DBCS 329 SGL Study Guide

Ted Harmasinski Case 31 Objectives

PREPARED BY: The D2 Class

Pathology
1. Discuss the etiology, epidemiology, pathophysiology and treatment for Acute Bacterial
Sialadenitis. Explain why alcohol and coffee consumption could contribute to this problem.
Sources:
Current Medical Dx & Tx Chapter 8. Ear, Nose, & Throat Disorders (Lawrence R. Lustig, MD, Joshua
S. Schindler, MD)
Tintinallis Emergency Medincine Section 12. Pediatrics Chapter 118. Neck Masses in children
(Osama Y. Kentab, Nadeemuddin Qureshi)
What is Sialadenitis?

Acute bacterial sialadenitis in the adult most commonly affects either the parotid or submandibular gland.
It typically presents with acute swelling of the gland, increased pain and swelling with meals, and
tenderness and erythema of the duct opening. Pus often can be massaged from the duct.
Ductal obstruction, often by an inspissated (dried up) mucous plug, is followed by salivary stasis and
secondary infection. The most common organism recovered from purulent draining saliva is S aureus.
The causative organism is usually S aureus or Streptococcus, as well as gram negative and anaerobic
bacteria it is considered to be polymicobial in origin
o (Gram-negative bacilli include pigmented Prevotella, Porphyromonas, and Fusobacterium)
Careful examination reveals swelling over the angle of the mandible and the face
Sialadenitis often occurs in the setting of dehydration or in association with chronic illness. Underlying
Sjgren syndrome may contribute.
In the setting of acute illness, a severe and potentially life-threatening form of sialadenitis, sometimes
called suppurative sialadenitis, may develop
Treatment consists of intravenous antibiotics such as nafcillin (1 g intravenously every 46 hours) and
measures to increase salivary flow, including hydration, warm compresses, sialagogues (eg, lemon drops),
and massage of the gland.

Epidemiology

The incidence of community-acquired acute bacterial sialadenitis is unknown. However, 0.01% to 0.02%
of patients admitted to hospital and 0.02% to 0.04% of post-surgical patients develop this condition.
Chronic recurrent sialadenitis occurs 10 times more frequently in adults than in children, with an age
range of 40 to 60 years in adults and 4 months to 15 years in children.

2. Discuss the etiology, epidemiology, pathophysiology and treatment for sialolithiasis.

Sources:
o
o

Lalwani, Anil K.. Current diagnosis & treatment in otolaryngology head & neck surgery. 2nd ed.
New York: McGraw-Hill Medical, 2008. Print.
Tintinalli, Judith E., and J. Stephan Stapczynski. Tintinalli's emergency medicine: a comprehensive
study guide. 7th ed. New York: McGraw-Hill, 2011. Print.

Pathophysiology/Etiology
Saliva contains minerals aggregates of mineralized debris in the duct form sialoliths
These salivary duct stones contain primarily hydroxyapatite, calcium phosphate, and/or calcium carbonate.
These aggregates form a nidus, promoting calculi formation, salivary stasis, and eventually obstruction.
Recurrence of sialoliths is about 20%. Correcting risk factors can decrease recurrence rate.
Risk factors:
Long illnesses with DEHYDRATION
Gout
Diabetes
HTN
Xerostomia
If obstruction is not relieved, local inflammation, fibrosis, and acinar atrophy may ensue
Other complications include salivary stasis, acute infection (acute suppurative sialadenitis), and abscess
formation
Epidemiology
Men>women, 30-60 yrs old most common
Submandibular gland (Whartons duct) most commonly affected (80-90%) because of its more viscous
secretion, its longer, ascending course, and its higher content of calcium and phosphate. 10-20% are found in
the parotid and they are rarely found in the sublingual and minor salivary glands.
Clinical Features
Recurrent swelling and pain in the gland, exacerbated when eating. Swelling may subside after an hour
Prolonged obstruction can lead to acute infection and increasing pain and erythema of the gland
Pt may report occasional sand-like foreign bodies in the mouth
Radiographs may reveal radioopaque stones
Diagnosis
Diagnosis is clinical
A stone may be palpated within the duct or gland
A conservative course of tx shold precede imaging studies
Imaging studies include x-rays, sialography, and/or CT and MRI scans
Tx
Conservative tx: treatment with analgesics, antibiotics (if there is concurrent infection), massage, and
sialogogues such as lemon drops. Palpable stones in the distal duct may be digitally milked from the duct.
Ductal papilla can be dilated with ease. Graded lacrimal probes are used serially, and the stone is expressed.
If the stone is too large, a more invasive intraoral procudre is done under local or general anesthesia. The duct
is cannulated and an incision is made over the stone to allow extraction. No closure of the incision is made.
Symptomatic stones embedded in the body of the gland may necessitate surgical excision of the gland

