
dentin and to carve amalgam. These can be sharpened with handpiece stones. Handpiece
stones can be used primarily to sharpen spoon excavators.

Chisels - used mainly to cut enamel. Chisels can be grouped as:

1. Straight, slightly curved, or bin-angle-primarily used for planing or cleaving enamel.
Characterized by a blade that terminates in a cutting edge formed by a one-sided bevel.

2. Enamel Hatchets-chisel bladed instruments with the cutting edge in the plane of the handle.
They come paired left and right. Designed to most effectively plane enamel of the facial and
lingual walls of a Class II amalgam preparation. It is the only instrument that allows the dentist
to have proper access to the margins and that imparts the proper cavosurface angle to the
margins.

3. Gingival Margin Trimmers-similar in design to the enamel hatchet, but has a curved blade and
angled cutting edge. Primarily used for beveling gingival margins, and for rounding or beveling
the axiopulpalline angle of Class II preparations.

The number of bevels that make up the cutting edge can classify hand cutting instruments (i.e. enamel
hatchets and chisels have single bevels, while ordinary hatchets like excavators have two bevels (bi-beveled).
• Dental hand cutting instruments are angled to provide better manipulative control, produce a better
distribution of force, increase efficiency, and establish proper balance when in use.

• 13-80-8-14 hand instrument is most applicable for placing retention grooves in the distal box of a
Class II amalgam preparation on a mandibular left 2nd premolar.

Instruments Used to Trim Restorative Materials (not for cutting tooth structure):
1. knives (finishing, amalgam, gold)-used to trim excess filling material on the facial and lingual surfaces.
2. files-used to trim excess filling material, especially at gingival margins.
3. discoid-cleoid-used mainly for carving occlusal anatomy in unset amalgam restorations.

3 Major Parts of Hand Cutting Instruments:

1. Handle-the part of the instrument held or grasped during activation of the blade. It can be single
or double ended .

2. Shank-connects the blade to the handle. It can be straight or angled (mon-angle, bi-angle, or
triple-angle), meaning one, two, or three angles in the shank. *Proper balance of the instrument
occurs by angling the shank so the cutting edge of the blade is within 2mm of the handle's long c:J C)
-c
axis. To keep the blade within 2mm of the long axis, the shank is angled . I'T'I
:z: I'T'I
..... :::0
cn~
.....
:::0<
-
3. Blade-the working end of the instrument, connected to the handle by the shank. Blades are of -< I'T'I

many designs and sizes, depending on their function .

Nib - is not a major part of a hand cutting instrument. Rather it is the working end of a non-cutting
instrument (i.e. burnisher or condenser). It corresponds to the blade of a hand cutting instrument.

Cutting instruments have formulas that describe the dimensions and angles of the working end:
• 1st number: blade width in tenths of a millimeter.
• 2nd number: primary cutting edge angle in centigrades.
• 3rd number: blade length in millimeters.
• 4th number: blade angle in centigrades.

• Many instruments have 3 measurements in their formulas. #12 in formula 12-5-6 indicates the blade
is 1.2mm wide.
401
 BURS
Bur Parts:
1. Shank-the part that fits into the handpiece. 3 most common shanks (straight, latch-type angle,
and friction-grip angle).

2. Neck-the intermediate portion of a bur that connects the head to the shank. Functions to transm it
rotational and translational forces to the head.

3. Head-the working part of the bur, the cutting edges perform the desired shaping of tooth structure.
Abur's shape refers to the contour of the head. Basic head shapes (round, inverted cone, elliptical, and
fissure (plain, cross-cut, or tapered). Within a given series of burs, the smaller numbers represent smaller
burs, larger numbers represent larger burs.

Types of Burs:
1. Steel Bur-used mainly for finishing procedures.
2. Carbide Bur-used for cavity preparation and performs best at HIGH SPEEDS.

Bur Blades: each bur blade has two sides and three important angles:
1. Rake face-side toward the direction of cutting. The surface (side) of the blade that contacts the
tooth surface and faces in the direction of bur rotation.

2. Clearance face-the surface (side) of the blade that faces away from the direction of bur rotation.

3. Rake angle-the angle made between the line connecting the edge of the blade to the axis of the
bur and rake face. This angle can be positive or negative. Rake angle is the most important
design characteristic of a bur blade.
• Soft materials like acrylics are cut most effectively with (+) angle burs, while extremely hard
and brittle materials (amalgam) are best cut with (-) rake angle burs.

• Carbide burs-used for cutting tooth structure, and usually have (-) rake angles and edge
angles of _90°. To be most effective, these burs should be rotating rapidly before contacting
the tooth. For most effective cutting, a bur should be rotating rapidly before contacting the tooth.

• On a carbide bur, a greater number of cutting blades indicates/results in less efficient cutting
and a smoother surface.

4. Edge angle-the angle of a bur blade formed between the rake face and clearance face.

5. Clearance angle-the angle formed between the clearance face and a tangent to the path of
rotation. Another important factor in blade design, that serves to eliminate friction between the clearance
face and new tooth structure exposed by the cutting edge. The greater clearance angle, the less friction.
co
,..., .."
:z: ,...,
..... ::a Factors that Influence Tooth Temperature During Cutting:
cn~
.....
::a < -
-< ,...,
• Bur sharpness and diameter.

• Bur-to-tooth contact time and amount of force applied to the bur.

• Type of coolant used (water is best); air may dehydrate the tooth or cause the tooth to be
hypersensitive by drawing odontoblasts into the dentinal tubules).

• Dangers of using air as a coolant while cutting with ultra-high speed are that it may dehydrate the
tooth, cause tooth hypersensitivity, and/or draw odontoblasts into the dentinal tubules.

• Factors that Influence Tooth Temperature During a Cutting Procedure: bur diameter and
sharpness, bur-to-tooth contact time, type of coolant used, and amount of force applied to the bur.

402
For an efficient 4-handed dental delivery system, the chairside assistant's position is HIGHER than
the dentist.
• The hand instrument to be transferred to the dentist is held by the assistant between the thumb and
forefinger.

• Whatever equipment is used, it should be compatible for the dentist and assistant.

• Venting the suction exhaust to the building exterior can reduce health hazards to office staff from the
central suction unit.

• The rotary instrument that produces the roughest tooth surface after use is a cross-cut tapered
fissure bur at slow speed.

• A lesser number of blades on a bur results in more efficient cutting, but a rougher surface. Cross-
cut fissure burs at high speed are this type.

• Greater number of cutting blades on a bur, the less efficient cutting, but smoother surface (polishing
burs are this type) .

Types of Dentin:
1. Primary Dentin-forms the initial shape of the tooth, and is deposited before completion of the
apical foramen.

2. Secondary Dentin-dentin formed AFTER completion of the apical foramen at a slower rate than
primary dentin as functional stresses are placed on the tooth. It is a regular and uniform layer of
dentin around the pulp cavity. The junction between primary and secondary dentin is characterized
by a sharp change in the direction of the dentinal tubules.

3. Reparative Dentin-formed very rapidly in response to irritants. Throughout life, dentin responds
to environmental changes (normal wear, caries, operative procedures). These changes initiate
the deposition of reparative dentin which is limited to the site of irritation. The composition or
reparative and secondary dentin is same, except reparative dentin is more irregular and they
differ only in location and deposition. If the environment insult is strong enough, it will kill the
odontoblast and its tubular process, leaving the tubule empty. If there is a collection of empty
tubules (dead tracts), in time these dead tracts calcify and become sclerotic dentin.

4. Sclerotic Dentin-are dentinal tubules that become calcified.

CI CI
,..., -0
:z: ,...,
..... ::c
v;~
.....
::c <:
-
-< ,...,

403
 NOTES OPERATIVE TEST QUESTIONS

• Low coefficient of thermal conductivity is the property most characteristic of current available cement
bases.

• Aluminum oxide disks provide the most desirable finished surface for a composite resin.

• When two teeth have Class II lesions adjacent to each other, the operator should prepare the larger
lesion first and fill the smaller lesion first.

• Class Vcavities are found in the gingival 1/3 of facial and lingual surfaces of anterior and posterior
teeth.

• One month after polishing a Class Vamalgam on a mandibu lar right first molar, the gingival tissue
was receded apically from the gingival margin of the restoration. The dentist should suspect
irreversible tissue change related to finishing.

• The most important consideration for pulp protection in restorative techniques is thickness of
remaining dentin.

• Arestorative material that has a high proportional limit, compared with one with a lower proportional
limit, invariably has more resistance to permanent deformation.

• Contact areas between maxillary premolars are normally found on the facial half of the proximal
surface.

• Place a liner of calcium hydroxide, coat the entire area with cavity varnish followed by a zinc
phosphate cement base is the procedure recommended when deep caries has been excavated and
the cavity is close to the pulp.

• The discolored, corroded, superficial layer frequently seen on the surface of a dental amalgam
restoration is a sulfide.

• In a restorative problem involving all teeth in the mouth, the protrusive condylar path inclination
has its primary influence on the mesial inclines of mandibular cusps and distal inclines of maxillary
cusps.

• Static registration of dynamic occlusion is the functionally generated occlusal registration in an

indirect gold casting technique.

• An indispensable factor in the etiology of dental caries is activity of oral microorganisms.

• The outline form of a cavity preparation is the shape or form of the preparation on the tooth surface.

• It is preferable to prepare narrow cavities rather than wide cavities in order to conserve tooth strength.

• Most detrimental to the strength of a posterior tooth in a cavity preparation is an increase in F-L
...,
CJ C
..."
width .
:z: ...,
..... :::c
c;;;~
..... - • Preparations of Class I cavities forthe reception of amalgam, direct filling gold , and gold inlay have
:::c<
-< ..., in common is divergence of mesial and distal walls occlusally.

• A patient returns to the office one week after a tooth was restored and complains of an intermittent,
vague pain in the same quadrant. The thermal reaction test produces a quick, sharp pain that passes
away immediately. The EPT produce more response than normal. The condition probably is hyperemia
of the pulp.

• Alcohol, calcium hydroxide, ethyl chloride, and silver nitrate, and 10% H202 cannot be used on dentin
as a cavity medicament.

404
• Zinc Chloride-agent most likely to cause necrosis of the sulcular epithelium and adjacent layer of
C.T. when impregnated into string used for tissue retraction. EPI, aluminum sulfate, and aluminum
chloride do not cause necrosis.

• Local anesthetics aid in reducing flow of saliva during operative procedures by reducing sensitivity
and anxiety during tooth preparation.

• To provide proper deflection patterns for food during mastication that will minimize the potential for
gingival irritation, the contact area between premolars is positioned to create a wide lingual and
narrow facial embrasure.

• The bevel on the cavosurface angle of an on lay preparation permits closer adaptation of the gold
margin structure because the thinner margin of the gold overlying the bevel is more adaptable.

• A typical polymer-reinforced ZOE cement retains approximately 20% by weight of polymethyl

methacrylate in the powder component.

• Examination of a patient with a hypersensitive tooth reveals an obviously leaking temporary

restoration that when removed, discloses a good cavity preparation of average depth with no carious
debris and no pulpal exposure. Suspecting a possible hyperemic pulp, the dentist should place an
anodyne dressing of zinc-oxide eugenol.

• A patient returns to the dentist two weeks after a gold onlay was cemented with zinc phosphate
cement complaining of moderate sensitivity to cold. Occlusion is evaluated, and the onlay is not in
hyperocclusion. The dentist should advise the patient to avoid extreme temperatures and that the
sensitivity to cold will gradually decrease.

• Use of a gold casting instead of dental amalgam should be considered in the restoration of an MOD
carious lesion on a maxillary second molar when the preparation is wider than a third of the
intercuspal distance.

• A zinc oxide-eugenol cement base is contraindicated for use with self-curing resin restorative
materials because the cement interferes with polymerization of the resin.

• In differentiating predisposing and inducing factors in the genesis of pulpal pain, an example of
inducing factor is a thermal change.

• Clinically, a maxillary left first molar shows an extensive proximal carious lesion. Hot beverages
trigger a sharp, momentary pain in the carious molar. Acute pulpitis, exposed sensitive dentin , or
partial necrosis of the pulp tissue without periapical involvement can be considered as potentially
causing the patient's complaint (not acute maxillary sinusitis).

• The principal mechanism of the systemic action of fluoride in reducing caries activity most likely is
the result of reduction of enamel solubility as its content of fluoride increases.

• The bur should be tilted lingually when preparing the occlusal aspect of a Class II preparation on a
mandibular first premolar to prevent encroachment on the facial pulpal horn and maintain dentinal
support of the lingual cusp.
...,
co
.."
::z: ...,
• When sealants are placed and maintained over pits and fissures, the effect on progression of carious ..... ::0:0

lesions is decreased development of new lesions and decreased progression of pre-existing lesions. .....-
cn~
::0:0<
-< ...,

• There are no real adverse systemic reactions to gingival retraction cord impregnated with aluminum
chloride.

• Faults in Class II restorations may be predisposing factors to periodontal disease include: gingival
overhang, weak proximal contact, broad F-L contact, and improperly shaped occlusal embrasure.

• Radiographic signs of trauma from occlusion: hypercementosis, root resorption, alteration of lamina
dura and periodontal space.

405
 • Periapical Film-film of choice to evaluate root surfaces, supporting bone, and PDL space (not for
occlusal or proximal caries).

• The marginal ridges of posterior teeth are frequently involved in cast restorations. It is usually
necessary that the restored marginal ridges be in contact with the cusps of opposing teeth and
rounded to help form occlusal embrasures.

• Good oral hygiene and fluoridation will least protect groove defects.

• Dentin is less dense than gold, enamel, amalgam, and porcelain.

• Ayoung adult suffers a traumatic blow to the face displacing lingually a maxillary central incisor.
There is no evidence of tooth fracture clinically or radiograpically. The initial treatment of choice is
to reposition the tooth and stabilize the tooth with a splint and relieve the occlusion.

• The occlusal surface of a wax pattern should be carved to obtain desired occlusal contacts.

• When designing an MO cavity preparation for an inlay, the greatest mechanical advantage to prevent
proximal displacement of the restoration is obtained by establishing an occlusal lock or dovetail.

• Pulp capping has the most favorable prognosis in a situation where there is a mechanical exposure
in a clean, dry field in a developing tooth .

• Progressive destruction of periodontal tissues after restorative procedures is most likely due to rough
surfaces and ill-fitting margins.

• A mechanical separator is inserted between the maxillary right 2nd premolar and first molar. The
space gained is provided mostly by movement of the premolar.

• If in the preparation of a Class II cavity the pulpal wall is established perpendicular to the long axis
of the tooth, the tooth most likely to have a pulp exposure is the mandibular 1st premolar.

• In comparison with poly (methyl-methacrylate), composite resin has a lower coefficient of thermal
expansion, lower polymerization shrinkage, greater compressive strength, and greater stiffness.

• The direction of retention pin holes should be parallel to the nearest external surface.

• Viewed from the occlusal, the contact area between maxillary premolars is normally positioned at the
junction of the facial and middle 1/3 of the crowns.

• One week after cementation of an MOD onlay on a maxillary molar adjacent to an existing amalgam,
the patient reports sensitivity to cold and pressure of the tooth . The most likely cause is
hyperocclusion.

• Acharacteristic common to all inlay preparations for Class II cavities is lack of undercuts.

• Permanent distortion or change in the shape of a casting alloy during its clinical use probably
indicates that the elastic limit was exceeded.

CJ C> • In an MOD cavity prepared for a cast gold onlay, the axial walls should converge slightly from the
..... ""C
:z: .....
..... :::t> gingival walls to the pulpal wall.
c:;;:=
..... -
:::t>c:
-< ..... • In a restorative problem involving all teeth in the mouth, the protrusive condylar path inclination
has its primary influence on the resultant morphology of mesial inclines of mandibular cusps and
distal inclines of maxillary cusps.

• Chronic Caries is caries characterized by a small lesion and dark-brown leathery dentin.

• The higher strength and hardness of die stone (Type IV) compared with plaster (Type II) gypsum are
due to the lesser amount of water required by the die stone for solution and wetting during mixing.

• AClass Vcarious lesion on the maxillary left canine usually has a conical decay pattern with the base
of the cone in the enamel portion on the facial surface.

406
• The DEJ is the area of the tooth most sensitive during cavity preparation .

• The jaw relationship most frequently used in the actual design of restorations is the acquired centric
occlusion.

• The principal reason for a cavosurface bevel of an inlay preparation is to improve marginal
adaptation.

• From facial to lingual, the axiopulpalline angle of an onlay preparation is longer than the axiogingival
line angle.

• Adental assistant holds the hand instrument to be transferred to the dentist between the thumb and
forefinger.

• Fine-grained dental casting alloys have higher strengths than coarse-grained alloys because the
motion of dislocations in the fine grains is stopped sooner by a grain boundary.

• Undercuts, parallel walls, and dovetails are configurations within cavity preparations that contribute
to retention form.

• Av-shaped or wedge-shaped ditch gingival to the CEJ in teeth with some gingival recession indicates
abrasion.

• The binder in casting investments strengthens the investment and contributes to the overall
expansion of the mold through its setting and hygroscopic expansions.

• Superficial decalcification and staining are evident in the buccal groove of a mandibular molar. The
treatment of choice is enameloplasty, limited to the superficial depth of the decalcified enamel.

• To minimize the possibility of porcelain fracture in a metal-ceramic restoration, one should avoid the
use of a casting with sharp angles and use a porcelain that has a coefficient of thermal expansion
close to that of the alloy.

• Complete seating of a Class II cast restoration can be verified clinically by radiograph ic examination
and examination of the gold-tooth margin with a sharp explorer when the restoration is seated in the
tooth.

