Acknowledgements 12-2-2013

This study guide was first shared with me by Dr. Tom Becker May
27,2008.
The first update was done by Dr. Gary Matt and released March,
2010.
This again was updated/revised by Dr. Mike Morris about 1.5 yrs
ago. Dr. Matt Dietrich recently updated/revised it for the Fall
2013 Oral exams. This includes the regenerative section, which
was added by Dr. Julie Berkhoff.
I wish to thank all of these individuals for their willingness to
share with others this information.
Sincerely,
Dr. Keith V. Krell

ABE Oral Board Study Guide

Synopsis of Dr. Krells conference
call 9-19-13
1. Interpret the radiograph, describe what you see in the photo (buccal
space swelling left side).
2. Ask for additional/missing info: 1st Medical hx( "I would like to know
the pts med hx, and also ask for vital signs). Ask for the objective
exam (percussion,palpation,pulp vitality,perio probings). So 5
things: Med hx, vitals,dental hx, radiographs, objective exam
3. Medical hx: That is why we know the med hx from earlier, else you
can't answer this question. How would you change your treatment
based on the med hx? Would you pre-med, Consider med hx and
anesthesia, analgesics, abx.
4.They will ask you to make a dx. They could ask you about referred
pain.
5.Etiology to this case. Micro-bacteria responsible, he mentioned to
check Sedgley's review of micro from Phillie.
6.Pathogenesis: They make ask you what facial spaces are involved. Is
it more difficult to obtain anesthesia? He said you can basically quote
the "Ohio state group for any anesthesia question". He did say its
better to quote the primary author, but if you forget its better to say
something.
7.Treatments: How would you treat this case? Retx, place CaOH, see
the pt for 2 appts. Justify with evidence. They may say the pts leaving
the country tomorrow, what treatment would you do then?
8. Biologic considerations:e.g. How does anesthesia work? Sargentis
paste, what evidence would you use to refute the use of it?
9.Complications with procedure: this can be medical or dental.eg. Pt
loses consciousness, file separates, perforation? Med emergency,
activate EMS, call 911, CPR guidelines (KNOW)
10. Give prognosis: Retx success? compare with initial tx success.

Update: June 2013

2

Topic List:
1. Tooth Morphology
2. Radiographic Exam
3. CBCT and Endo
4. Subjective / Objective Exam
5. NS RCT
6. Procedural Errors
7. Emergency TX / Flare-ups
8. Infections
9. ReTX
10.
S RCT
11.
Trauma
12.
Anesthesia
13.
Endo-Perio
14.
Endo-Pedo
15.
Endo-Ortho
16.
Resorption
17.
Bleaching
18.
Materials
19.
Restoration
20.
Pulpal Pathosis
21.
Periapical Pathosis
22.
Anatomy
23.
Microbiology
24.
Inflammation
25.
Immunology
26.
Pain
27.
Pharmacology
28.
Prognosis / Outcomes
29.
Regenerative Endodontics

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TOOTH
Max. Central
Incisor
Max. Lateral Incisor

CANALS

CONFIGURATION
Type I: 100%

AUTHOR
Vertucci (Dye)

Dens in Dente: .04-10%

52% DB dilaceration

Hovland
Chohayeb

Max. Canine
Max. 1st Premolar

1 canal - 9% 8%
2 canals 85% 87%
3 canals 6% 5%

Apex: 26%
69%
5%

Carns & Skidmore

(resin casts)
Vertucci
Sieraski- T-trough
Tamse-furc groove P
aspect B root
Vertucci (Dye)

(2 roots 57% / 3 roots - 6%)

Max. 2nd Premolar

Max. Molars

1 canal 48%
2 canals 51%
3 canals 1%
MB2 located 1.8mm L MB2:
Hand inst.: 54%
Burs: 31%
Microscope: 10% (Total=95%)
77% 2 canals in MB root clinical
60%/35% overall, 66/40 (retx)
85% >10 deg curvature P root

At the Apex:
1 canal - 75%
2 canals 24%
3 canals 1%
MB2:
type I: 5%
type II: 49%
type III: 46%

Kulild & Peters

61% were type III

Neaverth

Clinical-5616 teeth (6
endodontists)

Wolcott
Bone & Moule
Yang & Yang

5% incidence of C shaped
(Chinese)
Mand. Incisors

2 canals: 41%

type I: 59%
type II: 40%
type III: 1%

Benjamin & Dawson

(radiographic study)

Mand. Canine

2 canals: 22%
30%/25%/22% - apex 3/2/6

type I: 78%
type II: 16%
type III: 6%

Vertucci (Dye)

70%/29.5%/0.5% - 74/25.5/0.5
apex

type I: 76%
type IV: 24%
(14% C-shaped)