3. Discuss the etiology, epidemiology, pathophysiology and treatment for parotid pleomorphic
adenoma. Discuss why treatment could lead to palsy.
Sources: Dr. Gordons Salivary Gland Pathology Lecture, eMedicine: Pleomorphic Adenoma
I. BACKGROUND
Also referred to as a benign mixed tumor
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Most common type of salivary gland tumor

Most common tumor of parotid gland
Three components:
o 1) An epithelial cell component
o 2) A myoepitheilial cell component
o 3) A stromal (mesenchymal) component
Pleomorphic = variable appearance seen by light microscopy
o Mixed epithelial (left) and mesenchymal cell components (right)

Carcinoma Ex Pleomorphic Adenoma

o Cancer may develop in 10-20% of pleomorphic adenomas if left untreated
o Sudden change of size, facial nerve involvement, ulceration and pain
o Usually an adenocarcinoma
o 5 year survival is 24% with treatment

II. ETIOLOGY
Unknown, but the incidence of this tumor has been found to increase 15-20 years after exposure to
radiation
Possibly Simian virus (SV40)
III. EPIDEMIOLOGY
Most common salivary gland tumor in both children and adults (45-75% of all salivary gland neoplasms)
Annual incidence: ~2-3.5 cases per 100,000 population
Occurs in individuals of all ages
o Most common in the third to sixth decades
o Average age at presentation is between 43 and 46 years
Seen more often in females than males (2:1 ratio)
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IV. PATHOPHYSIOLOGY
Epithelial elements may be arranged in duct-like structures, sheets, clumps and/or interlacing strands and
consist of polygonal, spindle or stellate-shaped cells (hence pleomorphism).
Areas of squamous metaplasia and epithelial pearls may be present.
The tumor is usually enveloped by a fibrous capsule of varying thickness and often incomplete.
The tumor often extends through these discontinuities but is not a sign of malignant transformation as it
does not invade surrounding tissues.
V. TREATMENT
The most common and effective treatment: complete surgical resection
Needle biopsy is highly recommended prior to surgery to confirm the diagnosis
Radiotherapy
o Physicians may feel that follow-up radiation treatment is necessary
o The National Institute of Health (NIH) does not recommend radiation therapy in all cases and
suggest that it is reserved for specific patients with surgical difficulties because radiation therapy
could increase the likelihood that any recurring tumors become malignant.
VI. ADVERSE OUTCOMES
The surgical risks involved in the removal of the tumor vary with the tumor itself.
o A smaller, more confined tumor will be easier to remove and therefore be less likely to cause
damage to the facial nerve located nearby.
o A tumor that extends to a wider area may carry heavier risk.
Bells Palsy
Facial paralysis due to Lyme disease, typhoid fever, trauma, temporal bone
fracture, tumors including acoustic neuroma and herpes virus
Nerve weakness could occur for up to four months after surgery, but this generally does not require any
therapy. Permanent nerve damage rarely occurs.
The possibility of infection exists with any surgical wounds, but can be treated with antibiotics.

4. Discuss the etiology, epidemiology and pathophysiology of gestational diabetes.

3-10% of pregnancies depending on population group studied

40-60% of women with GDM show no symptoms
For women who have had gestational diabetes there is a 40% chance of developing diabetes within 10
years after pregnancy.