• A tray used for making an impression for a cast restoration with polysulfide impression material
must be rigid, have occlusal stops, and be coated with an adhesive cement.

• Pulpal trauma caused by ultra-high speed cutting is related to the remaining thickness of dentin,
pressures placed on the instrument while cutting, coolant used while cutting, and bur sharpness.

• Fluoride ion is easily exchanged for hydroxyl ion in the lattice structure of enamel because the fluoride
ion is slightly smaller than the hydroxyl ion and the fluoride ion has a greater affinity for the
hydroxylapatite crystal than the hydroxyl ion.

• Objectives of electrosurgical procedures before making impressions for cast restorations: hemostasis,
access to cavosurface margins, minimal areas of coagulation , and reduction of the inner wall of the
,...,
CJ CJ
."
gingival sulcus. :z: ,...,
..... :::a
v;!:i
..... -
• Elastic impression materials like reversible hydrocolloid or polysulfide rubber require proper soft :::ac::
-< ,...,
tissue management. Effective tissue displacement is accomplished by placing chemical-impregnated
cords into the sulcus & electrosurgery.

• Resistance form in a cavity preparation is achieved by pulpal and gingival walls perpendicular to
occlusal forces and proper angulation of cavity walls.

• Radiographic signs of trauma from occlusion include: hypercementosis, root resorption, alteration of
lamina dura and periodontal space.

• The location of the gingival margin in the preparation of proximal cavities for a cast restoration is
influenced by theh amount of retention required, need to extend gingivally to clear the contact area,
and convenience form.

407
 • Main disadvantages of using polymethyl-methacrylate as a restorative material are its low resistance
to abrasion and high coefficient of thermal expansion.

• Common signs of trauma from occlusion include: mobility, thermal sensitivity, sensitivity to
percussion, and attrition of the enamel (not thickening of cementum).

• When a tooth has a hyperemic pulp, pain of short duration may occur, pain is intensified by applying
cold, and the tooth may respond at low levels (decreased current) to an EPT.

• Considerations that must be incorporated to result in an efficient four-handed dental delivery system
of dental care: equipment selection, standardization of instruments, positioning of patient, dentist,
and auxiliary, transfer of instrument techniques, and standardization of operatory design.

• Two months after placing a large MOD inlay in a maxillary 2nd premolar, the patient has dull pain
on pressure and some thermal sensitivity. Potential causes include a cracked tooth or the tooth is in
supraocclusion .

• Precautions that should be taken when making an acrylic resin temporary restoration for a large
MOO onlay preparation: polymerization should not go to completion in the mouth, overextended resin
should be removed, open margins are avoided, and undercuts in the preparation should be blocked out.

• The porcelain of a metal-ceramic crown is separated at the porcelain-metal interface. Technical or

clinical problems that may have caused the separation are "degassing" metal at too Iowa
temperature and fusing the opaque coat of porcelain at too Iowa temperature.

• Properties usually found in materials that consist of ionic bonds are brittleness and high melting point
(not weakness).

• In an MOD cavity in a second premolar prepared for amalgam, the matrix is placed around the tooth.
Before inserting the amalgam, tapered wedges are placed interproximally to obtain close adaptation
of the matrix at the gingival margins and the band is burnished into contact with the adjacent teeth.

• Effects of cold working a metal are decrease in ductility and increase in hardness.

• Drugs that act as anti-sialogogues: Atropine and Methantheline (Banthine).

• Daily application of 1.23% acidulated phosphate fluoride in fitted trays for 4 minutes each is the most
effective way to increase the fluoride content in the external layers of teeth.

• The use of retraction cord impregnated with 8% racemic EPI may be hazardous for some patients
because of its potential for systemic action.

• The 8% racemic EPI-containing cord for tissue management during cast gold procedures, may prove
hazardous for some patients because of its systemic vasoconstricting action.

• The direction of mesial and distal walls of a Class V amalgam cavity preparation is determined by
the direction of the enamel rods.

• Adding difunctional monomers is the procedure indicated to produce cross-linking during

c
,..., CI
.."
:z: ,..., polymerization of a linear polymer.
- f ::<:I
c;;~
- f _
::<:1<:
-< ,..., • It has become necessary to remove a conservative DO inlay from a maxillary second premolar. The
method of choice is to cut through the isthmus to remove the proximal and occlusal in two pieces.

• The greatest potential hazard of chronic mercury toxicity comes from inhalation of mercury vapor.

• Outline form of a cavity preparation is the shape or form of the preparation on the tooth surface.

• The amount of force needed to compact direct filling gold properly is influenced mostly by the surface
area of the condenser.

• Areason for sealing caries into the cavity is to allow formation of secondary dentin before complete
excavation.

408
• Adaptation of a matrix band to the gingival aspect of a Class II amalgam cavity preparation may be NOTES
most difficult in an MO preparation of a maxillary first premolar.

• The external shape of an initial Class V carious lesion in enamel is related to the contour of the
gingiva.

• During preparation for a cast gold restoration, the tooth tissue that is weakened by the cavity
preparation and subjected to damage by the forces of mastication must be reduced and covered by
the cast restoration.

• Different microstructure has been described for gold foil, mat gold, and granular (powdered) gold. It
has been demonstrated at the microscopic level that void spaces remain in any compacted gold.

• The contact area on the distal surface of a maxillary first premolar should be placed in the occlusal
third of the proximal surface with the lingual embrasure greater than the facial embrasure.

• The strength of dental investments for gold alloys is dependent upon the amount of gypsum.

• Treatment of choice for hypersensitive erosion areas is to apply a sodium fluoride paste.

• Dental floss is applied to the distal bow of the clamp and allowed to extend from the mouth so that
the clamp may be easily retrieved if it slips from the clamp forceps or the tooth.

• When seating a quadrant of onlays, the occlusal relationship should be opposing teeth contacting
the castings to the same degree the teeth contact on the opposite side.

• The occlusal isthmus of an MO dental amalgam restoration is more resistant to fracture if the
axiopulpalline angle is rounded.

• With respect to the relationship between marginal leakage of an amalgam and the age of the
restoration, marginal leakage decreases as the restoration ages.

• Afundamental guideline that governs the outline form of a Class II cavity preparation is to extend
the margins until sound enamel is obtained within the cavity outline.

• Contact areas are always carefully restored to protect the gingival tissues.

• Reversible hydrocolloid has the longest shelf life.

• Carboxylic acid is the component that could replace eugenol in a zinc-oxide paste.

• Chelation-a chemical phenomena common to zinc oxide-eugenol and polycarboxylate cements.

• The gingival contour of a cast restoration that replaces the coronal portion and part of the root portion
of a posterior tooth should be an extension of the original contour of the clinical crown to the gingival
margin of the restoration.

• Direct pulp capping is indicated when there is an accidental mechanical exposure in a clean,
dry field.
CJ CJ
• On a carbide bur, a greater number of cutting blades results in less efficient cutting and smoother ,.,., -0
:z: ,.,.,
surface. ......
cn~
""
...... -
""<
-< ,.,.,
• Improved zinc oxide-eugenol materials serve as good temporary restorations pending placement of
a permanent restoration because they have excellent marginal seal, have a therapeutic palliative
effect on the dental pulp, have thermal insulation qualities comparable to dentin, and maintain
opposing and adjacent teeth in their respective positions.

• In constructing a custom tray to use with polysulfide rubber material, the thickness of the rubber
should be even throughout to allow for dimensional accuracy.

• Cavosurface margins or wall junctions of an onlay cavity should be beveled where the pulpal wall
meets the axial wall, gingival bevel meets the proximal external planes, and where the external planes
of the proximal portion join the bevel of the occlusal portion.

409
 • The principal component of dental plaque is MICROORGANISMS.

• Apatient reports for treatment after sustaining a blow that resulted in a crown fracture of a maxillary
second premolar 2mm apical to the anatomic crown. The patient had previous extensive periodontal
surgery and has been practicing excellent oral hygiene. The treatment of choice is RCT followed by
an appropriate restoration.

• The primary purpose of careful restoration of contact areas is to protect gingival tissues.

• Examination of a patient with a hypersensitive tooth reveals an obviously leaking temporary

restoration that when removed, discloses a good cavity preparation of average depth with no carious
debris and no pulpal exposure. Suspecting a possible hyperemic pulp, the dentist should place an
anodyne dressing of zinc oxide-eugenol.

• The drinking water supply of a Midwest town has a natural fluoride level of 0.6ppm. If the fluoride
level is raised by O.4ppm, tooth decay among grade school children is expected to decrease by -40%
after seven years.

• In diagnosing interproximal carious lesions (Class II & III) that cannot be explored directly, a
good supplement to the radiograph is examining for color changes or loss of translucency
beneath marginal ridges.

• Apatient returns to the dentist office two days after placement of an MO inlay in a maxillary premolar.
His complaint that the tooth is sensitive to chewing pressure indicates a need for occlusal adjustment.

• Reversible pulpitis changes to irreversible pulpitis primarily because of invasion of microorganisms.

• As the fluoride concentration in drinking water is increased from Ippm to 4ppm, caries incidence
remains essentially the same, but mottling of enamel increases.

• Using the pick-up and delivery technique, the thumb and first two fingers on the assistant's hand
form the "delivery" portion.

• A 16-year old patient has a large, radiolucent carious lesion on the distal aspect of a first molar.
Treatment of choice is to remove the superficial portion of the decayed tooth tissue and place an
indirect pulp cap.

• Air bubbles and fracture of the investment are casting defects that are prevented by vacuum
investing.

• Two weeks ago, well-finished onlays were seated on a maxillary second premolar and first molar. The
patient now has a fractured lingual cusp on the first premolar of the same arch. Possible causes are
the onlays are in infraocclusion, the onlays accentuated a previous non-working contact on the first
premolar, or the patient recently bit into a hard object.

• Low polymerization shrinkage and low coefficient of thermal expansion are properties that enable
com posite resins to be placed by the bulk technique with achievement and maintenance of reasonably
good adaptation to cavity walls.
c::JC
..., ""C
:z: ..., • Materials contraindicated for placement under and in contact with composite resin are varnish and
...... ""
v;~
...... - zinc oxide-eugenol.
"" c::
-< ...,
• Pulp has several defense mechanisms to protect it from irritation: sclerotic dentin, reparative dentin,
and vascularity.

• The use of propantheline bromide (Pro-Banthine) to control salivary secretion is contraindicated in

patient with glaucoma or cardiovascular distress.

• Marginal ridges of posterior teeth are frequently involved in cast restorations. It is necessary that the
restored marginal ridges be in contact with the cusps of opposing teeth and be rounded to help form
the occlusal embrasures.

410
• Objectives of electrosurgical procedures before making impressions for cast restorations are
coagulation, hemostasis, access to cavosurface margins, and reduction of the inner wall of the
gingival sulcus.

• Incorporating additional moisture during mixing will accelerate the set of polysulfide impression
material and a zinc oxide-eugenol impression paste.

• The axial wall of a large Class Vcavity prepared for direct filling gold is convex in a M-D direction in
order to conserve tooth tissue and minimize pulpal irritation.

• Selection of appropriate bases and liners to restore the axial wall of a Class II restoration depends
on the biologic effect required and thickness of remaining dentin.

• The bur should be tilted lingually when preparing the occlusal aspect of a Class II dental amalgam
preparation on a mandibular first premolar to prevent encroachment on the facial pulp horn and
maintain dentinal support of the lingual cusp.

• Pre-set trays, choice of equipment, and standardized work patterns are closely linked to work
simplification.

• In developing cavosurface angles for all types of restorative materials normally used in posterior
teeth, desirable features include margins of the restoration placed in areas more easily cleaned,
enamel rods supported by dentin, and a definite cavosurface angle.

• Research data indicates that pit and fissure sealants are retained best on maxillary and mandibular
premolars.

• Features of tooth morphology responsible for food deflection include marginal ridges, facial and
lingual contours, and facioproximalline angles (not central fossae) .

• The least likely microbial species found in dental plaque is Staphylococcus aureus.

• With careful technique, soft tissue management for elastic impressions is usually safely
accomplished by using a cotton cord, alum -impregnated cord , EPI-impregnated cord (not a zinc
chloride-impregnated cord).

• A 12-year old boy has deep fissures but no apparent caries on his permanent molars. The least
acceptable treatment for this condition is to place a conservative amalgam restoration. You can
place pit and fissure sealants, treat with topical fluoride, perform enameloplasty, or simply nothing.

• The margin of a preparation for casting should NOT be placed in a wear facet area. It can be placed
in a lingual bevel, marginal ridge, or gingival sulcus.

• Adentist is preparing tooth #30 for an occlusal amalgam restoration . Once the ideal outline form and
depth are established, the dentist notes that caries remains on the facial, pulpal, and lingual walls
of the preparation . The next step in treatment is to extend the outline form .

• Shim stock is the best method for evaluating centric occlusion on a newly placed onlay restoration.
C> C)
• Adentist inadvertently sealed a small carious lesion in the occlusal surface of a maxillary first molar. ,..,., ."
:z: ,..,.,
..... ::a
This would most likely result in arrested caries. cn~
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• A Class II cavity preparation in a primary molar for dental amalgam restoration will not require a
gingival bevel because the enamel rods in the area incline occlusally.

• Likely causes of rampant caries in geriatric patients are poor oral hygiene, decreased salivary flow,
and medication side effects (not a change in oral microflora).

• During the preparation of a Class II cavity, the facial pulp horns of a mandibular first premolar are
most likely to be subjected to an accidental pulp exposure.

• The most effective way to reduce injury to the pulp during a restorative procedure is to minimize
dehydration of the dentinal surface.

411
 N • In determining the caries rate for older adults, and epidemiologist usually uses the DMFT index
because it can be difficult to ascertain why teeth are missing. Both the statement and reason are
correct and related.

• Acomposite restoration is wider than the diameter of the light tip of the curing unit. In this situation,
the restoration is cured by placing the tip stepwise over each area and exposing each area for the
required time.

• The major difference between a Class Vcavity preparation for amalgam and for composite resin by
the acid-etch technique is the angulation of the enamel cavosurface margins.

• The wave length of light emitted by a light-curing unit should be checked periodically with a dental
light meter. This meter detects light only in the range of 400-499nm.

• The syringe material that is most rigid, thus the most difficult to remove from the mouth is polyether.

• When cementing a cast restoration, the dentist should apply the cement on both the restoration and
preparation.

• When seating a casting, the practitioner usually finds the initial interferences at (on) the proximal
contacts.

• If after six weeks, a pulp-capped tooth were asymptomatic, one can conclude that the lack of adverse
symptoms might be temporary (you cannot conclude that pulp capping was a success or that
reparative dentin formation at the exposure site was complete) .

• To prevent physical injury most effectively when using pickling solutions, dentists should wear
safety goggles.

• Mechanical (brush and floss) is the current method-of-choice for removing or disrupting bacterial
masses in the mouth.

• In selecting a dental base, the dentist should give the greatest consideration to the thickness of
remaining dentin.

• The cusps to be restored with dental amalgam should be reduced by 2mm while forming a flattened
surface.

• Currently, bonding of composite restorative materials to dentin depends on difunctional coupling

agents.

• The dentist plans to make an impression of an onlay preparation. To prepare the tissues around the
preparation for the procedure, this dentist will use electrosurgery. When correctly used, electrosurgery
will remove a thin layer of crevicular gingival tissue.

• Adentist is restoring an endodontically treated posterior tooth with a pulp chamber-retained amalgam
restoration. Ideally, the dentist should place the amalgam 3mm deep into each root canal to obtain
satisfactory retention.
...,
CI 0
.....
::z ..., • Retention of fissure sealants is chiefly the result of mechanical microretention .
..... :=
cn!:i
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• For most effective cutting and long usefulness of a tungsten carbide bur, it should be rotating rapidly
before contacting the tooth.

• The primary determinant of the outline form of a Class Vpreparation is the extension of the carious
lesion.

• Ateen-aged patient presents with numerous proximal carious lesions that undermine the occlusal
enamel. The treatment of choice is to restore the involved teeth as rapidly as possible using dental
amalgam.

412
• Following cleansing of a tooth, new plaque growth accumulates mainly on the interproximal
surfaces.

• A dentist anticipates the possibility of a pulpal exposure of a vital, asymptomatic tooth during a
cavity preparation. In this situation, the dentist should leave the carious material in the deeper
areas, base, and restore appropriately.

• A dentist adjusts the shade of a restoration using a complementary color. This procedure results in
decreased value.

• The materials used in the "walking bleach" technique are sodium perborate and 30% aqueous H202'

• Convenience for access, and size, shape, and location of caries determines the outline form for a Class
III composite restoration (extension for prevention does not determine outline form).

• Reasons for beveling a preparation for a restoration with composite resins: to increase surface area
of enamel for etching, to expose the ends rather than the sides of enamel rods, and to enhance the
enamo-resin marginal seal.

• Increment thickness most affects curing a light-activated composite resin.

• Two adjacent cavities involving proximal contact can be prepared and restored with composite resin
at one appointment because access to adjacent cavities is simplified and color matching is easier.
Doing this does not enhance the restoration of contact.

• Before adhesion can take place between a liquid and solid, it is essential that the liquid surface
exhibit a small contact angle with the solid.

• A 33-year old female patient states her mandibular first molar has been hurting since the recent
placement of an amalgam restoration. She describes the pain as mild-to-moderate, non-spontaneous,
but provoked by cold, heat, and sweets. These symptoms correspond with reversible pulpitis.

• The dentist will use the acid-etch technique to make a minimal cavity preparation for composite
resin. Advantages of this technique are it conserves tooth structure and improves restoration
esthetics. It does not provide greater access for finishing procedures.

• A practitioner is restoring the mesio-occlusal marginal ridge of a maxillary left second molar. If the
marginal ridge is higher than the adjacent tooth, then it can create a problem in retrusive excursion.

• Tooth bleaching affects a color change in both dentin and enamel.

• Surface characteristics of a restoration affect its perceived form because a surface smoother than
normal will give the impression of a larger size.

• Fluoride therapy and occlusal sealants modify the HOST the most.

• 1.5mm is the optimal reduction of the lingual cusps on tooth #3 to receive an MODL onlay.

• Class I carious lesions are the least likely to occur on the lingual surfaces of mandibular incisors.
CI
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• Orange stain is used to change the hue of porcelain color. :z: .....
..... ::c
cn!:i
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• Green and orange stains on maxillary incisors can usually be attributed to poor oral hygiene. ::c -==
-< .....

• Aproperly trimmed wooden wedge will protect the gingival tissue, provide space for the matrix band,
and reduce moisture leakage into the cavity preparation. It will not prevent overcontouring of the
contact area .

• The best measure of the potential clinical performance of a casting alloy is its ADA certification.

• Stiffness or rigidity is measured by the modulus of elasticity.

413
 N • An 82-year old women presents with a large four-surface pin-retained amalgam on tooth #3. The
dentist notes minor recurrent caries along the faciocervical amalgam margin. The treatment of
choice is to repair the defect (do not replace the restoration or prepare the tooth for a crown).

• The light source affects the perception of color because the light source must contain the color's
wavelength to be matched in order to see that color.

• Dextranase is the enzyme when incorporated into a mouthwash is most likely to interfere with
microbial aggregation in the plaque mass.

• Microorganisms gain entrance to the dental pulp mainly by way of a carious lesion.

• In humans, mercury from dental amalgam restorations is most efficiently absorbed by inhalation of
mercury vapor.

• The use a retraction cord impregnated with racemic EPI is hazardous for some patients due to a
potential for systemic action (increase HR and BP).

• During completion of an MOD onlay preparation, it becomes necessary to extend the distogingival
margin subgingivally to the levellmm occlusal to the alveolar crest. The next step is to perform a
crown lengthening procedure.

• To minimize fovial fatigue when making a shade selection on a patient, the dentist should use an
observation time of 5 seconds or less.

• A study to compare mouthwash A with mouthwash B to reduce halitosis is being planned. The null
hypothesis for this study should be there is no difference in effectiveness between mouthwash A
and mouthwash B.

• The most frequent cause of failure of dental amalgam restorations is improper cavity design.

• Pit &fissure caries has a conical configuration on both sides of the DEJ, thus the bases of both
cones are at the DEJ.

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414
EHAPTEH 1$

415
 NOTES BEHAVIORAL MANAGEMENT &THERAPY
Psychosocial Factors that strongly influence behavior: attitudes, beliefs, values, family, society, cul-
ture, and education . Behavior is a determined, purposeful unit of activity.
• Determined-the assumption that behavior is lawful and has determinants.
• Purposeful-the assumption that behavior is goal-oriented, that is seeks to achieve positive and
reduce negative need or motivationa I states.
• Unit of Activity-what a person does that can be reported or described as discrete elements.

Ex: teeth do not behave, individuals behave. Observing that a pulpal or periodontal problem exists is a
common behavior for the dentist. Avoiding the dentist, even though an objective need exists and the
patient requires treatment, is a common behavior for patients. Both meet the criterion of being deter-
mined, purposeful units of human activity.

BEHAVIORAL DEVElOPMENT - any observable response mediated through the neuromotor sys-
tem. To understand the development of human behavior, you must understand the basic concepts of
maturation and learning. There are 4 major fields of behavior:
1. Personal Social-is usually a function of environment, work, play, and society.
2. Motor-starting point to access maturity.
3. language-vocalization, words, sentences, facial, and manual movements.
4. Adaptive-use of motor capacity and solutions to practical behavior.

BEHAVIOR MANAGEMENT - the means by which the dental health team effectively &efficiently
performs treatment for the patient while simultaneously instilling a positive attitude. Most researchers
believe changes in behavior are a prerequisite to changes in attitude.

Ex: Ashley, a 32-year-old women, comes in for her routine cleaning appointment. Stephanie, the hy-
gienist finds that Ashley has not been following the home care program recommended six months ago.
Stephanie believes Ashley's problem is a management deficiency, not a skills deficiency. Thus, the
best course of action for Stephanie to take is to meet with her supervising dentist to determine the
future course of action.

• Since this is not a skills deficiency problem, reviewing homecare techniques is not going to solve the
problem . Ashley knows what to do. Now Stephanie and Ashley's supervising dentist needs to find a
way to motivate Ashley to find the time to brush and floss.

• The most effective way to teach oral hygiene skills is by having the patient participate in repeated,
supervised training sessions.

• The best time to determine a patient's plaque index (to assess the effectiveness of patient homecare)
is at the beginning of the appointment. Rather than just asking about the patient's homecare skills,
have the patient demonstrate their brushing/flossing skills.

• Maintaining a 4-year-old child's healthy dentition starts with educating the parent.

• Having your teeth cleaned and examined regularly and keeping them clean daily at home is the best
way to prevent periodontal disease.

• Patient information required to plan dental hygiene care includes: health & dental history, dietary
analysis, and periodontal examination.

416
7 Steps in the Educational Process:
1. Step 1 (Recognizing Needs)-the dentist recognizes educational needs as he checks for treatment
NOTES
needs. Then, the dentist helps the patient recognize his own needs.
2. Step 2 (Expressing Needs)-the dentist records educational needs and helps the patient state
his own needs.
3. Step 3 (Stimulating Motivation)-motivation arouses and maintains interest. The dentist may
appeal to inner needs or use artificial stimuli.
4. Step 4 (Setting Goals)-goals may be short-term or long-term guides to activity. The goals must
be meaningful, attractive, and attainable.
5. Step 5 (Acting to Achieve Goals)-activity is necessary to learning. The activity should be
directed toward specific goals.
6. Step 6 (Reinforcing Learning)-review and repetition aid in retention of learning.
7. Step 7 (Evaluating Results)-aids in judging what the patient has learned and how effective
the dentist's teaching has been. This can help clarify or redefine the goals.

Each learning situation will not follow these steps in this exact sequence, but most learning situa-
tions will include all of these steps in some form.

Needs & Learning:

• Needs are driving forces that prompt a person to act. Motivation stimulates a person to act on his
needs and is a fundamental part of every learning situation. Motivation can be artificial or built-in .
Needs and goals may provide motivation, and patients rarely learn without some motivation.
Motivation arouses and maintains interests.

• Short-range goals are less remote and more easily attained than long-term goals. Goals should be
attractive and attainable to be meaningful. Goal-directed activity is required for learning.

• The learning process is continual and multiple, and occurs as a person attempts to satisfy needs.

• Telling a person what he needs may convince him that a behavior change is desirable.

• Expressing needs helps pinpoint them for the dentist and patient.

• Recording educational needs can be as important as recording treatment needs.

BEHAVIOR MODIFICATION (BEHAVIOR THERAPY) - a type of psychotherapy that attempts to

modify observable, maladjusted behavior patterns by substituting a new response or set of responses to a
given stimulus. Psychologists have developed many techniques to modify patient behavior by using the
principles of learning theory. Examples of techniques/methods used mainly in pediatric dentistry:

1. Classical Conditioning (Pavlovian or Respondent Conditioning)-a mechanism by which

behavioral responses are learned. Operates by associating one stimulus with another. A
stimulus leads to a response. If individuals in white coats give painful injections that cause
crying, the sight of an individual in a white coat soon may provoke a crying outburst. If this is not
reinforced, the conditioned response will no longer occur (extinction of the conditioned behavior).
Classical conditioning is a form of learning in which a previously neutral stimulus comes to
elicit a given response through associative training.

2. Operant Conditioning-the consequences of a behavior is in itself a stimulus that can affect

future behavior. The consequences that follow a response alter the probability of that response
occurring again in a similar situation . It is a form of learning in which the person undergoing
therapy is rewarded for the correct response and punished for the incorrect response. There are
4 types of operant conditioning distinguished by the nature of the consequence: positive &
negative reinforcement, omission, and punishment.

417
 • Behavior Shaping (Successive Approximation)-an operant conditioning technique used in behavior
therapy in which new behavior is produced by providing reinforcement for progressively closer
approximations of the final desired behavior. It is a common non-pharmacologic technique.
• Proponents of this theory believe that most behavior is learned, and learning is the establishment
of a connection between a stimulus and a response. Thus, it is sometimes called the "Stimulus-
Response Theory" (SR Theory).
• When shaping behavior, the dentist assistant or dentist is teaching a child how to behave. Young
children are led through these procedures step-by-step.
• Behavior Shaping is regarded as a learning model. A general rule about learning models is the
most efficient learning models are those that follow the learning theory model most closely.
• Ex: attempting to change several aspects of a patient's oral hygiene regimen should be done one
aspect at a time (sequentially). Have the patient mimic the correct oral hygiene behavior to
increase the chances of succeeding in changing the patient's behavior.

3. Aversion Conditioning-a technique in which punishment, unpleasant or painful stimuli are used
in the suppression of undesirable behavior. In dentistry it is called the "Hand-Over-Mouth"
technique (HOME).

4. Observational learning (Modeling or Behavior Shaping)-a behavior acquired through initiation

of a behavior observed in a social context. There are two distinct stages in observational learning:
acquisition of the behavior by observing the behavior and the actual performance of the behavior.
Having an open dental office design may aid in the dentist in this method. Children can watch
other cooperative children, and this may rub off on them. Modeling is a technique in which the
person learns a desired response by observing it being performed. Relative maturity modifies
expectations of a child's behavior in that a child cannot be expected to learn a mode of behavior
until he has matured to a stage at which he is ready for such learning.

5. Systemic Oesensitization-a technique used to eliminate maladaptive anxiety associated with

phobias. The procedure involves the construction by the person of a hierarchy of anxiety
producing stimuli and the general presentation of these stimuli until they no longer elicit
the initial response of fear.

Communication is basic to all aspects of the dentist-patient relationship. Without proper communi-
cation (verbal or non-verbal), dentist-patient relationships would fail. Acceptable non-verbal behavior
varies with age, sex, ethnic background, geographical region, culture, and situation.
• When communicating with children, try to reinforce positive behavior by telling the child exactly
what he is doing well.
• Non-verbal behaviors: posture, facial expression, eye-contact (most important), body position
(physical proximity), and gesticulations. Eye Contact is the primary non-verbal cue that two or
more people use to regulate verbal communication. Eyes are directed toward the patient and
engage the patient's eyes as frequently as is comfortable for the speaker and listener.

Types of Questions: These are all VERBAL communication behaviors.

1. Open-Ended Questions: requests information in the patient's own words and specifies a general
content area. Ex: "How are you doing with your brushing and flossing?" When presenting
treatment plans always use open-ended questions (questions that cannot be answered with a
simple "yes" or "no"). Open-ended questions are the most effective in helping patients to express
their understanding of the proposed treatment plan. When reviewing oral hygiene, have the
patient repeat what you have gone over with them.
2. Direct Questions: questions that ask the patient for a specific bit of information. Ex: "Is it easier
to hold the brush this way?"
3. Probing Questions: Questions that ask for more specific information that the patient offers
spontaneously. Ex: "What else did you notice about your gums?"
4. laundry-list Questions: Questions that ask the patient to respond from among a list of alternative
adjectives or descriptions provided. Ex: "Is the pain throbbing, aching, dull, or sharp?"
5. leading Questions: Questions that entice a patient to answer a specific way. Ex: "You are not
afraid of needles, are you?"
6. FaCilitating Questions: questions that encourage the patient to say more without specifying an
area or topic. Ex: "How are you?"

418
AVERSIVE CONDITIONS of interaction between the dentist & patient: psychophysiological reactions,
stress, anxiety, fear, and pain. These conditions are perceived as aversive and the dentist-patient in-
teractions seeks to MINIMIZE them.

NON-AVERSIVE CONDITIONS are perceived as non-aversive, and the dentist-patient interactions seeks
to MAXIMIZE them.
• Communication-gathering information, identifying problems, giving information
(as in case presentations).
• Preventive oral-health behavior.
• Management of exceptional patients such as the physically or emotionally disabled. For these
patients, gradually expose them to the dental office.

Specific Ways to Effectively Communicate with Patients:

• Describe, be specific, be responsive, time appropriate, and pay attention (the best way to show a
patient you care about what he/she is telling you is to use EYE CONTACT). Do not evaluate, be
general, be evasive or premature, too deep, or inattentive or wander.

Aggression:
1. Constructive Aggression-an act of self-assertiveness in response to a threatening action for
purpose of self-protection and preservation.
2. Destructive Aggression-an act of hostility unnecessary for self-protection or preservation
directed toward an external object or person.
3. Inward Aggression-destructive behavior directed against oneself.
4. Aggressive personality-a personality with behavior patterns characterized by irritability,
tantrums, destructiveness, or violence in response to a frustration.

Stress, Anxiety, & Fear are simultaneously negative or aversive emotional states, full of symptoms
that can motivate through a process of threat appraisal. The interaction of the intensity of an emo-
tional response with threat appraisal determines the content of the behavior that will follow (whether
or not to show up at the dentist's office, to submit to an injection, to accept the need for an extraction
or filling, etc.)

1. Anxiety-a state or feeling of apprehension, uneasiness, agitation, or uncertainty resulting from

the anticipation of some threat or danger, usually of intrapsychic rather than external origin,
whose source is generally unknown or unrecognized. The ANXIOUS patient is usually considered
the most difficult patient. Most dentists become anxious with an anxious patient. Most patients
who are anxious have had a traumatic experience in a dental or medical setting. Ways to
reduce patient anxiety:
• Explain procedures before doing them and forewarn about the possibility of pain.
• Give the patient some control over the procedures and pain (i.e. raise your hand if you
feel anything).
• Build trust between you and the patient.
• Watching a patient's eyes or eyebrows is a good indication if the patient feels pain
during dental treatment.

2. Fear-anticipation of a threat elicited by an external object generally agreed to be harmful. In

evaluating a patient's dental fears, take note of what the patient says, how he/she behaves, and
how they appear while in the dental office. Fear is distinguished from anxiety on the basis of
the person's ability to locate the threatening agent "out there" and to recognize the clear
presence of a behavior that will reduce perceived danger. Patients who are fearful or anxious
will do anything to put off making dental appointments.

3. Stress-a general disturbance in psycho-physiological adaptation. It implies a person who is being

maladaptively influenced by more than one negative or aversive factor. Stress is mostly
associated with response aspects.

419
 Parent Types:
1. Manipulative Parents: have excessively demanding attitudes that usually start with
appointment times and can extend to directing the course of diagnosis or treatment.
2. Overprotective Parents: insist on remaining with the child in the dental operatory, regardless of
the situation or child's age. Pointing to the lack of apprehension of a young child and the
importance of establishing a one-to-one relationship between the child and dentist, usually
satisfies most overprotective parents. Overprotective parents usually have children who are
shy, docile, and manageable.
3. Hostile Parents: question the necessity for treatment usually due to distrust, not curiosity.
4. Neglectful Parents: fail to maintain appointments, miss recall visits, or do not oversee the
child's oral hygiene.

Children with defiant behavior are usually stubborn or spoiled. For hostile or angry children, try to
identify the underlying source of these emotions (this holds true for adult patients too).

Health Belief Model-a conceptual framework that describes a person's health behavior as an ex-
pression of his or her health beliefs. HBM was designed to predict a person's health behavior, includ-
ing the use of health services and to justify intervention to alter maladaptive health behavior. Health
Belief Model suggests that individuals will act to prevent disease only when they believe they are
susceptible to disease. A patient's compliance is affected by their perception of a disease's severity
and length of a treatment regimen. Components of the Health Belief Model:
1. person's own perception of susceptibility to a disease or condition.
2. likelihood of contracting that disease or condition.
3. person's perception of the severity of the consequences of contracting the condition or disease.
4. perceived benefits of care and barriers to preventive behavior.
5. internal or external stimuli that result in appropriate health behavior by the person.

UNIVERSAL PRECAUTIONS &WASTE MANAGMENT

STANDARD ("UNIVERSAL") INFECTION CONTROL PRECAUTIONS - a method of infection
control in which all human blood and certain body fluids (saliva in dentistry) are treated as if known
to be infectious for HIV, HBV, HCV, and other blood borne pathogens. The same infection control pro-
cedures are used for all patients.

• Athorough medical history is obtained for all patients at the first visit and updated and reviewed at
subsequent visits. However, since not all patients with infectious diseases can be identified from a
medical history, physical exam, or readily available lab tests, the CDC introduced the concept of
"Standard Precautions".

• Universal precautions are effective in preventing disease transmission from dental worker to
patient, patient to dental worker, and patient to patient.

OCCUPATIONAL SAFETY & HEALTH ADMINISTRATION (OSHA) - a federal agency created by

Congress in 1970 to protect WORKERS from hazards in the work place. OSHA is concerned with regu-
lated WASTE within the dental office. According to OSHA, "regulated waste" includes:
• Blood or other potentially infectious materials (including saliva) in dental procedures.
• Items that would release blood and other potentially infectious materials (including saliva), if
com pressed.
• Items caked with dried blood or other potentially infectious materials capable of releasing these
materials during handling.
• Contaminated sharps
• Pathological and microbiological waste containing blood or other potentially infectious materials
(including saliva).