What group is at the highest risk?

Obese mothers
Family history of Type II Diabetes
Maternal age >35y/o
Previous pregnancy with GDM
Polycystic Ovary Syndrome (common female endocrine disorder)
Ethnicity African American, Native American, Hispanic, Pacific Islanders, South Asia
Potential complications for offspring
Large for gestational age Macrosomia
Delivery complications C-section
Childhood obesity (future type II diabetes)
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Hypoglycemia
Jaundice
Still birth (mother has seizure)
Pre-eclampsia: characterized by high BP (>140/90) + protein in urine of pregnant women. Leads to
eclampsia seizure/coma.
Low birth weight due to management with diet and medication

Pathophysiology
Exact mechanism is not know.
Pregnancy hormone and other factors are thought to be related:
o Human placental lactogen (human chorionic somatomammotropin)
Hormone similar to growth hormone
Present only during pregnancy
Decreases maternal insulin sensitivity
Interferes with insulin receptor at cell signaling level
Cortisol
o Response to stress
o Gluccocorticoid increases blood glucose through gluconeogenesis
Others including: estradiol, prolactin, progesterone
Possible mechanisms include :
o Single Gene Mutation, Autoimmunity, Obesity and more which result in inappropriate insulin
balance.
Symptoms
Increased thirst
Increased Urination
Blurred Vision
Fatigue
Nausea
Vomiting
Bladder Infection/Yeast Infection
Treatment
Dietary intervention followed by insulin injection if diet alone does not work
Glipizide
sulfonylurea increase insulin production from B-cells in pancreas by binding to K-channels on B-cells: cells
cannot hyperpolarize-membrane becomes more+, leads to an influx of calciumincrease insulin secretion
Metformin
Decreases glucose production in liver & act as antagonist to glucagon.

Microbiology
5. Describe the polymicrobial nature of the etiology of acute bacterial sialadenitis in the parotid
gland.
Source: Oral and Maxillofacial Pathology Book + Dr. Ks Lecture on Salivary Glands

Most cases of acute bacterial sialadenitis are caused by Staphylcoccus aureus, but may also rise from
streptococci or other organisms, i.e., gram-negative and anaerobic bacteria
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According to Dr. K - Staph aureus (mixed): S. aureus colonizes around duct orifice
Treatment
o symptomatic supportive care, IVF hydration and antibiotics
o Augmentin, Unasyn, Cephalosporin
o Clindamycin, zithromax, biaxin (not erythromycin-high resistance)
o Not oxacillin or dicloxacillin (anti-staph, but high resistance)
o May need surgical incision and drainage

6. Discuss the rationale for culture and sensitivity analysis for Acute Bacterial Sialadenitis.
Source: Current Diagnosis & Treatment Ch.15, Dr. Flick Lecture, Dr. K Lecture
Acute Suppurative Parotid Sialadenitis
Seen with changes in fluid balance: elderly, debilitated, malnourished
Trauma, sepsis, surgery, fever
Usually bilateral (if unilateral, R>L)
Mean age = 60
Slightly more in males
Staph aureus (mixed): S. aureus colonizes around duct orifice
Clinical rapid onset of painful swelling; palpation shows no flow, with purulence
Start of with Empiric Antibiotic Use
Predictable bacterial etiology
Routine culture and sensitivity is not cost effective or beneficial
Use narrowest spectrum antibiotic, less disruption of GI flora, less resistance development
Least toxic and lowest side effects
Follow with Culture and Sensitivity when:
Rapidly progressive infection
Non-responsive infection
Recurrent Infection
Compromised Host Defenses
Treatment symptomatic supportive care, IVF hydration and antibiotics
Augmentin, Unasyn, Cephalosporin
Clindamycin, zithromax, biaxin (not erythromycin-high resistance)
Not oxacillin or dicloxacillin (anti-staph, but high resistance)
May need surgical incision and drainage
Antibiotics targeted against S aureus should be started immediately and continued for 710 days. Culture
testing and sensitivity may be necessary to rule out abscess formation or stone (sialolithiasis) in patients who
do not improve clinically after several days of appropriate therapy.