420
Regulated waste MUST be placed in containers that are closable, constructed to contain all con-
tents and prevent leakage, and labeled appropriately. The container must be closed prior to removal
to prevent spillage or protrusion of contents. The rule also requires that if the outside of the container
becomes contaminated, it must be placed in a second container with the same characteristics. The
need for a second container is extremely unlikely in a dental office.

HAZARDOUS WASTE - waste causing harm or injury to the environment (not all hazardous waste
is toxic/poisonous).

TOXIC WASTE - waste capable of causing a poisonous effect.

INFECTIOUS WASTE - waste that contains strong enough pathogens in sufficient quantity to
cause disease. All infectious waste is contaminated, however, not all contaminated waste is infec-
tious (may not be able to cause disease).

AIDS prompted OSHA to adopt the Bloodborne Pathogens Standard for Dentistry. OSHA is also con-
cerned with Hepatitis B and other blood borne diseases, but AIDS is the disease that prompted regula-
tory action.
• In 1986, unions representing healthcare workers petitioned OSHA for an emergency rule to protect their
members from workplace exposure to the human immunodeficiency virus (HIV) and hepatitis Bvirus
(HBV) . OSHA denied the petition, but agreed to adopt a permanent rule on exposure to blood borne
pathogens through the regular rule making process. It took five years to develop the rule which now
applies to hospitals, physician offices, nursing homes, other healthcare settings, emergency
response personnel, funeral homes, and dental offices.

• Bloodborne Pathogens-pathogenic microorganisms present in human blood that can cause disease
in humans.

• Other potential infectious materials (OPIMs): human body fluids (semen, vaginal secretions, CSF,
synovial fluid, pleural and pericardial fluids, peritoneal fluid, amniotic fluid, & saliva in dental
procedures). Only in dental procedures is saliva considered a potentially infectious material. Also
any unfixed tissue or organ is considered an OPIM.

OSHA BlOODBORNE PATHOGENS STANDARD - a comprehensive rule that sets forth the spe-
cific requirements OSHA believes will prevent the transmission of blood borne diseases to EMPLOYEES
(not patients or employers). OSHA requirements:
• Employers covered by BPS must make exposure determinations and develop an exposure control plan.
Employers must use engineering and work practice controls to prevent employee exposure, and
develop a system to evaluate exposure incidents.

• BPS requires training of all employees who provide or assist in providing patient care and training
to those who clean operatories, instruments, and gowns.

• Through the OSHA Bloodborne Pathogen Standard, OSHA directs that uniform clothing worn in the
dental office is laundered at the dental office or by an outside service, NOT at an employee's
home. Offices must use barrier techniques, communicate hazards to employees (training),
perform proper cleaning of the office, and offer Hepatitis Bvaccinations.

• Standard (formerly "Universal") infection control precautions for bloodborne pathogens requires
changing gloves BETWEEN ALL PATIENTS. Gloves and gowns are required when you reasonably
anticipate skin contact with blood or other potentially infectious materials, including saliva. Thus,
if you reasonably anticipate the forearms will be spattered with saliva or blood, then the forearms
must be covered.

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 N • Any gown or clinic jacket that prevents blood or other potentially infectious materials (including
saliva) from reaching work clothes, street clothes, or skin is considered adequate. Fluid-resistant
gowns are not required unless it is anticipated that large amounts of blood, saliva, or other body
fluids will soak through the gown to the employee's clothing. OSHA considers cotton or
cotton/polyester clinic jackets or lab coats as satisfactory barriers for most routine dental procedures.
When surgical procedures are performed involving large quantities of blood (i.e. trauma surgery),
additional personal protective equipment like long-sleeved gowns are required. According to OSHA,
the selection is to be based on the quantity and type of exposure expected.

• When handling chemical agents or cleaning a dental office, always wear protective eyewear, mask,
and heavy-duty utility or nitrile gloves.

• Wearing gloves, protective eyewear, and a facemask is recommended WHEN TREATING All
PATIENTS. Masks and protective eyewear are required when splashes, spray, splatter or droplets of
blood or other potentially infectious materials (including saliva), may be generated and eyes, nose,
or mouth contamination can be reasonably anticipated. Aface shield may be substituted for masks
and eyewear if you prefer.

• Face mask should be changed BETWEEN PATIENTS (every patient) or more often if heavy spatter
is generated during treatment. CDC recommends the mask to be changed between patients or
during patient treatment if the mask becomes wet or moist from within or without.

• The rule states that if eyewear is required, if must be goggles or glasses with solid (not perforated)
side shields.

• Center for Disease Control suggests a new mask for EACH PATIENT. Masks should have at least
95-99% filtering efficiency for small particle aerosols 1-3 m.

Human Immunodeficiency Virus (HIV) the most infectious target of Standard (Universal) Blood Pre-
cautions. While HBV is the most infectious bloodborne pathogen, it is not the most infectious target
of Standard Blood Precautions. Infection control precautions are aimed at preventing its viral trans-
mission and are also effective in preventing HIV &HCV cross-infection.

HEPATITIS BVIRUS (HBV) - poses the greatest occupational healthcare worker risk for blood-
borne infection. The basis of the current standard (formerly "universal") infection control precautions
were first recommended by the CDC in 1987 to protect healthcare workers from occupational transmis-
sion of all blood borne infectious diseases during the provision of patient care. While many health pro-
fessionals focused on HIV, evidence demonstrated that HBV was responsible for infection in 10-30% of
exposed, susceptible healthcare workers. HBV concentrations in blood of a chronic carrier can range
between 1-100 million virions/ml, in contrast to significantly lower viral loads shown for both HIV and
AIDS infected patients. Precautions that minimize potential HBV infection/spread prevent cross-infec-
tion of less infectious microorganisms.

• Exposed employees who have declined the Hepatitis Bvaccination can change their mind at any
time and receive FREE vaccination.
• Exposed employees who have begun their Hepatitis Bvaccination series can work at their jobs
even though the series is not complete.
• Dentists must provide "at-risk" employees with protection from HEPATITIS B. The federal standard
for occupational exposure to bloodborne pathogens requires employers to provide the Hepatitis
Bvaccination. Employers must offer the vaccination (and boosters if these are recom mended in the
future) to all employees who have occupational exposure at no cost to the employees. The employee
may refuse the vaccination, but OSHA will require proof that an employee has refused.
• Employers must offer the vaccination to a new employee within 10 working days of initial assignment
to a position involving exposure. OSHA requires the employee to be trained regarding Hepatitis Band
the vaccination prior to being offered vaccination.
• Hepatitis B virus infection commonly occurs by sexual intercourse, prenantal transfer, and
percutaneous inoculation.

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HEPATITIS CVIRUS (HCV) - transmitted primarily in infected blood via accidental needle-
sticks, blood transfusions, or drug addicts sharing contaminated syringes. Historically, parenteral
drug abusers, people receiving transfusions, organ recipients, and hemophiliacs receiving Factor VII
or IX are at high risk for HCV infection. More recently, people receiving tattoos or undergoing body
piercings have been infected via contaminated, unsterilized needles.
• Viral concentrations detected in hepatitis Cvirus infected patients range between numbers for
HBV and HIV. Thus, we target the most infectious blood borne pathogen with our infection control
standards.

OCCUPATIONAL EXPOSURE - defined by OSHA as any reasonably anticipated skin, mucosal,

eye, or parenteral contact with blood or other potentially infectious fluids during the course of
one's duties while at work. OSHA includes saliva in dental procedures in the definition of "other po-
tentially infectious materials" because saliva can be mixed with blood in some dental procedures.
Thus, OSHA concluded that saliva should be treated as potentially infectious even though scientists
believe blood borne diseases are not transmitted via saliva. The following are included in procedures to
evaluate an exposure incident:
• State the policies that were in place at the office at the time of the incident.
• State the engineering controls (i.e. needle recapping device, sharps container, rubber dam) and
work practices that were in place at the office at the time of the incident.
• State the personal protective equipment (gloves, lab coats, etc.) that were in use at the office
at the time of the incident.

EXPOSURE INCIDENT - a specific occupational incident involving the eyes, mouth, other mucous
membranes, non-intact skin, or parenteral contact with blood or other potentially infectious materials
(including saliva). An injury from a contaminated sharp is the most common exposure incident.
After a report of an exposure incident is made, the employer must make immediately available at no
cost to the employee, a confidential medical evaluation and follow-up that includes:
• Documentation of route(s) of exposure and circumstances in which the incident occurred.
• Identification and documentation of the source individual (patient), unless the employer can establish
that identification is not feasible or prohibited by state or local law.
• Results of testing of the source individual's blood, it the patient is available.
• Collection and testing of the employee's blood AFTER consent is obtained.
• Medically indicated prophylaxis
• Counseling
• Evaluation of reported illnesses in the weeks after the incident.

The employer MUST provide the following information to the health care profeSSional who performs
the evaluation:
• Acopy of the OSHA standard.
• Description of the employee's duties as they relate to the incident.
• Documentation of route(s) of exposure and circumstances under which exposure occurred.
• Results of the source individual's blood testing if available.
• All medical records relevant to treatment of the employee (including vaccination status)
which are the employer's responsibility to maintain.

EXPOSURE CONTROL PLAN - the standard requires that every employer have a written expo-
sure control plan designed to eliminate or minimize employee exposure to bloodborne diseases.
The plan must set forth office policies and protocols to protect employees from these diseases. OSHA
requires the plan to contain these elements:
• how and what schedule your office is implementing OSHA's requirements for barrier techniques,
hepatitis Bvaccination, housekeeping, disinfection of contaminated work surfaces/equipment,
handling regulated waste, post-exposure evaluation and follow-up, communication of bloodborne
pathogen hazards to employees, and record keeping.
• The exposure control plan should outline office protocol for when gloves, gowns, masks, and eyewear
(or faceshields) are used. When and how you will provide training for employees, your specific
practices for disinfection, how you launder gowns (on-site or using a service), where to keep your
records (training and medical records, and OSHA standard) .
• Office policy on the hepatitis B vaccination, and office protocol for handling regulated waste.

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 The Exposure Control Plan must be accessible to employees and must be updated at least annually
and whenever necessary to reflect office changes (i.e. new procedures that affect occupational expo-
sure and new positions). The plan must be provided to OSHA upon request.

Employers must ensure that ALL employees with occupational exposure participate in a training
program at no cost, during working hours, with material appropriate to the education, literacy, and
language of the employee. Training is critical to OSHA compliance and must include:
• Acopy of the standard and explanation of its contents.
• A general explanation of the epidemiology, symptoms, and modes of transmission of
blood borne diseases.
• An explanation of the office's exposure control plan, and how the employee can obtain a copy of it.
• Information about the office's protocol for gloves, gowns, masks, and eyewear (or faceshields),
including the type of equipment available, its location and when it is to be used , and how it is to be
removed, handled, decontaminated, and disposed.
• An explanation of how to recognize tasks that may involve occupational exposure and how to prevent
or minimize such exposures (i.e. how to use a sharps container properly).
• Information on the hepatitis Bvaccine, including efficacy, safety, how it is administered, vaccination
benefits, and that the vaccination is free of charge.
• Information on how to handle emergencies involving occupational exposure (what actions to take
and who to contact).
• An explanation of the office protocol for handling exposure incidents like injuries from contaminated
sharps, how to report the incident, follow-up medical care, and evaluation.
• An explanation of the biohazard labels used in the office.
• An opportunity for interactive questions and answers with the trainer.

OSHA REGULATES CONTAMINATED SHARPS - Contaminated sharps are any contaminated

object that can penetrate the skin, including, but not limited to needles, scalpels, broken glass,
broken capillary tubes, and exposed ends of dental wires. There may be other objects used in the
dental office that are sharps, and if they become contaminated with blood or other potentially infec-
tious materials (including saliva), then they must be regulated.

RECAPPING SHARPS - the rule generally prohibits bending, recapping, breaking, shearing,
or removing sharps. However, recapping with a one-handed method or using a mechanical device is
permitted if the employer can demonstrate that not alternative is feasible, or that such action is re-
quired by a specific medical procedure. The rule's introduction lists the administration of an anes-
thetic as a medical procedure that may require recapping (i.e. reinjection of the same patient to
enhance the local anesthetic).

ANTI-RETRACTION VALVES - valves used on handpiece and air-water syringe hoses to prevent
the retraction of fluid back into the tubing (they prevent patient fluids from getting into the water
lines) and reduce the risk of cross-contamination other patients.

• Center for Disease Control &Prevention (CDC) recommends a minimum of 20-30sec of flushing
water lines between patients, and several minutes of flushing water lines if the system has been idle
for a period of time (i.e. over the weekend).

• Hand-pieces and reusable air-water syringe tips must be autoclaved between patients. Disposable
air-water syringe tips are available. Disposable saliva ejectors cannot be reused.

• FDA (Food &Drug Administration}-a branch of the U.S. Department of Health &Human Services
that determines which drugs and medical services can be marketed in the U.S. The FDA requires
both drug safety and efficacy. FDA is also responsible for regulating hand pieces and recommending
sterilization procedures to the CDC.

• Drug Enforcement Administrations (DEA)-a branch of the U.S. Department of Justice that
determines the degree of control for substances with abuse potential (Schedules I-V).

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The most commonly used dental materials deemed HAZARDOUS by OSHA are mercury, nitrous
oxide, &chemicals used to develop film.
• When working with or handling mercury, work in a well-venti lated space, avoid direct skin contact
with the metal, and store scrap amalgam in tightly sealed containers covered with sulfide solution
(an effective agent to suppress or eliminate the emission of mercury vapor from the scrap).

• When working with x-ray processing solutions, use protective eyewear & rubber gloves, work in a
well-ventilated area, and store solutions in tightly covered containers.

• The acceptable maximum exposure level allowed by OSHA for nitrous oxide is 1000ppm.

MATERIAL SAFETY DATA SHEETS (MSDS) - documents that contain information concerning a
hazardous chemical. Chemical manufacturers and importers are required to obtain a material
safety data sheet for each hazardous chemical they produce or import. Distributors are responsible
for ensuring their customers are provided with a copy of these MSDS. Employers must have an MSDS
for each hazardous chemical they use, and may rely on the information received from their suppliers.

• The role of MSDS under the rule is to provide detailed information on each hazardous chemical
(including its potential hazardous effects, physical and chemical characteristics, and
recommendations for appropriate protective measures). This information is useful to employers
responsible for designing protective programs, and to workers.

• If you are not familiar with the MSDS and chemical terminology, you may need to learn to use them
yourself. A glossary of MSDS terms may be helpful in this regard. Most employers using hazardous
chemicals will primarily be concerned with MSDS information regarding hazardous effects and
recommended protective measures.

• MSDSs must be readily accessible to employees when they are in their work areas during work
shifts. You must decide what is appropriate for your particular office. Some employers keep MSDSs
in a binder in a central location. As long as employees can access the information they need, any
approach can be used. Employees must have access to the MSDS themselves.

Infection control training records and medical records if the employee is involved in an occupa-
tional exposure MUST be maintained. The employer must maintain a medical record for each em-
ployee whose job involves occupational exposure to blood and other potentially infectious materials.
The employee's medical record must include:
1. Employee name and SSN.
2. Copy of the employee's hepatitis B vaccination status (dates and medical records
regarding the employee's ability to receive the vaccination).
3. Medical opinions and evaluations.
4. Test results
5. Details about exposure incidents (routes of exposure and how the exposure occurred).

Medical records MUST be maintained for the duration of the employment plus 30 years, and must be
kept strictly confidential. However, each employee is entitled to review their medical record. Also, the
OSHA-required records must be transferred to the new owner. If you go out of business and there is no new
owner, you must notify the Director of the National Institute for Occupational Safety and Health (NIOSH) at
least 3 months before you intend to dispose of the records and offer to transmit the records to NIOSH.

ENVIRONMENTAL PROTECTION AGENCY (EPA) - regulates waste transportation from the

dental office.

• The CDC considers the following groups as "high-risk": IV drug users, homosexual/bisexual males,
people receiving transfusions or blood products, and health care workers who may come into
contact with body fluids.

• OSHA considers part-time, temporary, and probationary workers as employees.

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 • It is important that the employer stress to employees that Hepatitis B has been a long-standing
occupational threat in dentistry. HBV is a hardy virus that only takes a low concentration to
transmit the virus and infect someone.

• Dental healthcare workers are at greatest risk for contracting HEPATITIS. As a dentist (employer),
you must offer to provide vaccination to all employees who have occupational exposure. Any FDA-
approved hepatitis vaccine is acceptable (Recombivax HB & Engerix-B).

• Hepatitis B virus is usually transmitted by percutaneous inoculation, sexual intercourse, or

prenatal transfer.

• Treat each patient and instrument as potentially infectious (Standard Infection Control Precautions).

PUBLIC HEALTH
QUALITY ASSESSMENT - the measure of the quality of care provided in a particular setting. Qual-
ity assessment is limited to the appraisal of whether or not standards of quality have been met.

QUALITY ASSURANCE - tthe measurement of the quality of care and implementation of any
necessary changes to maintain or improve the quality of care rendered. Quality assurance includes
the additional dimension of action to take the necessary corrective steps to improve the situation in
the future. Concepts that relate to quality assurance:
1. structure-the layout and equipment of a facility.
2. process-involves the actual services that the dentist and assistant perform for patients,
and how well they perform.
3. outcome-the change in health status that occurs as a result of the care delivered.

FALSE NEGATIVE TEST RESULT - a test result that erroneously excludes an individual from a
specific diagnostic or reference group, due mainly to insufficient exact methods of testing. Simply
stated, if a diagnostic test fails to identify a case of true disease, it is a false negative result.

FALSE POSITIVE TEST RESULT - this result erroneously assigns an individual to a specific diag-
nostic or reference group, due particularly to insufficiently exact methods of testing.

Sensitivity & Specificity are INVERSELY proportional. As the specificity of a test increases, the
sensitivity decreases.
• Sensitivity-ability of the test to diagnose correctly a condition or disease that actually exists. Sensitivity
measures the proportion of people with a disease who are correctly identified by a positive test.
Sensitivity is defined as the number of true positives (TP) divided by total number of potential positive
findings (true positives and false negatives) in the sample. Sensitivity = TPITP + FN.

• Specificity-ability of the test to classify health. Specificity is defined by the number of true negative
(TN) results divided by the total number of false positive (FP) + true negative (TN) results in a sample.
Specificity = TN/FP + TN .

• Prevalence-the number of OLD cases of disease present in a population at risk at a specific period
of time. It is the proportion of persons in a population suffering from a particular disease at a
given point in time. A proportion expressed as a percentage of the population.

• Incidence-number of NEW cases of a specific disease occurring within a population at a certain

amount of time. Expressed as a rate (cases)/(population)/(time). Incidence is a "rate" that requires
a unit of time.

• Frequency-a cou nt.

• Epidemiology-the study of the incidence, prevalence, mode of transmission, and control of

diseases in a defined human population to establish programs to prevent and control
their development and spread.
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CHILD ABUSE - Dentists are morally, ethically, and legally obligated to report a suspected case NOTES
of child abuse. Once an injury or a suspicious nature is observed , the dentist's first and immediate
responsibility is to protect the child.
• Reports should be made to the designated state agency (Social Services or Police) . Dentists must
familiarize themselves with the exact procedures to be followed in their states.

• Child abuse most commonly involves newborns and children up to age 3 years.

• Dentists are also ethically obligated to identify and refer cases of domestic violence. Practitioners
should be familiar with the physical signs of domestic violence, especially since 68% of battered
women injuries involve the face, 45% the eyes, and 12% the neck.

MANAGED CARE - an arrangement where a third-party payer (insurance company, federal govern-
ment, or corporation) mediates between doctors and patients, negotiating fees for services and over-
seeing the types of treatment provided.

• Types of Managed Care Practices: HMO, PPO, IPA.

• PPO (Preferred Provider Organization)-typically involves contracts between insurers and dentists.
Patients can choose their dentist depending on if the dentist participates in the PPO arrangement.

• Participants of HMOs are much more limited in their dentist selection because they have to stay
with in network.

THIRD-PARTY DENTISTRY - a system where a provider of dental coverage contracts to pay for
part of a patient's dental treatment.

The major forms of third-party reimbursement currently in use are:

• Usual, customary, and reasonable (UCR) fee, Table of Allowance, Fee Schedules, and Capitation .

• Capitation-a fixed monthly payment paid by a carrier to a dentist based on the number of patients
assigned to the dentist for treatment. The capitation fee is the same regardless of how much or how
little care is delivered. Capitation is the most popular managed care payment method.

• Closed Panel of Providers-dental services provided by salaried dentists at specified locations only.

• Open Panel of Providers-dental services provided by any dentist willing to accept

third-party payment.

DENTAL INDEX - a data collection instrument used to numerically express the oral health
status of a population .
1. DMFT Index (Decayed-Missing-Filled Teeth Index)-an irreversible index (measures conditions
that cannot be reversed like caries) applied only to permanent teeth. DMFT index results yield
a group's caries susceptibility. DMFT has received universal acceptance, and is probably the
best known of all dental indices. DMFT is the best caries index to use if the major purpose of
an epidemiologist's research is to determine caries susceptibility as opposed to immediate
treatment needs. DMFT determines the total dental caries experience (past and present) but is
only used for permanent teeth. It has received universal acceptance and is the best know of all
dental indexes. DMFT Index Limitations:
• DMFT values are not related to the number of teeth at risk.
• DMFT index can be invalid in older adults because teeth can become lost for
non-caries reasons.
• DMFT index can be misleading in children whose teeth have been extracted for
orthodontic reasons .
• DMFT cannot be used for root caries and cannot account for sealed teeth.

2. DEFT Index (Decayed, Extracted, Filled Teeth)-used for the primary dentition.

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 3. DMFS Index (Decayed, Missing, Filled Surfaces)-the same as DMFT, but records involved
tooth surfaces.

4. Gingival Index (GI)-a reversible index used to assess the severity of gingivitis based on color,
consistency, and BOP.
• Gingivitis is most commonly scored with the gingival index of Loe & Silness which grades the
gingiva based on the four surfaces of each tooth based on inflammation and bleeding.
• GI, Papillary, Marginal, &Attached Gingiva Index (PMA Index) are confined to measurements
within the gingiva . PMA index is used to record the prevalence and severity of gingivitis in
school children. The presence or absence of gingivitis is noted in the gingival papillae,
gingival margin, and attached gingiva.

5. Periodontal Index (PI)-a reversible index that measures conditions that can be changed (plaque
and bleeding). Measures the periodontal condition of a population. Used to assess the prevalence
of periodontal disease in populations of people. The best time to perform this index is at the
beginning of the appointment.
• The condition of the gingiva AND bone are estimated individually for each tooth. A progressive
scale that gives little weight to gingival inflammation, and more weight to alveolar bone
resorption is used for scoring.
• Scores from each tooth are added together, then is divided by the number of teeth in the
mouth to give the patient's periodontal disease index. This score reflects the average status
of periodontal disease in a given mouth without reference to the type or causes of disease.
The community's score is the average of individual scores of persons examined.

6. Simplified Oral Hygiene Index-a reversible index used to measure oral hygiene status by
estimating the tooth surface covered with materia alba and/or calculus.

7. Plaque Index (PI) of Silness & Loe-a reversible index to assess the THICKNESS of plaque at the
gingival margin (measures oral debris). Used to determine plaque accumulation. The best time
to per10rm a plaque index is at the beginning of the appointment. The plaque index is a specific
index for scoring plaque and oral debris. It was derived from the papillary, marginal, and
attached gingiva index (PMA).
• The plaque index is based on an assessment of the severity and location of soft debris
aggregates in terms of scores 0, 1,2,3. A plaque score of "0" means the gingival area of the
tooth surface is plaque free. The examination is made by passing a probe over the tooth surface
into the gingival sulcus. If no soft material adheres to the probe, the area is given a "0".
• A plaque score of "I" is given when plaque cannot be observed on the tooth, but is
observed on the probe.
• A plaque score of "2" is given when a thin to moderately thick plaque layer is visible to the eye.
• A plaque score of "3" is given when a heavy accumulation of plaque fills the area between the
gingival margin and the tooth surface, or fills the interdental area.
• In this system, the most stress is placed on the THICKNESS OF PLAQUE at the gingival margin
area on all four sur1aces of each tooth. The scores of all three areas of all teeth are added
then divided by the number of teeth.
• The plaque index has been extensively used, but does NOT have universal acceptability.
• Some studies show 80-90% of children have inflammatory periodontal disease (gingivitis
or periodontitis) by age 15. Localized acute gingivitis is the most common form.
Epidemiologic studies show the strongest relationship between prevalence and severity of
periodontal disease with oral hygiene and age.

8. Sulcus Bleeding Index (SBI)-used to determine the bleeding and gingival health.

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 ........

VITAL STATISTICS - quantitative data routinely collected by epidemiologists and public health pro-
fessionals on mortality, morbidity, natality, birth-death ratios, and crude death ratios. Vital statis-
tics are quantitative methods to monitor and evaluate the life history of a specific population. Vital
statistics identify community health needs, estimate healthcare costs, and evaluate health pro-
gram effectiveness.
1. Mortality (Death Rate)-number of deaths caused by a specific disease. It is the ratio of the
number of deaths caused by the disease, to the total number of cases of the disease at a
specific time.
2. Morbidity-the incidence of a specific disease within a given population.
3. Natality (Birth Rate)-the ratio of births to the general population .
4. Birth-Death Ratio (Vitallndex)-the number of births in a given year divided by the number
of deaths in a given year. It is an indication of the population growth, stability, and reduction.
5. Crude Death Rate-ratio of the number of deaths occurring within a given time period and
population to the total population during that time.

PUBLIC HEALTH - the science & art of preventing disease, prolonging life, and promoting physical
health &efficiency through organized community efforts.
• 3 principles of public health: a problem exists, solutions exist, and solutions to the problem
are applied.
• Public health problem does NOT always result in government passing new laws against a problem
nor result in public demand for immediate government intervention.
• Apublic health problem must meet these criteria:
1. Awidespread condition or situation that is the actual or potential cause of morbidity
and/or mortality.
2. Involves a perception by the public, public health authorities, and government that a public
health problem is occurring.

Most important concept of Winslow's definition of public health is PROMOTION THROUGH ORGANIZED
COMMUNITY EFFORT.

DENTAL PUBLIC HEALTH - science and art of preventing and controlling dental disease, and pro-
moting dental health through organized community efforts. Aform of dental practice that serves the
community as a patient rather than serving the individual. Dental public health involves providing
dental education to the public, research, and applying research findings with the administration of
dental care programs for groups, and the prevention and control of dental disease through a commu-
nityapproach.

Fundamental principles of public health are prevention, cost-efficiency, and teamwork. Prevention
is the major objective of public health programs because it entails ethics, teamwork, and cost-effi-
ciency. It is more ethical to prevent disease than to cure it. Teamwork is necessary to handle large
groups efficiently. Cost-efficiency plays a major role because prevention is cheaper than a cure.

• Education plays an important role in public health because it decreases the need for government
intervention. When people learn why regulations are of value, they will comply. Ex: when people learn
how many lives are saved annually by seat belts, they are more inclined to wear them .

• Any school-based program to promote oral health should have these fundamental components:
1. Oral health services: involves preventive procedures, health screening and treatment,
referral, and follow-up.
2. Health instruction: includes personal and community health topics.
3. Healthy environment: attention to all aspects of the school environment that could affect the
health of students or school personnel. The more successful school-based programs use a
high degree of active involvement of the participants.

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 NOTES RANDOMIZED STUDY - a study where All subjects have an equal chance of being assigned to
either the study or control group. Statistical probability is such that the assumption can then be
made that the groups differ ONLY in terms of the agent under study. Any uncontrolled variables influ-
encing the outcome are likely to affects subject in both groups equally. Thus, researchers prefer the
"random assignment method" for placing subjects into either the study or control group.

BLIND STUDY - a study where subjects are unaware of if they are in a test or control group. One
way of achieving a blinded study is using placebos.
cDouble Blind Study-neither participants (subjects) nor examiners know the group allocations (test or
control grou ps).

Two Variables Used in Research Studies:

1. Dependent variable-the variable whose value depends on those of others (i.e. in the formula
x = 3y + z) x is the dependent variable.
2. Independent variable-the variable whose value determines the other variable values
(i.e. x = 3y + z) y &z are the independent variables.

The ethical rules and principles of professional conduct for the practice of dentistry are set forth in the
ADA's publication "Principles of Ethics and Code of Professional Conduct". The ethical principles
found in this code are justice, autonomy, and beneficence.
1. Justice-the quality of being impartial and fair.
2. Autonomy-to inform patients about treatment, to be truthful, and protect their confidentiality.
3. Beneficence-to be kind and give the highest quality of care one is capable of providing.

The dentist is responsible for providing information and dental care. However, the patient is ultimately
responsible for maintaining his/her own oral health (brushing, flossing, etc.).

GOOD SAMARITAN LAW - a law enacted in all states that provides immunity from suit for speci-
fied health practitioners who render emergency aid to victims of accidents, provided there is no evi-
dence of gross negligence. Not all states include dentists in the Good Samaritan law.

INFECTION CONTROL
OPPORTUNISTIC INFECTION - an infection caused by normally non-pathogenic microorgan-
isms in a host whose resistance has been decreased or compromised.
• The percentage of people living with a wide variety of immune compromised conditions continues
to increase. Along with the clinical manifestations of those types of diseases, there can be
accompanying deficiencies in aspects of host-immune defenses. The severity of deficiency can range
from mild, to life-threatening, and predispose the compromised person to infections by organisms
that would not usually occur in other people with intact innate and specific immunity.

Infection Control:
• Exposure is not synonymous with infection.
• Do not disinfect when you can sterilize.
• Known AIDS patients can be treated using Standard Bloodborne Precautions.
• It is not possible or necessary to sterilize all environmental surfaces that become contaminated
during patient care. In many instances, because of the relatively low risk of microbial transmission,
thorough cleaning of surfaces is sufficient to break the cycles of cross-contamination and cross-
infection. Thus, sterilization of all clinical instruments and inanimate environmental surfaces is
NOT mandatory.

Personal protective equipment clinic jackets are required to be lONG SLEEVE, HIGH NECK for opti-
mal protection and to minimize the potential for exposed skin contact that can become contaminated
with a patient's blood, saliva, or other potentially infectious material.

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BACTERICIDAL - an antibacterial solution that directly KILLS bacteria. Bactericidal agents are
preferred to "bacteriostatic" chemicals because bacteriostatic do not directly kill or inactivate
microbes, but merely inhibit their metabolism and replication. Thus, these organisms can remain vi-
able, but inactive for extended intervals. Application of a bactericidal agent or process ensures micro-
bial inactivation.

SANITIZATION - a type of antimicrobial treatment (i.e. used for drinking water) to lower the total
microbial load to safe public health levels. Used to treat water supplies to reduce microbial levels to
safe public health levels.

STERILIZATION - the process of KILLING (or removing) all microorganisms (including bacterial
spores) on an object or in a material (i.e. liquid media). Sterilization is the complete destruction of
all forms of microbial life (including SPORES) without particular reference to microbial organisms.
The limiting requirement is destruction of heat-resistant spores.

• Sterilization involving the use of HEAT is recommended for all instruments used in the mouth.
Heat is the most efficient, reliable, and biologically monitorable sterilization method. During a
routine cycle using an autoclave, unsaturated chemical vapor sterilizer, or dry-heat unit, CElL DEATH
OCCURS because the heat inactivates critical enzymes and other proteins within microbial cells.

• DO NOT DISINFECT WHAT CAN BE STERILIZED.

• Sterilization is the use of physical or chemical procedures to destroy ALL microbial life (including
bacterial endospores). Sterilization refers to the absence of all living forms.

• The recommendation stating that all reusable items that come into contact with a patient's blood,
saliva, or mucous membranes must be sterilized using heat is now routinely accepted and used in
dental facilities.

• PRE-CLEANING is the most important step in instrument sterilization. Debris acts as a barrier to
the sterilant and sterilization process. Ultrasonic instrument cleaning is the safest and most
efficacious method of precleaning.

• Heat sterilization is the most EFFICIENT way to kill microbes. Heat is the most efficient, reliable,
and biologically monitorable sterilization method. During a routine autoclave cycle, unsaturated
chemical vapor sterilizer or dry heat unit, cell death occurs via heat inactivation of critical enzymes
and other proteins within microbial cells.

• The recommendation that all reusable items that contact a patient's blood, saliva, or mucous
membranes must be sterilized using heat is now routinely accepted and used in dental facilities.

• The immersion of dental instruments in cold disinfectants will not destroy spores or hepatitis
viruses (they are resistant to physical and chemical agents).

• liquids are generally sterilized by filtration. The most commonly used filter is composed of
nitrocellulose and has a pore size of 0.22 m. This size retains all bacteria and spores. Filters work by
physically trapping particles larger than the pore size.

RAPID HEAT TRANSFER STERILIZATION - provides a very fast cycle time, no dulling of cutting
edges, & dry instruments after the cycle. FDA-approved, forced air, dry heat convection ovens are
appropriate for sterilizing heat-stable instruments and other reusable items used in patient care. They
use a higher temperature than other dry heat units, and there is controlled internal air flow within
the chamber. In contrast to traditional dry heat sterilizers, a rapid heat transfer unit can sterilize
items in much shorter times, while offering the advantages of dry heat. Rapid Heat Transfer Sterili-
zation requires 375°F (191 °C) for 12 minutes for wrapped instruments, and Smin cycle time for
unwrapped instruments.

431
 N DRY HEAT STERILIZATION - proper time &temperature for dry heat sterilization is 320°F
(160°C) for 2hrs, or 340°F (170°C) for 1hr. Items usually sterilized by dry heat can be autoclaved .
They should be removed immediately after cycle to diminish the possibility of instrument corrosion and
dulling of sharp points or edges (carbon steel instruments). Dry heat destroys microorganisms by
causing COAGULATION OF PROTEINS.

• Instruments MUST BE DRY before using dry heat sterilization and ethylene oxide sterilization,
because water interferes with the sterilization process.

• Dry Heat Advantages: effective/safe for sterilizing metal instruments, and does not dull or
corrode instru ments.

• Dry Heat Disadvantages: long cycle, poor penetration, and ruins heat-sensitive materials.

AUTOCLAVE (MOIST HEAT STERILIZATION OR "SATURATED STEAM") - proper time and

temperature for autoclaving is 250°F (121°C) for 15-20 minutes. These conditions yield 151bs of
pressure of steam per square inch. MOIST HEAT destroys bacteria by denaturation of high protein-
containing bacteria. Autoclave provides sterilization when used at the 250°F (121 °C) for 15-20 min
because it applies the heat under pressure, which greatly speeds up the protein denaturation process
(compared to boiling water). Usually only 10 minutes is required to destroy all bacteria, but the in-
creased time is allowed for penetration when instruments are wrapped in thick towels. Autoclaving ef-
fectiveness is best determined by culturing bacterial spores. Spore testing of autoclave units is
recommended weekly.