Pharmacology
7. Describe Furosemide according to the pharmacology template. How would Furosemide contribute
to Acute Bacterial Sialadenitis?

Furosemide

A sulfonamide-derived loop diuretic used in the management of edema associated with congestive heart
failure, cirrhosis, and renal disease
Pharmacodynamics
o Competes with Cl- for the Na/K/2Cl symporter in the ascending limb of the Loop of Henle, thus
inhibiting sodium and chloride re-uptake from the filtrate
Also increases excretion of Ca, Mg, bicarbonate, ammonium and phosphate
o Ion concentration increases in the filtrate and decreases in the renal medulla, resulting in less
water being resorbed via osmosis and resulting diuresis
o The renal vasodilation and net decrease in blood volume from diuresis result in decreased blood
pressure and help decrease tissue edema
Pharmacokinetics:
o Minimally metabolized in the liver
o 50-80% excreted unchanged in the urine w/in 24h, remaining via feces
Renal disease may increase the proportion cleared through the feces
Adverse effects
o Excess amounts of drug may result in fluid and electrolyte depletion
o Adrenal cortex may try to compensate for diuresis by releasing aldosterone which increases
sodium resorption and potassium and hydrogen excretion, may result in metabolic alkalosis
o Hyponatremia, hypokalemia, hypocalcemia, hypochloremia and hypomagnesemia must be
monitored for
Dental considerations:
o Diuretic properties may result in dehydration and a resulting decrease in salivary flow, which can
lead to sialadenitis via a retrograde bacterial infection
o No documented issues with local anesthetic administration

Periodontics
8. Discuss the etiology, epidemiology, pathophysiology and treatment for localized severe chronic
periodontitis
Source: Kacy Jos LI
Chronic periodontitis, formerly known as adult periodontitis or chronic adult periodontitis is the more
prevalent form of periodontitis.

Slowly progressing disease

However, in the presence of systemic or environmental factors that may modify the host response to
plaque accumulation (i.e. diabetes, smoking, or stress) disease progression may become more aggressive
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Most frequently observed in adults, however, it can occur in children and adolescents in response to
chronic plaque and calculus accumulation
Recently defined as an infectious disease resulting in inflammation within the supporting tissues of the
teeth, progressive attachment loss, and bone loss
Periodontal pocket formation is usually a sequel of the disease process, unless gingival recession
accompanies attachment loss, in which case pocket depths may remain shallow even in the presence of
ongoing attachment bone loss

Clinical featuresGeneral characteristics:

Supragingival and subgingival plaque accumulation that is frequently associated with calculus formation,
gingival inflammation, pocket formation, loss of periodontal attachment and loss of alveolar bone
Gingiva ordinarily is slightly to moderately swollen and exhibits alterations in color ranging from pale red
to magenta
Loss of gingival stippling and changes in the surface topography may include blunted or rolled gingival
margins and flattened or cratered papillae
In many patients, the changes in the color, contour, and consistency that are frequently associated with
gingival inflammation may not be visible on inspection, and inflammation may be detected only as
bleeding of the gingiva
Gingival bleeding, either spontaneous or in response to probing is frequently
Inflammation-related exudates of crevicular fluid and suppuration from the pocket also may be found
In some cases, probably as a result of long standing, low-grade inflammation, thickened, fibrotic marginal
tissues may obscure the underlying inflammatory changes
Pocket depths are variable; both horizontal & vertical bone loss can be found
Tooth mobility often appears in advanced cases when bone loss has been considerable
Diagnosis
Clinically diagnosed by the detection of chronic inflammatory changes in the marginal gingiva, presence
of periodontal pockets, and loss of clinical attachment
Radiographically diagnosed by evidence of bone loss
Findings may be similar to those seen in aggressive disease. A differential diagnosis is based on the age of
the patient, rate of disease progression over time, familial nature of aggressive disease, and relative
absence of local factors in aggressive disease compared with the presence of abundant plaque and
calculus in chronic periodontitis
Disease distribution
Chornic periodontitis is considered a site-specific disease. The clinical signs of CP namely inflammation, pocket
formation, attachment loss, and bone lossare considered to be due to the direct, site-specific effects of
subgingival plaque accumulation.
It may be described as being localized when few sites (<30%) demonstrates attachment and bone loss or
generalized when many sites (>30%) around the mouth are affected.
Disease severity