• Spore-forming pathogens provide the ultimate test for efficacy of sterilization. Since bacterial
spores are resistant to boiling (lOO°C at sea level), they must be exposed to a higher temperature.
This temperature cannot be achieved unless the pressure is increased. For this purpose, an autoclave
chamber is used where steam at a pressure of 15lbs/in reaches a temperature of 121°C for 15-
20min. This kills even the highly heat-resistant spores of Clostridium botulinum (causes botulism)
with a margin of safety.

• Saturated steam (autoclave) is the most practical, economical, most currently effective sporicide,
and the most efficient method for destroying viral and fungal microorganisms.

• Steam autoclaves operate at either 121°C (250°F) at a pressure of 15lbs/square inch (psi) for 15-
20 minutes, or at 134°C (270on at a pressure of 30psi for a minimum of 3 minutes ("flash cycle"),
To effectively kill all living organisms, the minimum required temperature is 121°C (250°F) .

• Autoclaving time varies directly with the type of load placed into the chamber. The 3-minute "flash
cycle" is best indicated for unwrapped instruments. For wrapped instruments, a longer
sterilization cycle is required to permit adequate penetration of steam for proper disinfection.

UNSATURATED CHEMICAL VAPOR STERILIZATION (UCVS) - the proper time and temperature
is 270°F (132°C) for 20-40 minutes. These conditions yield 20lbs of sterilizing vapor pressure. The
main operation of CVS is similar to steam sterilizers, but rather than using distilled water, UCVS uses
a solution of alcohol, formaldehyde, ketone, acetone, and water to produce the sterilizing vapor.

• The temperature and pressure required for chemical vapor sterilizers is greater than for autoclave.

• MAIN advantage of this system is it does not rust or corrode metal instruments and carbon steel.

• Disadvantages: instruments must be dried completely before processing, a special chemical solution
must be used, and it destroys heat-sensitive plastics.

432
GLUTARALDHYDE (2%) - an alkalizing agent highly lethal to essentially all microorganisms. It NOTES
takes lOhrs to kill bacterial spores when a dental instrument is placed in a 2% glutaraldehyde solu-
tion. If the lOhr sufficient contact time is provided, there is absence of extraneous organic material.

• Glutaraldehyde Advantages: most potent category of chemical germicide, capable of killing spores
(after 10hrs), EPA registered as a chemical sterilant, and can be used on heat-sensitive materials.

• Glutaraldehyde Disadvantages: long period required for sterilization, allergenic, not an environmental
disinfectant, and extremely toxic to tissues.

• Used in hospitals to sterilize respiratory therapy equipment.

ETHYLENE OXIDE GAS STERILIZATION - used extensively in hospitals to sterilize heat-sensi-

tive materials like surgical instruments and plastics. It kills by alkylating proteins and nucleic
acids (it is an alkylating agent that irreversibly inactivates cellular nucleic acids (DNA) and pro-
teins). It is a slow process (10-16hrs) depending on the material to be sterilized. This gas is fairly
toxic to humans and is flammable, so its use is limited.

• Ethylene oxide gas has been widely used as a sterilization agent, especially for pre-packaged, disposable
plastic ware in hospitals. Exposure of materials to ethylene gas must be performed in special sealed
chambers, and items must be cleaned and dried thoroughly before the sterilization process.

• Advantages: highly penetrative, does not damage heat-sensitive materials (rubber, cotton, plastics),
evaporates without leaving a residue, and works well for materials that cannot be exposed to moisture.

ANTISEPTICS - are chemical safe to be administered to external body surfaces or mucous mem-
branes to decrease microbial numbers. Antiseptics cannot be taken internally. Antiseptics are chemi-
cal agents similar to disinfectants, but can be applied onto living tissues (i.e. hand-washing) to
remove accumulated transient microorganisms, and temporarily lower the concentration of normal,
resident flora. Soap only removes microorganisms.

• "Antiseptic" best relates to a handwash agent. Antiseptics are used for antimicrobial agents applied
onto living tissues.

• Liquid antimicrobial preparations (antiseptics) for handwashing: chlorhexidine gluconate,

parachlorametaxylenol, idophors, and triclosan.

• Alcohol-the most widely used antiseptic, and is used to reduce the number of microorganisms
on the skin surface in a wounded area. Alcohol denatures proteins, extracts membrane lipids, and
acts as a dehydrating agent, all of which contribute to its effectiveness as an antiseptic. Even some
viruses (lipophilic viruses only) are inactivated by alcohol.

• Isopropyl Alcohol-also used for hand hygiene procedures, but products containing 60-80%
alcohol DO NOT use water, thus is a waterless hand hygiene agent. Isopropyl alcohol (90-95%)
is the major form used in hospitals.

• Phenol-the original disinfectant used in hospitals, but is rarely used today because it is
too caustic.

433
r= -

• Advantages of using alcohols (70% isopropyl & 70% ethyl alcohol) as surface disinfectants:
alcohols are bactericidal, tuberculocidal, and are economical. Alcohols are NOT sporicidal.

• Alcohol Disadvantages: alcohol evaporates too quickly and has diminished activity against
viruses in dried blood, saliva, and other secretions on surfaces due to the presence of tissue
proteins and glycoproteins that render alcohol ineffective. Thus, alcohols are not effective surface
cleansing agents (i.e. cleaning a dental operatory after treatment).

• Ethanol (70%)-widely used to clean skin prior to immunization or venupuncture.

• Iodine-the most effective skin antiseptic used in medical practice that acts as an
oxidizing agent, and irreversibly combines with proteins.

DISINFECTION ~ process of reducing the numbers or inhibiting growth of microorganisms (espe-

cially pathogens) to the point that they do not pose a threat of disease. Disinfection uses chemical
agents to destroy pathogenic microorganisms, but not necessarily all pathogens or resistant
spores on INANIMATE surfaces. Disinfection is less lethal than sterilization, and involves a chemical
process of microbial inactivation that destroys virtually all pathogenic microorganisms on inanimate
surfaces, but not necessarily all microbial forms (spores). Disinfection is the killing of many, but not
all, microorganisms. It does not include the destruction of bacterial spores.

DISINFECTANTS ~ antimicrobial chemical agents (solutions, sprays, or wipes) used to destroy/kill

microorganisms on when applied to inanimate objects/surfaces like countertops, lights, bracket
trays, headrests, light handles, dishes, tables, floors. Disinfectants are not safe to use on living tis-
sues (however antiseptics are safe). Thus, are only applied to inanimate objects. Disinfectants are
germicidal (kill) and prevent pathogenic microorganism growth (microbiostatic)

• Alcohols, Chlorhexidine, & Quaternary Ammonium Compounds are disinfectants.

• Water-based disinfectants are better than alcohol-based disinfectants.

• Pump spray disinfectants are better than aerosol spray disinfectants.

• Quaternary Ammonium Compounds-cationic detergents used as disinfectants & antiseptics. Gram

(+) bacteria are most susceptible to destruction. These compounds are NOT sporicidal, tuberculocidal,
or viricidal, and are inactivated by anionic detergents (soaps and iron found in hard water). Ex:
Benzalkonium Chloride.

• Cationic Detergents-quaternary ammonium compounds widely used for SKIN ANTISEPTICS.

Detergents are "surface-active" agents composed of a long ch ain, lipid-soluble, hydrophobic portion,
and a polar hydrophilic group that can be a cation, anion, or non-ionic group. These surfactants
interact with the lipid in the cell membrane through their hydrophobic chain, and with the surrounding
water through their polar group and thus, disrupt the cell membrane.

• Anionic Surface-Acting Substances/Detergents-are synthetic anionic detergents and soaps that

alter the nature of interfaces to lower surface tension and increase cleaning. Their primary value is
their ability to remove microorganisms mechanically from the skin surface. *Non-ionic chemicals
DO NOT have anti-microbial properties.

434
 .- '

• Cleaning surfaces PRIOR to disinfection in clinical settings is required to REDUCE the

concentration of pathogens. The simplest way to approach environmental surface disinfection is to
adhere to the aseptic technique of CLEANING IT FIRST. All disinfectant products include specific label
instructions for cleaning PRIOR TO DISINFECTION. Cleaning physically removes debris, reduces
the number of microorganisms present, and removes blood, tissue bioburden, and other debris that
can interfere with disinfection.

• Mycobacterium Tuberculosis is the marker microorganism for intermediate surface disinfection.

Antimicrobial activity against MT is recognized as a significant benchmark criterion for disinfectant
effectiveness. While tuberculosis is not transmitted via inanimate environmental surfaces, its
morphology and structure make tubercle bacilli relatively resistant to penetration by many low-
level disinfectant chemicals.

• Intermediate level agents like phenols, iodophors, hypochlorite, and certain preparations
containing alcohols and other cleaner disinfectant chemicals can penetrate the wax and lipid outer
layers surrounding mycobacteria.

CHLORHEXIDINE GLUCONATE & TRICLOSAN - handwash agents with broad antimicrobial ef-
fect. They also have "substantivity" or a residual action on washed tissues for extended periods of time.

CHLORINE - a powerful oxidizing agent that inactivates bacteria and most viruses by oxidizing free
sulfhydryl groups. Chlorine is the active component of hypochlorite (bleach) and is used as a disinfectant.

PASTEURIZATION - the treatment of dairy foods (milk) for short intervals using HEAT to
kill certain disease-causing microorganisms. The target of pasteurization is to destroy
MYCOBACTERIUM TUBERCULOSIS.

Concentration &contact time are critical factors that determine the effectiveness of an antimi-
crobial agent against a particular microorganism. Any or all three of the major portions of microbial
cells can be affected: cell membrane, cytoplasmic contents (especially enzymes), and nuclear material
(DNA, RNA).

Studies show an increased risk of developing an allergic reaction to latex protein (Type 1) or cer-
tain chemicals used in the latex manufacturing process (Type IV) in certain groups of people. Cur-
rent information has NOT shown a cross-reaction between pollen allergies and water-soluble latex
allergens. Individuals who are predisposed to readily developing Type I hypersensitivity reactions
(i.e. people who are atopic), can become sensitized to latex allergens more readily than people
with few or no allergies.
• Latex Allergy Risk Factors: rubber industry workers, atopy, persons with multiple surgeries and
banana allergies, and spina bifida.

Antigens most responsible for an immediate Type I allergic reaction to natural rubber latex are
PROTEINS. Only a few of the 250 proteins are found in sap of the rubber tree.

• Hevea brasiliensis-water-soluble macromolecules that can leach out of latex gloves when a person
perspires, or may be detected on surfaces of other products containing natural rubber latex (NRL).
These proteins cause Type I, immediate, IgE-mediated reactions to natural rubber latex.

• If a patient develops a Type I, immediate allergic reaction to latex during dental treatment, the next
time you treat them wear VINYl or NITRILE gloves.

435
 NOTES • Awide variety of latex-alternative infection control items appeared in the market within the last
10 years. The most widely recognized are newer generations of vinyl or nitrile gloves that do not
cross-react with latex allergens. Products designated "hypoallergenic" are no longer labeled
latex alternatives since they contain latex with a chemical coating over the latex.

• Recent studies show not all latex-allergenic people were able to use hypoallergenic gloves, since
many Type I allergic individuals still developed allergic manifestations when using these gloves.

IRRITATION DERMATITIS - the most common form of an adverse epithelial (skin) reaction
noted for healthcare professionals. Many published reports have cited data suggesting 20-30% of
healthcare workers suffer occasional or chronic dermatitis on their hands.

The most common manifestation is irritation dermatitis (a non-specific immune reaction often caused
by contact with a substance that physically or chemically damages the skin). The condition is aggra-
vated by frequent handwashing, residual glove powder left on hands, and the harshness of repeated
use of some antiseptic handwash agents. Healthcare workers who live in colder climates may also ex-
perience chapping during the winter months.

AMERICANS WITH DISABILITIES ACT - both state and federal statutes define disability as
having a physical or mental impairment that substantially limits one or more major life activities
of the individual, a record of such impairment exists, and the patient is regarded as having
such impairment.

• Dentists cannot deny anyone care due to a disability and cannot dismiss employees due to a disability.

• Dental offices must undergo structural changes to allow access for the disabled.

• HIV patients are protected under the Americans with Disabilities Act.

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436
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437
 RADIOLUCENCY & OSTEORADIONECROSIS
Radiographs show shading from black to white (most radiolucent to most radiopaque). From least to
most radiopaque: (POL space, dentin, enamel, ZOE, and amalgam).

Radiopaque Structures & Dense Materials: metals, enamel, dentin, and bone that INHIBIT the passage
of x-rays and appear WHITE on the processed film. Less radiation penetrates the structure and reaches
the film.

RADIOLUCENT STRUCTURES AND MATERIALS - less dense materials like soft tissue and air
space that appear gray to black on processed film) ALLOWING RADIATION to pass through by absorbing
very little radiation. More radiation penetrates the structure and reaches the film.
• Radiolucent Lesions-appear every time bone is DESTROYED. Unilocular & Multilocular are terms
only used to describe radiolucent lesions.

1. well-defined unilocular (one cavity): border is well-defined. Most benign lesions are
unilocular, well-defined .
2. well-defined multilocular: border is well-defined with several cavities.
3. well-defined honeycomb or soap bubble (multilocular):
4. diffuse-cannot follow the border of the radiolucency: 90% of the time it is cancer.
If loss of cortical plates, the first diagnosis is cancer.

OSTEORADIONECROSIS - the necrosis of bone produced by ionizing radiation that is more

common in the MANDIBLE than maxilla due to the richer vascular supply to the maxilla, and because the
mandible is more often irradiated. The most common factors precipitating osteoradionecrosis are pre-
irradiation & post-irradiation extractions, and periodontal disease. Damage to blood vessels (not
nerves or muscles) predisposes a patient to developing osteoradionecrosis. A complications that can
occur with patients taking IV Bisphosphonates or oral bisphosphonates for more than three years
orally (i.e. Fosamax).

Osteoradionecrosis is more common IN THE MANDIBLE probably because of the richer vascular supply
to the maxilla and the fact that the mandible is more frequently irradiated. Caution with patients on IV
bisphosphonates or if taking oral bisphosphonates (i.e. Fosamax).

• May occur after dental extractions.

• The most common factors precipitating osteoradionecrosis are pre and post irradiation extractions
and periodontal disease.

438
HAMULAR PROCESS - the bony projection that arises from the SPHENOID BONE and extends
downward and slightly posteriorly. On the radiograph, it is seen in proximity to the posterior surface of
the maxillary tuberosity. It varies greatly in length, width, and shape among patients. It usually exhibits
a bulbous point, but sometimes the point is tapered.

CORONOID PROCESS - this image of the mandible often appears in the periapical radiographs of
the MOLAR REGION of the MAXILLA. As the mouth is opened, the coronoid process moves forward, and
thus comes into view most often when the mouth is opened to its fullest extent at the time the exposure
is made. It is evidenced by a tapered or triangular radiopacity that can be seen below, or sometimes
superimposed on the molar teeth and maxilla.

Dental Radiographs should be retained INDEFINITELY. The dental record must include documentation
of informed consent and the exposure of radiographs (i.e. number and type of films, rationale for exposure
and interpretation) . Legally, dental radiographs are the PROPERTY OF THE DENTIST. However, patients
have a right to reasonable access to dental radiographs, which includes having a copy forwarded to
another dentist.

• Patients may refuse dental radiographs, but the dentist must decide whether an accurate diagnosis
can be provided, and whether treatment can be provided.

• No document can be signed by the patient that releases the dentist from liability.

DIGITAL RADIOGRAPHY - requires LESS radiation than traditional radiography because the sensor
is more sensitive to x-rays. Also, radiation exposure to the patient is reduced 50-80% with digital
radiography. The sensor is used in place of film in digital radiography. Intra-oral, panoramic, &
cephalometric images can all be obtained digitally.

Advantages:
• Superior gray-scale resolution. The human eye can only appreciate 32 shades of gray. The traditional
radiograph differentiates 16-25 shades of gray, while the digital image uses up to 256 shades of gray.

• Less patient radiation and increased speed of image viewing.

• Decreased cost of equipment and film, image enhancement (this may also be a disadvantage in
legal issues since the image can be manipulated), superior patient education tool. Although initial
set-up costs for digital radiography can be significant, the elimination of film, darkroom chemicals,
and equipment reduces maintenance costs.

• Each digital sensor costs between $5,000-$7,500 (initially expensive, but over the long-term, the
office will save money due to savings in time, no film required, developing chemicals, etc.) . Digital
radiography is the absolute future in dentistry.

DIGITAL SENSOR

439
 STORAGE PHOSPHOR IMAGING SYSTEM - a type of digital imaging system that uses a
REVERSIBLE IMAGING PLATE rather than a sensor to record the image. The plates are more flexible, thus
more comfortable for the patient.

DIRECT DIGITAL IMAGING SYSTEM - uses an intraoral sensor attached to a fiberoptic cable.

Indirect Digital Imaging System - scans an existing radiograph and digitizes the image.

Charge-Coupled Device (CCD) - currently the most common digital image receptor. It is a solid
state detector with a silicon chip embedded in it (it is the electronic circuit in the silicon chip that is sensitive
to x-rays). CCD technology is also used in home video cameras, fax machines, and telescopes.

PRIMARY RADIATION - the radiation generated at the ANODE of the x-ray tube that is attenuated
by the filter and object. The amount of primary radiation follows the inverse square law measured from
the focal spot. The attenuation of primary radiation is measured with a narrow beam geometry to include
all secondary (i.e. scattered radiation).

SECONDARY RADIATION ("SCATTERED RADIATION") - arises from interactions of the primary

radiation beam with atoms in the object being imaged. Since scattered radiation deviates from the
straight line path between the x-ray focus and image receptor, scattered radiation is a major source of
image degradation in both x-ray and nuclear medicine imaging techniques. When x-ray radiation passes
through a patient, 3 interactions can occur (coherent scatter, photo electric absorption, and Compton
scattering). Of these, most scattered x-rays in diagnostic x-ray imaging arise from Compton scattering.
ALEADED, RETANGULAR cone (PID) best reduces the amount of scatter radiation to the patient as this
greatly reduces the size of the beam.