Mild: more than 1 to 2 mm of clinical attachment loss

Moderate: 3-4mm of clinical attachment loss
Severe: 5mm or more of clinical attachment loss

Epidemiology:
Estimate of 64.7 million adults have chronic periodontitis (moderate/mild > severe)
Adults aged 65 years and older, 64% had either moderate or severe periodontitis
Highest in men, Mexican Americans, adults with less than a high school education, adults below 100%
Federal Poverty Levels (FPL), and current smokers
Resources: Prevalence of Periodontitis in Adults in the United States: 2009 and 2010 from Journal of Dental
Research. www.jdr.sagepub/com
Etiology:
Periodontitis is considered to be a multifactorial disease in which the normal balance between microbial plaque
and host response is disrupted.
Local factors

Prior history of periodontitis need continuous monitoring and maintenance of periodontitis to prevent
a reoccurrence of disease
Plaque accumulation on tooth and gingival surfaces at the dentogingival junction (considered primary
initiating agent)
Increase in proportion of gram-negative organisms in subgingival plaque biofilm

Plaque accumulation is the primary initiating agent in periodontal destructionanything that facilitates plaques
accumulation or prevents plaque removal by oral hygiene procedures can be detrimental to the patient.
Plaque retentive factors
Important in the development and progression of CP because they retain plaque microorganisms in close
proximity to the periodontal tissues, providing an ecologic niche for plaque growth and maturation

Calculus is considered the most important plaque retentive factor retain and harbor plaque bacteria on
its rough surface
Subgingival and/or overhanging margins of restorations
Carious lesions that extend subgingivally
Furcations exposed by loss of attachment and bone
Crowded and malaligned teeth
Root grooves and concavities

Systemic factors
While the rate of progression of plaque-induced chronic periodontitis is generally slow, in a patient with a
systemic disease the rate of destruction may be significantly increased

Diabetes
Severe periodontitis has been observed in individuals with primary neutrophil disorders
agranulocytosis, neutropenia, Chediak-Higashi syndrome, and lazy leukocyte syndrome
More frequent and severe periodontitis has been observed in individuals who exhibit secondary
neutrophil impairment Down syndrome, Papillon-Lefevre syndrome, and inflammatory bowel disease
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Environmental & behavioral factors

Smokingmore attachment and bone loss, more furcation involvements, deeper pockets, more
supraginigval and less subgingival calculus, and less bleeding on probing
Emotional stress associated with necrotizing ulcerative disease and influence the extent and severity of
chronic periodontitis

Genetic factors

Frequently seen among family members and across different generations within a family, suggesting the
possibility of a genetic basis to the susceptibility to periodontal disease
Recent studies have demonstrated a familial aggregation of localized/generalized aggressive periodontitis
No clear genetic determinants have been described for patients with chronic periodontitis, a genetic
predisposition to more aggressive periodontal breakdown in response to plaque/calculus accumulation
may exist
o Recent data indicate that a genetic variation or polymorphism in the gene encoding interleukin 1alpha and interleukin 1-beta is associated with an increased susceptibility to a more aggressive
form of chronic periodontitis in subjects of Northern European origin
o Recent study suggested that patient with the IL-1 genotype increased the risk for tooth loss by 2.7
times; those who were heavy smokers and IL-1 genotype negative increased the risk for tooth loss
by 2.9 times; the combined effect of IL-1 genotype and smoking increased risk of tooth by 7.7
times

Pathophysiology

Increase in proportion of gram-negative organisms in subgingival plaque biofilm, with specific increases in
organisms known to be exceptionally pathogenic and virulent.
Bacteroides gingivalis, B. Forsythus, and Treponema denticola are frequently associated with ongoing
attachment and bone loss in chronic periodontitis
The mechanism by which attachment and bone loss occurs have not been clearly delineated, but these
bacteria may impart a local effect on the cells of the inflammatory response and the cells and tissues of
the host, resulting in a local, site-specific disease process.