• In performing normal dental diagnostic procedures, the operator receives the greatest hazard
from secondary (scatter) radiation.

COLLIMATION - the control of the SIZE &SHAPE of the x-ray beam using metal plates, slots, or bars
to confine and direct radiation (i.e. x-rays or gamma rays) to a specific region and/or to discriminate
against radiation from unwanted directions (i.e. scattered radiation) . In x-ray imaging systems, a
collimator mounted to the x-ray tube is used to define the dimensions of the beam which is to be incident
on the subject and detector. To minimize radiation dose and to comply with government regulations, a
certain level of precision must be maintained.

• It is a basic rule of radiation hygiene that the radiation beam be as small as practical. For intra-
oral radiography, by state law, the diameter of a circular beam of radiation at the patient's skin
cannot be larger than 2.75 inches. One can use a diaphragm or metal cylinders, cones, or tubes to
collimate the beam.

• These devices reduce the amount of radiation received by the exposed tissues and the radiation to
surrounding tissues due to x-ray beam divergence.

X-ray beam is composed of rays of different wavelengths and penetrating power (polychromatic)
because the potential across the x-ray tube constantly changes as the kilovoltage changes:

• Short wavelength (high energy) x-rays: have great penetrating power (are useful) . Short wavelength
x-rays are produced at higher kilovoltages and penetrate objects more readily (these form the image
on the film).

• Long wavelength (low energy) x-rays: are produced at lower kilovoltages (kVp) thus have low
penetrating power (are easily absorbed), and do not reach the film in reasonable quantities because
they are attenuated by the soft tissues. Low energy rays only add to the total amount of radiation the
patient receives. Aluminum discs are used to "filter" out these USElESS long wave rays to increase
the overall quality of the x-ray beam .

440
FILTRATION - the removal of parts of the x-ray spectrum using absorbing materials in the x-ray
beam. The x-ray spectrum reaching the patient is filtered by attenuating material in its path. Filtering
the beam is used to modify the spectral or spatial distribution of x-ray (or both). Filtration reduces
patient dose, contrast, & film density.

1. Inherent filtration-the filtration of an x-ray beam by any parts of the x-ray tube or tube shield
through which the beam must pass. The parts include the glass envelope of the x-ray tube and
OIL surrounds the x-ray tube to cool the tube to dissipate heat, and the exit window in the tube
housing. The inherent filtration corresponds to -0.51mm of aluminum.

2. Added filtration-obtained by placing thin sheets of aluminum in the cone to filter the
useful beam further.

3. Total filtration of the x-ray beam before it reaches the patient consists of the inherent filtration
+ added filtration. The recommended total is the equivalent of 0.5mm (below 50 kVp) and
2.5mm (over 70 kVp) of aluminum .

When taking radiographs, the operator should STAND AT LEAST 6 FEET AWAY from the patient to reduce
radiation exposure to the operator and should also stand behind a lead shield if possible. The operator
should NEVER remain in the room holding the x-ray packet in place for the patient. If a film must be
held in place by someone else (i.e. for a child), drape the parent and have him or her hold the film. All
dental personnel should wear film badges that monitor exposure dosages.

1. The operator must avoid the primary beam by positioning themselves at a 90°-135°
angle to the bea m.

2. Always maintain proper infection control when taking and processing dental radiographs!

EKTA-SPEED FILM - provides the MOST EFFECTIVE way to REDUCE exposure time, amount of
radiation reaching the patient, and amount of scatter radiation (secondary radiation) to the dentist.

Additional Factors that Reduce Patient Radiation:

• Lead apron & thyroid (cervical) collar-is the most effective at stopping x-rays, so patient should
always wear both . The cervical collar protects the thyroid gland .
• Increasing filtration using an aluminum disk.
• Lead diaphragms placed within the cone of an x-ray tubehead .
• Collimating an x-ray beam .
• Ekta-Speed Film
• Increasing the source-film distance.
• Intensifying screens-used for all extra-oral radiography (panoramics, cephalometrics).

Committee on Radiation Protection of National Bureau of Standards: recommends a person who works
near radiation be exposed in 1 year to a maximum dose of 5 REM (0.1 REM per week). Secondary
(scatter radiation) is the greatest hazard to the dental team.

• MPD (Maximum Permissible Dose of Radiation Exposure). The yearly MPD for a non-occupationally
exposed person is 0.5 REM and 5 REM for people who work near radiation.

Sequence of Radiation Injury:

1. Latent Period-period of time between radiation exposure and onset of symptoms. It may be short
or long, depending on the total dose of radiation received and amount of time it took to receive
the dose.

2. Period of Cell Injury-comes after the latent period. Cellular injury may cause cell death, changes
in cell function, or abnormal mitosis of cells.

3. Recovery Period-the last event in the sequence of radiation injury. Some cells recover from the
radiation injury, especially if the radiation is "low level".

441
 N Effects of radiation exposure are ADDITIVE, and the damage that remains non-repaired accumulates
in tissues. The cumulative effects of repeated radiation exposure can lead to various serous health
problems (i.e. carcinogenesis, which leads to various carcinomas, genetic mutations that cause birth
defects, different leukemias, and cataracts) .

Carcinogenesis &Genetic Mutations are important and serious effects of repeated exposure to low
doses of x-radiation . The mechanisms involved are due to frame-shift mutations, synergism with
chemical carcinogens, and altered DNA repair enzyme functions .

Cells in the body have different sensitivities to radiation. In general , the greater the rate of potential
for mitosis and the more immature the cells and tissues, the more susceptible or sensitive these
cells are to radiation.

• Radiosensitive Cells: small lymphocytes (immature blood cells), bone marrow, reproductive cells
(sperm/ova), and immature bone cells.
• Prostate gland is very sensitive to radiation.

• Hemopoietic tissue is the most sensitive to radiation

• Radioresistant Cells: mature bone, muscle, and nerve (pulp).

• Muscle cells are the most radioresistant.

RADIATION ABSORBED DOSE ("RAD") - a measure of the energy imparted by any type of ionizing
radiation to a mass of any type of matter. The traditional unit of absorbed dose is the "rad".

EQUIVALENT DOSE ("DOSE EQUIVALENT") - the correct unit of measurement used by the dentist
to compare the biologic-risk effects/estimates of different types of radiation damage to a tissue or
organ.

EFFECTIVE DOSE - used to estimate the risk in humans.

EXPOSURE - a measure of radiation quantity, the capacity of the radiation to ionize air. Roentgen (R) is the
traditional unit of radiation exposure measured in air. Roentgen only applies to x-rays and gamma rays.

X-rays have more energy than light. -1 % of the energy released in the x-ray tube is released
as x-rays.

ELECTROMAGNETIC RADIATIONS - includes microwaves, x-radiation, visible light, and gamma

radiation . X-rays &gamma rays are types of non-particulate radiation energy.

PANORAMIC RADIOGRAPH - an extra-oral radiograph where a bite piece is held between the
patient's front teeth. This bite piece should either be sterilized after each use, or covered with a disposable
plastic slipcover.

• Indications: diagnose oral pathology not visible on periapical radiographs, treating planning
(especially orthodontic cases) , evaluation of anomalies, as one part of the follow-up evaluation in
surgical and trauma cases, edentulous patients prior to fabrication of full dentures, and in patients
unable to tolerate intra-oral radiographs.

• Advantages: shows areas that may not be visible on a full-mouth series (and shows both arches on
the same film). Greater patient comfort (eliminates gagging), and requires less time than a full-
mouth series. Panoramic radiograph is the screening x-ray for pathology of the jaws. It is excellent
for third molar pathology and to observe the TMJ, sinuses, and in sialography (a technique used
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442
• Disadvantages: provides less image detail & definition than periapical radiographs due to
intensifying screens, movement of the x-ray tube and film, and increased object-film distance.
• loss of image detail (making it difficult to diagnose early carious lesions). Bite-wing x-rays are
required to diagnose carious lesions.
• Image distortion due to increased object-film distance.
• Inadequate for interproximal caries detection or detecting periodontal breakdown (bone loss) .
• Proximal overlapping (especially in posterior areas).
• Added exposure to a large area of body tissue in addition to the oral tissues.

Poor definition of interproximal caries. However, by supplementing a panoramic with posterior or anterior
bitewings, a more complete radiographic survey of the patient is obtained. The panoramic is NOT a
substitute for intra-oral films.

Pamoramic Positioning Errors:

1. Chin Tilted too Far Upward: a positioning error most likely to cause a REVERSE OCCLUSAL PLANE
CURVE on a panoramic radiograph . A "reverse occlusal plane curve" is where mandibular
structures look narrower and maxillary structures look wider (looks like a "frown").

2. Chin Tilted too Far Downward: occlusal plane shows an excessive upward curve (looks
like a "big smile"), there is severe interproximal overlapping, and the anterior teeth appear
highly distorted .

CEPHALOMETRICS ("LATERAL HEAD RADIOGRAPH) - a technique employing oriented

radiographs for the purpose of making head measurements used to study craniofacial growth, diagnosis,
planning orthodontic treatment, and evaluation of treated cases. Cephalometries are useful to assess
tooth-to-tooth, bone-to-bone, and tooth-to-bone relationships. Serial cephalometric films can show
the amount and direction of growth.

• Lateral head radiograph (cephalometric x-ray) must be compared with "normal" lateral radiographs
from an accepted norm . Linear and angular measurements are obtained using known anatomical
landmarks in the lateral head radiography of the patient. These measurements are then compared
with those considered WNL, thus enabling the orthodontist to assess aberrations in the dentition and
jaw structures that cause malocclusion.

• Cephalometric radiographic analysis includes hard tissue structures (bone & teeth), and
measurements of soft tissue structures (nose, lips, soft tissue chin).

• Superimposition of longitudinal cephalometric studies is generally on a reference plane and

registration point to best demonstrate the growth of structures farthest from the plane and point.
The most stable area from which to evaluate craniofacial growth is the anterior cranial base due to
its early cessation (stopping) of growth.

BITEWING RADIOGRAPHS - an intraoral radiograph MOST useful to detect INTERPROXIMAL CARIES

and demonstrate alveolar bone resorption (periodontitis). Bitewings show the crowns of both maxillary
& mandibular teeth, but NOT the root apices. The main reason to take bitewings is to detect
interproximal caries.

• Bitewings are most useful to monitor the progression of periodontal disease as they show the
crestal bone levels and interproximal areas of both arches. For the film to be of diagnostic use, the
quality of the dimensional accuracy, open contacts, and optimum contrast and image clarity must
be excellent. When taking bitewings, the film is placed in either a horizontal or vertical position.

• Vertical bitewings-provide more periodontal information (i.e. bony defects and furcation involvement).
A fuzzy or indistinct image of crestal bone is often associated with early periodontitis. The vertical
bitewing angUlation should be between +8° and +10°. Vertical bitewings show more alveolar bone
than traditional horizontal bitewings.

• Adjust horizontal angulation to direct the central ray toward the center of the film.

443
 • Two bitewings are usually taken on a child (one on each side). If the child only has the primary
dentition, then #0 film is used. If the child has a mixed dentition, #1 film is used. Once the child has
2nd molars, two to four #2 films are used (if using 4 films, one film images the premolar area, while
the other images the molar area). Sometimes two, long #3 films are used (one per side) rather then
two #2 films on each side. This practice is not recommended due to the curvature of the arch, making
it difficult to open all contacts on one film.

SUBMENTAL-VERTICAL (SUBMENTOVERTEX) - an x-ray designed to diagnose BASILAR SKUll

FRACTURES, and provides some diagnostic information about the zygoma, zygomatic arches, and
mandible. This film is taken with the source below the mandible and the film above the head. The
submentovertex radiographic view is used when you suspect a fracture of the zygomatic arch.

SUBMENTOVERTEX IMAGE

'1 . mandibular C'ondyle .' , plQde

2. ooronoid prooess otr,..andibJe " al,pte!' plate '
4'.·~ar.otidoanal
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3: ariferior .VIall of Idelle dainial fossa
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6. foramen o'v'ale 18. nasal sept'um
7. It'la$toid airceUs 19: maxilier; sirius
8. sphehoicl sirius 20. hairollp
9Aateral viall of maxillatysiflus 21 . pharYflx
10. po~eriorCt,miaLto~sa 22: vertebrae
11. odont6idprooes'~ Ofaxfs 23.ari::h :Qfq~1
12. foramen magnum . . . .

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444
WATER'S VIEW - the standard radiograph of choice for showing an ANTERIOR VIEW of the
PARANASAl SINUSES and of the mid-face and orbits. This is a posterior-anterior projection with patient's
face lying against the film and the x-ray source behind the patient's head . Water's is one of the best films
for radiographic diagnosis of MID-FACIAL FRACTURES, sinus infections, and its view best demonstrates
lesions of the maxillary sinus.

WATER'S VIEW

445
 TOWNE'S VIEW - the best film to visualize the CONDYlES &NECK OF MANDIBLE from an AP
projection. The patient lies on his back with the film under his head. The x-ray source is from the front,
but is rotated 30° from the Frankfort plane and is directed right at the condyles.

• Towne's view is often of value to assess the status of the condyles, condylar neck, and rami
because superimposition of the mastoid and zygoma over the condylar neck region in the straight
postero-anterior projection often makes interpretation difficult. Towne's view eliminates this
superimposition to give good visualization of the condylar area and rami.

• Reverse Towne's View-used to identify fractures of the condylar neck and ramus area.

TOWNE'S VIEW

446
CONVENTIONAL TMJ RADIOGRAPHS - show the condyles position in the glenoid fossa, range of the NOlES
condyles' antero-posterior movement, and areas of bone destruction on the condylar heads.

DEVElOPER SOLUTION - a chemical solution that converts the invisible image on a film into a
visible image composed of minute masses of black metallic silver. Its function is to reduce silver halide
crystals to black metallic silver.

X-ray Developing Solution Contains 4 Chemicals:

1. Developing agent (hydroquinone)-a chemical compound capable of changing the exposed silver
halide crystals to black metallic silver, while producing no appreciable effect on the unexposed
silver halide crystals in the immulsion. It gives details to the x-ray image. Elon, also Quickly
generates gray tones on the x-ray image.

2. Antioxidant preservative (sodium sulfite)-prevents the developer solution from oxidizing in

the presence of air.

3. Accelerator (sodium carbonate)-an alkali that activates the developing agents and maintains
the alkalinity of the developer at the correct value. It softens gelatin of emulsion.

4. Restrainer (potassium bromide)-is added to developers to control the action of the developing
agent so it does not develop the unexposed silver halide crystals to produce fog.

When taking panoramic radiographs, if the films keep getting lighter &lighter after each development,
to correct this problem simply replenish the developing solution. As the developing solution gets
weaker, the films get lighter. Both the developing and fixing solutions should be replenished daily. These
solutions need to be changed regularly and the tanks scrubbed and cleaned.

• Factors that affect developing solution life: cleanliness of tanks, size & number of films processed,
and solution temperature.

• Yellowish-brown film is caused by insufficient fixing or rinsing.

• Fogged film may result from improper film storage or outdated films.

• Low solution levels will appear as developer cut-off (straight clear border) or fixer cut-off (straight
black border).

X-RAY FIXING ("FIXER") SOLUTION - a chemical solution whose function of is to STOP

development and remove remaining unexposed crystals. Fixing time is always at least twice as long
as the developing time. Fixer contains 4 chemicals:

1. Clearing agent (sodium or ammonium thiosulfate)-commonly called "hypo" dissolves and

removes underdeveloped silver halide crystals from the emulsion (one of the main functions of
fixing solutions). The chemical clears the film so the black silver image produced by the developer
is distinctly perceptible. When the film is improperly cleaned, the remaining unexposed silver
halide crystals darken upon exposure to light and obscure the image.

2. Antioxidant preservative (sodium sulfite)-prevents the decomposition of the fixer chemical.

3. Acidifier (acetic acid)-necessary for the correct action of the other chemicals and also neutralizes
any alkaline developer that may be carried over by the film or hanger.

4. Hardener (potassium alum)-shrinks and hardens the gelatin in the emulsion . It shortens
drying time and protects the emulsion from abrasion.

If a dried radiograph were processed a second time, there would be no change in contrast or density.

After processing a film, if it appears the color BROWN, the most likely cause is the fixing time was
not long enough. Afilm appears brown when it is not completely fixed.
447
 Common Darkroom Errors:
• Mounted films are improperly labeled (wrong patient name): because racks are not labeled properly.
• Fogged film (gray/lack of contrast) due to faulty safelight in the darkroom. White light leaking into
the da rkroom.
• lost films because films are not secured properly on the rack.
• Static marks (multiple black lines) due to friction when opening film packets causes static electricity.
• Overdeveloped film (dark) due to incorrect time (too long) and too hot a temperature.
• Underdeveloped film (light) due to incorrect time (too short), too cold a temperature, or weak
solutions that are old or diluted.
• Torn emulsion: films were allowed to touch or overlap while drying.
• Stained film (dark/white spots) due to dirty work surfaces, person developing film was sloppy.
• Scratched films (white lines): film emulsion removed by sharp object (fingernails/rack touching) .
• Clear films: emulsion washed away, films left in water (wash) for over 24hrs.
• Air bubbles (white spots): air trapped on the film surface while being placed in processing.
• Overbent films-causes crescent-shaped radiolucent marks due to cracked emulsion.