Resources: Carranzas Clinical Periodontology, 9th Edition. Pg 398- 407

Probing depths vs. Attachment level

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9. Discuss the etiology, epidemiology, pathophysiology and treatment of pregnancy tumors

Source: Dr. Gordons PPT, Oral Pathology Book, PubMed, Dr. Ashrafis PPT
Epidemiology:

Between 0.5% and 5% of pregnant females develop pyogenic granulomas in the oral cavity
o 75% of oral pyogenic granulomas occur on the gingiva
o More common on the maxilla and interproximally
Pyogenic granulomas can occur at any age with a predilection for females and children, or young adults
Appears to be similar in all races

Etiology & Pathophysiology:

Unknown, but associated with trauma, hormonal influences, viral oncogenes or underlying microscopic
arteriovenous malformations
It is neither infected nor a granuloma
Originally thought to be caused by pyogenic organisms, thus the name
Reactive lesion due to local irritating factors
Traumatic agents include gingival and periodontal irritants such as plaque accumulation,
calculus, overhanging margins, implantation of foreign material etc.
Independent of their exact nature, the traumatic insults induce inflammation, followed by repair with
production of excessive granulation tissue
Highly vascular proliferation that resembles granulation tissue
Numerous small and larger endothelium-lined channels are formed that are engorged with red blood cells
and organized in lobular aggregates
Surface becomes ulcerated with mixed inflammatory cell infiltrates of neutrophils, plasma cells and
lymphocytes
Gradual rise in development of these lesions throughout pregnancy may be related to the increasing
levels of estrogen and progesterone as the pregnancy progresses
After pregnancy and the return of normal hormone levels, some of these pyogenic granulomas resolve
without treatment or undergo fibrous maturation and resemble a fibroma

Treatment Options:

No treatment
o Due to the risk of complications and higher recurrence rate during pregnancy, treatment should
be deferred with the exception of cases featuring excessive bleeding and ulceration, or marked
functional and esthetic problems
Surgical Excision
o Excision should include the removal of the base of the lesions, with extension down to
periosteum, and curettage
o Extraction of associated teeth is rarely necessary
LASER Therapy
o If surgery is necessary, it is preferably done after the second trimester
o LASER is used over surgical excision due to the high content of vascular tissue (control of bleeding)
All obtained specimen should be evaluated microscopically to confirm the diagnosis

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10. Explain how Scaling and Root Planing (SRP) can help control periodontal disease. Discuss why a
reevaluation should be done 4-6 weeks after the SRP is performed.
Source: Carranzas Clinical Periodontology

Primary objective of SRP is to restore gingival health by completely removing elements that provoke gingival
inflammation (i.e., biofilm, calculus, and endotoxin) from the tooth surface
Instrumentation has been shown to reduce dramatically the numbers of subgingival microorganisms
o Shift in composition of subgingival biofilm from one with high numbers of gram-negative anaerobes to
one dominated by gram-positive facultative bacteria compatible with health
When biofilm and calculus form on enamel, the deposits are usually superficially attached
o Scaling is sufficient to remove deposits from enamel, leaving a smooth, clean surface
Root surfaces frequently have biofilm and calculus deposits embedded in cemental irregularities
o Subgingival calculus is porous and harbors bacteria and should be removed completely
o Root surfaces exposed to biofilm are contaminated by toxic substances (i.e. endotoxins)
Scaling alone is insufficient ; portion of root surface must be removed to eliminate these deposits
o Where cementum is thin, dentin may be exposed; not intentionally, but may be unavoidable
Re-evaluation should be done 4-6 weeks after the SRP, following a period of soft tissue healing
o Need to wait for re-epithelialization of wounds otherwise bleeding on probing can be expected
o Re-evaluation at this point is to check on the progress and success of the SRP therapy
o Can decide at this point what further treatment is needed (i.e. perio maintenance, surgery etc.)

11. Define the ADA and AAP classifications.

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12. Compare and contrast the biofilm for a patient with a healthy periodontium versus a patient with
Chronic Periodontitis. How does the biofilm change after scaling and root planing? Why does it
change?
Source: Ashrafis Periodontal lectures and Carrazas Clinical Periodontology

Bacterial plaque is made primarily of gram-postive bacteria cocci and rods. Some bacteria are more prevalent
than others, those prevalent bacteria include: P.gingivitis, T. forsynthis, P. intermedia, F. nucleantumDuring the
later stages of plaque formation, the mass of plaque will be made up of mostly gram-negative bacteria.Primary
Colonizers: streptococci and actinomycetesSecondary Colonizers: P. intermedia, P. loescheii, Capnocytophaga
spp., F. nucleatum, Porphyromonas gingivalis
The shift in bacterial plaque goes as follows.

Gram positive to gram negative

From cocci to rods to spirochetes
Non motile to motile
Facultative anaerobes to obligated anaerobes.
Fermenting to proteolytic

During the process of scaling and root planing, calculus and bacterial plaque are removed from the crown and
root surfaces. This bacterial plaque includes both early and late colonizers(responsible for inflammation present in
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periodontitis). Because the early colonizers have been removed, the late colonizing gram negative bacteria cannot
return, therefore allowing the overall health of the gingiva to improve. However, if the early colonizing bacterial
are allowed to return as bacterial plaque, the late colonizers can once again be present in the gingival pocket, lead
to further development of chronic periodontitis.

13. List and describe at least 5 periodontal conditions that require referring a patient to a
periodontist.
Source: SGL Assignment 1 Answer Handout
1. Persistent probing depths with bleeding on probing - a pocket is a risk factor for further periodontal
destruction
2. Vertical defects and furcation involvement which will need regeneration procedures
3. Lack of keratinized and attached gingiva that is causing problems for the patient or for teeth that are
receiving crowns or will be abutments to partial dentures
4. Crown lengthening surgery
5. Implants
6. Ridge augmentation procedures
7. AxiUm D0170 re-eval limited problem focus:
a. Use after SRP to evaluate success of perio treatment and need for referral

Clinical
14. Describe the rationale for use of the intracoronal and extracoronal RPD attachment systems.

Sources: https://open.umich.edu/sites/default/files/1029/JShotwell-Week10.pdf, RPD manual, Dr. Organs

lecture

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Types:
Advantages:

Disadvantages:

Intracoronal
Engage vertical walls built into the crown
of the abutment tooth to create frictional
resistance to removal (internal or
precision attachments)
Hannes anchor
Interlock
Occlusal forces exerted upon the
abutment tooth are applied close to the
long axis of the tooth
Enhance appearance of the RPD
eliminate need for facial clasps
Not readily dislodged because it can only
be removed in one direction

Additional tooth reduction required

Increase cost of RPD
Necessitate having to remake the fixed
retainer when they wear out
When used with distal extensions, add
higher stresses to the abutment teeth
Not good for people with limited dexterity
Retention is reduced with wear of the
retentive surfaces
The size of these attachments limits their
use, especially in vital teeth or small teeth
Sufficient crown height must exist for
adequate length for a positive friction fit

Extracoronal
Utilizes mechanical resistance to
displacement by components on or
attached to the external surface of an
abutment tooth
Bredent
Ceka
Normal tooth contour can be maintained,
minimal tooth reduction necessary and the
possibility of devitalizing the tooth is
reduced.
Path of insertion is easier for patients with
limited dexterity
Enhance appearance of the RPD (esthetic
advantage)
Use this when it is not possible to create a
box prep that will totally incorporate the
female element into the crown
Increase cost of RPD
Necessitate having to remake the fixed
retainer when they wear out
When used with distal extensions, add
higher stresses to the abutment teeth
Make oral hygiene more difficult
Resin bonding retention is inadequate
improves the tissue response below the
attachment
unfavorable stresses on the abutment
teeth