Common Errors When Taking Radiographs:

• light films (underexposed/image not dense enough): due to incorrect milliamperage (too low) or
exposure (too short), incorrect focal-film distance, or cone too far from the patient's face, or film is
placed backwards.
• Dark films (overexposed/image too dense): due to incorrect milliamperage (too high), exposure (too
long), incorrect kVp (too high).
• Double exposure: film was used twice.
• Fogged films (gray/lack of contrast): exposed to radiation other than from the primary beam .
• Poor contrast: incorrect kVp (too high).
• Poor film placement: film is not placed far enough back or not forward enough in the mouth .
• Blurred image: patient movement or drifting of the x-ray arm.
• Clear films: were not exposed to radiation .
• Artifacts: patient did not remove eyeglasses, jewelry, or removable prosthetic appliances.
Herringbone ("Diamond Effect")-a zig-zag pattern appears on the processed film when film is
placed backwards in the mouth. Developing solution on the film . Double exposure of film .

RADIOGRAPHIC TECHNIQUES
VERTICAL ANGULATION - directing x-rays so they pass vertically through the part being examined.
This is accomplished by positioning the tubehead and direction of the central ray in an up-and-down
(vertical) plane. Foreshortening &Elongation are produced by INCORRECT VERTICAL ANGULATION.

• Foreshortening-a shortened image is caused by excessive vertical angulation. The teeth APPEAR
TO SHORT due to either too much vertical angulation, or poor chair position.

• Elongation-an elongated image is caused by insufficient (too little) vertical angulation. Elongation
is the MOST COMMON error when taking dental radiographs where the teeth APPEAR TOO lONG
due to either too little vertical angulation, or the film not being parallel to the long axis of the teeth
or the occlusal plane not being parallel to the floor.

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448
 NOTES
VERTICAL ANGULATION

HORIZONTAL ANGULATION - maintaining the central ray at 0° as the tube is moved around the
head. This is accomplished by positioning the tubehead and direction of the central ray in a side-to-
side (horizontal) plane. The general rule for horizontal angulation is the central ray should be
perpendicular to the mean antero-posterior plane of the teeth being x-rayed.

• Overlapping-interproximal areas are overlapped due to incorrect horizontal tube angulation

(central x-ray was not directed perpendicular to the curvature of the arch and through the contacts) .
Overlapping reduces the diagnostic quality of film to detect interproximal caries since teeth
images are superimposed on each other).

The central ray is at 0° when the x-ray tube is adjusted so the central ray is parallel to the floor. If the
tubehead is directed at the floor, it is positive angulation. If the x-ray tubehead is directed toward the
ceiling, it is negative angulation.

BISECTING ANGLE TECHNIQUE - a technique based on the geometric rule of isometry which
states two triangles are equal if they have two equal angles and share a common side. The image on the
film is equal to the length of the tooth when the central ray is directed at 90° to the imaginary
bisector. Atooth and the radiographic image are equal in length when two equal triangles are formed
that share a common side (imaginary bisector). The bisecting technique works as follows to produce a
tooth image that is accurate if done correctly. Advantage: decreased exposure time.

• X-ray film is placed along the lingual/palatal surface of the tooth. At the point where the film contacts
the tooth, an angle is formed by the plane of the film, and the long axis of the tooth.

• The person taking the x-ray must visualize a plane that bisects this angle (this plane is the imaginary
bisector which creates two equal angles and provides a common side for the two imaginary equal
triangles. The central ray is positioned perpendicular to the imaginary bisector.

• Disadvantages: x-ray film image may be dimensionally distorted (amount may vary) ; due to the use
of a short cone (which causes divergent rays) the image is not a true reproduction of the object; may
not be able to judge the correct alveolar bone height.

Paralleling Technique based on the concept of parallelism since the film is placed parallel to the
long axis of the tooth being x-rayed, and the central x-ray beam is directed perpendicular or at right
angles to the long axis of the teeth &plane of the film. Afilm holder (XGP) must be used to keep the
film parallel to the long axis of the tooth .

• Advantages: little or no root superimposition on a maxillary molar view, accurate diagnosis of

periodontal bone height (given minimal distortion), and the image formed is dimensionally accurate.

449
 N • Disadvantages: film placement may be difficult in some areas (i.e. low palatal vaults) , increased
exposure time is required due to the use of a LONG CONE, and XCP holderslrings can be
cumbersome to work with and may cause patient discomfort. The object-film distance must be
increased to keep the film parallel, which results in image magnification and loss of definition. Also,
the source-film distance must be increased to compensate for the image magnification, and to
ensure that only the most parallel x-rays will be aimed at the tooth and film. Using a long cone to
increase the target-film distance (16 inch target-film distance) is required to provide greater
definition and less image magnification .

• AKA: XCP (Extension Cone Paralleling Technique), Right-Angle Technique, Long-Cone Technique.

BUCCAL OBJECT RULE ("TUBE SHIFT TECHNIQUE" OR "SLOB" RULE) - used to determine
an object's special position within the jaws. This technique uses two radiographs of an object exposed
with slightly different tube angulations, then compares the object's position on the radiograph with
respect to a reference point (i.e. the tooth root).

• SLOB (Same Lingual, OPPosite Buccal): if the object in question appears to move in the SAME
direction as the x-ray tube, then it is on the LINGUAL aspect. If it appears to move in the OPPOSITE
direction as the x-ray tube, then it is on the BUCCAL aspect.

• If the x-ray tube is shifted and directed from a mesial direction/angualtion, and the object in question
moves mesially from the reference point, then the object lies lingual to that reference point. The the
x-ray tube was directed from a mesial angulation, the special position of the object lies LINGUAL.
However, if the x-ray tube is shifted mesially and the object moves distally, it lies on the buccal
aspect of the reference point.

CERVICAL BURNOUT - a phenomenon caused by relatively low x-ray absorption on the mesial or
distal surfaces of teeth, between the edges of the enamel and adjacent crest of the alveolar ridge. Because
of this diminished x-ray absorption, these areas appear relatively radiolucent will ill-defined margins. It
is caused by the normal configuration of the affected teeth (CEJ) which results in decreased x-ray
absorption in those areas. These radiolucencies should be anticipated when viewing x-rays of almost
any tooth, and must not be mistaken for a carious lesion.

Inverse Square Law = original intensity = new distance2

new intensity original distance 2

Important: for a given beam of radiation, the intensity is INVERSELY proportional to the square of the
distance from the radiation source. The intensity of an x-ray beam at a given point is dependent on the
distance of the measuring device from the FOCAL SPOT. The reason for this decrease in intensity (the
reason it is inversely proportional) is because the x-ray beam spreads out as it moves away from the
source. The "spread out" beam is less intense.

450
FOCAL SPOT - the small area of tungsten on the anode (target) from which x-rays emanates and that NOTES
receives the impact of the speeding electrons. Focal spot is 1 of 3 factors that influences image
sharpness. The size of the x-ray tube focal spot influences radiographic DEFINITION.

• Target (tungsten targeU-a tungsten wafer embedded in the anode face at the point of electron
bombardment.

• Target Film Distance (source-to-film distance)-distance from the x-ray source (the focal spot on the
tungsten target) to the film. It is determined by the length of the cone (position-indicating device =
PID). Two standard target-film distances are used in intra-oral radiography.

1. 20cm (8 inches): is the short cone that exposes more tissue by producing a more divergent beam.

2. 41cm (16 inches): is the long cone that reduces the amount of exposed tissue by producing
a less divergent beam and a sharper image.

HALF -VALUE LAYER (HVL) - the amount of material required to reduce the intensity of an
x-ray beam to half. For x-ray beams, this is normally expressed in aluminum or copper thickness, but
may also be expressed in other materials or media (i.e. water). HVl is an indicator of the QUAlITY of an
x-ray beam.

Half-value layer is strictly defined for different quantities: photon fluence (# of photons/cm 2), energy
fluence (# of photons x photon energy/cm2) or absorbed dose. Intensity-a term commonly used, but is too
vague, thus is avoided.

• Due to the spectral nature of x-rays, HVl is not constant. When measuring multiple half-value layers,
the 2nd HVL is greater than the 1't HVL since the mean energy of the x-ray spectrum is increased
following the passage of the 1st HVL that results in x-rays becoming more penetrating.

• In oral diagnostic radiography, the HVl of the radiation beam is -2mm of aluminum (this means
50% of the x-rays exiting the vacuum tube are absorbed by 2mm of aluminum. Doubling the
thickness of aluminum will not absorb all of the x-rays, but one HALF of the remaining x-rays.

INTENSIFYING SCREENS - devices used in extra-oral radiography that convert x-ray energy into
visible light. The visible light then exposes the screen film. Thus, the radiation a patient receives is
decreased. Used for all extra-oral radiography (panoramics, cephalometrics) films to decrease the
amount of radiation exposure to patients.

CASSETTE HOLDER - a light-tight device used in extraoral radiography to hold film and
intensifying screens.

Radiograph Operator Controls 3 Factors:

1. Kilovoltage (kVp)-the quality or penetrating power of the x-ray beam that controls the speed
of ElECTRONS. The speed that electrons travel from the filament of the cathode to the anode's
target depends on the potential difference between the two electrodes (kilovoltage). Thus, this has
a very important effect on the x-rays produced at the focal spot. Kilovoltage has nothing to do with
the number of electrons that compose the stream flowing from cathode anode. The number of
electrons (which determines the quantity of x-rays produced), is controlled by the
temperature of the tungsten filament (milliamperage setting). The hotter the filament, the more
electrodes are emitted and available to form the electron stream (x-ray tube current). In the x-
ray tube, the number of electrons flowing/sec is measured in millamperes. The intensity of x-
rays produced at a particular kilovoltage depends on that number. Suitable ranges of dental x-
rays are 65-100 kVp

• Important: kilovoltage influences the x-ray beam and radiograph by altering contrast quality
(for patients with thick jaws, increase kilovoltage), determining the quality of the x-rays
produced, and determining the velocity of the electrons to the anode.

451
 NOTES • kVp most directly affects radiographic CONTRAST and predominantly determines the
penetrating ability of the x-ray beam.

• Setting the x-ray machine for a specific milliamperage actually means adjusting the filament
temperature to yield the current flow indicated.

• To increase film density: rnA, kVp, &time, and source-object distance.

• One effect of a change in kVp is a change in the x-ray's penetrating power. Increasing
kilovoltage (kVp): reduces subject contrast (and the longer scale of contrast) and produces
new, more penetrating x-rays, while emitting less penetrating x-rays that were also produced
at the lower kilovoltage. Increasing kVp causes the resultant x-ray to have AlONGER SCALE
OF CONTRAST. Decreasing kilovoltage: increases subject contrast (and the shorter the
scale of contrast).

2. Milliamperage (mA)-controls the number of x-rays produced (it's the quantity or number of x-
rays produced). Suitable ranges for dental x-rays are 7-15mA.

3. Exposure time-the length of time x-rays are produced and the time the patient is
exposed to them.

Some x-ray machines are calibrated in "impulses" (there are 60 impulses per second).

DENSITY - overall DARKNESS (blackness) of a radiograph that increases, as rnA, kVp, or exposure time
increases, and decreases as rnA, kVp, or exposure time decreases.

CONTRAST - the difference in the degree of blackness (density) between adjacent areas on a
radiograph. Only one exposure factor affects contrast (kilovoltage (kVp). Filtration also plays a role. Higher
kVp settings produce more shades of gray (low contrast).

• High contrast: very dark and very light areas.

• low contrast: many shades of gray, and is preferred in dentistry. Produced by higher kVp settings.

5 Rules to Create Accurate Images when taking x-rays:

1. Use the smallest focal spot that is practical. The size of the focal spot influences radiographic
definition or sharpness (they are inversely proportional, as focal spot decreases, image
sharpness increases). The operator cannot control the size of the focal spot.
2. Use the longest source-film distance practical in the situation.
3. Place the film as close as possible to the structure being radiographed.
4. Direct the central ray at as close to a right angle to the film as anatomical structures allow.
5. Keep the film parallel to the structure being radiographed.

Image Magnification is minimized by USING a lONG CONE.

Dental X-Ray Tube Parts:

1. Filament-a coiled tungsten wire in the cathode (+) that when heated to incandescence,
emits/produces the stream of electrons.

2. Molybdenum cup-houses the tungsten filament.

3. Electron stream-travels from the filament in the cathode to the tungsten target.

4. Tungsten target-located in the anode (-) to stop the stream of electrons.

5. Focal Spot-the portion of the tungsten target struck by the electron beam. It contains a small
area "focal spot" that the electrons strike to produce x-rays. The focal spot's size directly
influences x-ray definition (the larger the focal spot, the greater loss of image definition
and sharpness).
452
 6. Copper sleeve-located in the cathode.

7. Vacuum

8. X-ray beam-produced when the electron stream bounces off focal spot on the tungsten target

9. Leaded glass housing-houses the entire x-ray tube.

X-rays are generated when a stream of electrons (produced by the filament) travels from the
CATHODE ANODE and is suddenly stopped by its impact on the tungsten target. The filament is located
in the cathode and is made of tungsten wire. The small area on the target that the electrons strike is the
focal spot (the x-ray source).

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Prescribing Dental Radiographs:

• Dental radiographs are taken ONLY when needed as judged by each patient's needs. Decisions
about the number, type, and frequency of dental x-rays are DETERMINED ONLY BY THE DENTIST based
on each patient's needs. Every patient has a different dental condition, thus the frequency of x-rays
differs as well. There are guidelines published by the ADA that assist a dentist in prescribing the
number, type, and frequency of dental radiographs.

• Patients with tooth decay, periodontal disease, tooth mobility, pain in one or more teeth, or possible
impacted teeth need more frequent radiographic examinations than patients without such problems.
Apediatric patient who is caries free and asymptomatic, the child's first bite-wing radiographs
should not be taken until the spaces between the posterior teeth have closed.

• Occult Diseases-includes small carious lesions, cysts, &tumors that present no clinical signs or
symptoms. Because occult disease in the perioral tissues is rare (except for caries), a radiographic
examination of the jaws should NOT be done solely to look for it in an individual with teeth when
there are no clinical signs or symptoms. However, every x-ray taken must be evaluated for these
lesions. Remember: caries is an exception to the above ru le due to its much higher prevalence
compared to occult cysts or tumors.

453
 N RADIOGRAPHIC STRUCTURES

Mandibular Molar Region:

1. Nutrient Canal-radiopaque area just below the root apex.
2. Bony trabecular plate-the opaque line between the molars.
3. Inferior border of mandible-a radiopaque straight line running below the molar apices.
4. Submandibular gland fossa-a radiolucent space -6mm below the molar roots.
5. Inferior border of mandible-radiopaque structure/area far below the molar apices.

Mandibular Premolar Region:

1. CEJ (cemento-enamel junction)-appears as an opaque line.
2. Mental foramen-radiolucent space around the root apex of the 2nd premolar.
3. Submandibular gland fossa-a large radiolucent space -5mm below the MB root of the
mandibular 1st molar.
4. PDL-a radiolucent line between the lamina dura and root surface.
5. Film clip mark-a small dark dot.

454
Mandibular Anterior Region:
1. PDL space: radiolucent line
2. Genial tubercles: radiopaque mass
3. Lingual foramen: radiolucent circle.
4. Bony trabecular plate: radiopaque line
5. Marrow space: radiolucent space

Maxillary Molar Region:

1. Anterior wall of maxillary sinus-radiopaque line directly parallel and apical to the first premolar.
2. Inferior nasal concha-a radiopaque mass above the floor of the nasal fossa.
3. Floor of nasal fossa-radiopaque line perpendicular and apical the posterior teeth.
4. Inferior border of zygomatic process of maxilla-radiopaque line that appears the maxillary
sinus floor.
5. Posterior wall of zygomatic process of maxilla (sinus)-a radiopaque line that is directly parallel
and apical to the roots of the maxillary molars.
6. inferior border of zygoma (zygomatic arch)-radiopaque line that passes through the middle
third of the maxillary molars.
7. Floor of maxillary sinus-radiopaque line usually in the apical third of the maxillary molar roots.
8. Mucosa over the maxillary alveolar ridge-the radiopaque structure near the occlusal to the
maxillary molars.

455
 Maxillary Premolar Region:
1. Inferior concha-radiopaque
2. Anterior wall of maxillary sinus-radiopaque
3. Floor of nasal fossa-radiopaque
4. Maxillary sinus-radiolucent space
5. Floor of maxillary sinus-radiopaque line
6. Inferior border of zygomatic process of the maxilla-radiopaque
7. Lingual cusp of first premolar-radiopaque

Maxillary Anterior Region:

• lateral wall of Nasopalatine bone-an opaque line that parallels along the root apex up to the
maxillary sinus.
• Anterior wall of the maxillary sinus-appears as an opaque line above the root apices of the
maxillary anteriors.
• Nasopalatine fossa-a radiolucent structure lateral to the cervical third of the maxillary
centrals root.
• Soft tissue tip of the nose-an opaque structure just before the apex of the maxillary central.
• lamina dura-a radiopaque line that surrounds the root.
• Border of the maxillary sinus-an opaque line.
• PDl-a radiolucent line just between the lamina dura and root surface.
• Nasal Fossa Floor-an opaque line that resembles the floor of the maxillary sinus.
• lateral wall in nasopalatine canal-an opaque line that parallels along the root apex up to the
maxillary sinus.
• Ala of nose-an opaque line.
• Anterior wall of maxillary sinus-opaque line above the root apices of the maxillary anteriors.
• Maxillary sinus-the radiolucent space above the root apices.
• Lingual cusp of I't premolar-opaque area.
• Anterior nasal spine.
• Nasopalatine fossa; soft tissue tip of nose; alveolar crest of bone.

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