15. Describe advantages and disadvantages of intracoronal RPD attachment systems.

Source: From Attachment Systems and Connectors for FPDs Dr. Organ
Intracoronal RPD Attachment systems
-

Advantage
o Occlusal forces exerted on the abutment tooth are applied close to the long axis of the tooth
Disadvantage
o Additional tooth reduction

16. Describe advantages and disadvantages of extracoronal RPD attachment systems.

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17. Describe partial veneer crowns (3/4 crown) preparation principles: axial reduction, occlusal
reduction, proximal groove placement, and occlusal offset.
Source: Dr. Organs Lecture
Axial reduction 3 axial walls are prepared; 1mm axial reduction; 2-5 degrees of taper/wall; chamfer finish line.
Occlusal reduction 1.5mm on centric cusp; 1.0 on noncentric cusp; minimal metal display on buccal (bevel over
buccal cusp).
Proximal grooves retention grooves are placed with 169L carbide bur; grooves must be placed into the tooth at
least to the full diameter of the bur. Should be parallel to the axis of tooth preparation in the bucco-lingual plane
and convergent toward that axis in the mesio-distal plane; occlusal portion of the groove should be located
directly across from the interproximal contact point. Recommended occluso-gingival height for a proximal groove
is 4mm; gingival floor of groove should be flat and well defined; gingival floor of the groove should be 0.5 mm
above the finish line.
There should be 90-degree angle between lingual walls of proximal grooves and the axial walls to resist lingual
displacement of restoration. Proximal flares buccal wall of the proximal groove should be flared to remove
unsupported tooth structure.
Occlusal offset V-shaped groove that extends from the proximal grooves along the buccal cusp; occlusal offset
groove is placed with inverted cone bur; provides additional bulk to ensure rigidity of the restoration.

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18. Describe advantages and disadvantages of partial veneer crowns (3/4 crown).
Advantage of Crown
Conservation of tooth structure
Reduced pulpal and periodontal insult
during prep
Access to supragingival margins is
rather easy and allows the operator to
perform selected finishing procedures
Better access for OH
Less gingival involvement than with
complete coverage
Better seating of the restoration due
to ease of luting agent escape
Better visibility to check for proper
seating and cementation
Remaining intact tooth permits EPT
testing

Disadvantage of Crown
Less retention and resistance
Difficult prep
Some metal is displayed (poorer
esthetics)

19. Describe the phases of the treatment plan when each step of the implant procedure for a Single
Tooth Implant would occur.

Surgical placement of implants occurs in Phase II of Treatment planning, while the restorative part occurs
in Phase III when all other crowns and FPD are delivered.
There are 3 steps to implant placement.
o Phase I Surgery- Placement and time to osteointegrate,
o Phase II Surgery- Assessment of osteointegration and healing abutment placed,
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Restorative Phase - Steps leading to restoration such as provisional, abutment selection and
prosthesis delivery.

20. Describe the importance of the ferrule effect for a tooth preparation. What is a potential adverse
outcome of an inadequate ferrule effect? How can the ferrule effect be improved for a tooth
preparation?
Source: Dr. Organs 2012 Fall_Restoration of Teeth with RCT_TP_BB.pdf. DAOB 322.
An adequate ferrule effect is necessary to provide sufficient support from occlusal load forces. If a ferrule effect is
not obtained, there will insufficient retention for a crown and the uneven distribution of occlusal forces can cause
a vertical fracture in the root.
Ferrule effect can be improved for a tooth preparation by ensuring that there is 1.5-2.0 mm of sound tooth
structure from the core margin to the finish line. The crown should envelop the remaining sound tooth structure
to properly protect the tooth from fracture (vertical) after being prepared for a crown.
Options for improving ferrule effect include:

Crown lengthening
o Must be performed after completion of RCT and provisional placement
Orthodontic extrusion/forced eruption
Alveoplasty
Placement of the finish line subgingivally

21. Describe the instructions that you would provide for the dental laboratory in your lab prescription
as to how you want #6 and #11 PFM crowns designed so that these crowns will reflect the design
of your planned RPD.

Make sure there are guide planes and rest seats on the crowns

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