Baisden, Kulild &

Weller
Vertucci

type I: 97.5%
type IV: 2.5% (2-3X Af.
Americans)

Vertucci (Dye)
Trope, Elfenbein &
Tronstad

M root:
type II: 40%
type III: 60%

Skidmore & Bjorndal

(resin casts)

Mand. 1st Premolar

Mand. 2nd Premolar

Mand. 1st Molar

Mand. 2nd Molar

2 canals: 7%
3 canals: 64%
4 canals: 29%

3 roots: 2%

Chinese pop. with 3 roots: 15%

1 canal: 1%
1 root: 4%
2 canals: 4%
3 canals: 81%
4 canals: 11%

M root:
type I: 4%
type II: 52%
type III: 40%

D root:
60%
40%

D root:
85%
9%
1%

2.7%/8% C-shaped

Pomeranz-12% middle
M, 2% type III
Walker
Weine (radiographic)

Weine / Cooke & Cox

type I continuous,
uninterrupted

Melton, Krell & Fuller

(Fan and Cheung)

type II semicolon
type III 2 or more distinct
canals
type IV-single round or oval

Morphology Overview

Discuss the types and incidence of lateral / accessory canals?

DeDeus 27% overall incidence; found most often in the apical area (63%
are in apical 3mm)
Lateral found in the main body of the root canal
Secondary extends from the main canal to the PDL in the apical region
Accessory from the secondary canal branching off to the PDL
What is the incidence of furcation canals?
Gutmann 28%
Burch and Hulen 76%
Discuss canal classification?
Weine: Type I one canal; Type II 2 canals, one foramen; Type III 2
canals, 2 foramina; Type IV 1 canal, 2 foramina
Vertucci: 1, 2-1, 1-2-1, 2, 1-2, 2-1-2, 1-2-1-2, 3
Who discussed the anatomy of the pulpal floor?
Vigouroux & Bossan discussed subpulpal grooves & dentinal cornice
Krasner & Rankow
Law of Centricity: pulpal floor is located in the tooth center at the CEJ level
Law of Concentricity: walls of the pulp chamber are concentric to external
surface
Law of CEJ: landmark pulp chamber location
Law of Symmetry: Except Max molars, orifi are equidistant & perpendicular
from M-D line drawn through center of pulpal floor;
Law of Color Change: pulpal floor is darker than walls
Law of Orifice Location: orifi are located at the junction of the floor and walls
Discuss the apical constriction?
Stein & Corcoran Width of the CEJ was avg. .189mm (size 20 file)
Dummer 4 types of apical constriction: single constriction 46%; tapering
30%; multiconstricted 19%; parallel 5%; 6% were completely blocked; 0.89
mm from apex
Kuttler-0.306 mm, 0.524 mm from apex (young 18-25 yro), 0.274 mm,
0.659mm older (>55 yro)
Discuss Abnomalities of the Teeth:
- Sabala: 60% of canal aberration are bilateral (the most rare ones are 90%
bilateral)
MICRODONTIA
TEETH SMALLER THAN THEY SHOULD BE
MACRODONTIA
TEETH LARGER THAN THEY SHOULD BE

GEMINATION
SINGLE ENAMEL ORGAN ATTEMPTS TO MAKE TWO TEETH
TWO CROWNS ONE ROOT
FUSION
JOINING OF TWO DEVELOPING TOOTH GERMS
MAY INVOLVE ENTIRE TOOTH OR JUST CEMENTUM AND DENTIN
ROOT CANALS MAY BE SEPARATE OR SHARED
MAY BE IMPOSSIBLE TO SEPARATE FUSION OF A NORMAL AND SUPERNUMERY
TOOTH FROM GEMENATION
CONCRESCENCE
FORM OF FUSION IN WHICH ADJACENT TEETH ARE JOINED BY CEMENTUM
MOST COMMONLY SEEN BETWEEN MAXILLARY 2ND AND 3RD MOLARS
DILACERATION
EXTRAORDINARY CURVING OR ANGULATGION OF TOOTH ROOTS
CAUSE RELATED TO TRAUMA DURING TOOTH DEVELOPMENT
DENS INVAGINATUS
AKA DENS IN DENTE OR TOOTH WITHIN A TOOTH
EXADURATION OR ACCENTUATION OF THE LINGUAL PIT
MOST COMMON IN MAX LATERAL INCISSORS
Oehlers-Type I-confined within crn, Type II-blind sac invades root (may
communicate with pulp), Type III-penetrates thru the root and bursts apically or
laterally.
DENS EVAGINATUS
COMMON DEVELOPMENTAL CONDITION AFFECTING PREDOMINANTLY PREMOLAR
TEETH
ALMOST EXCLUSIVELY OF THE MONGOLOID RACE
FREQUENTLY BILATERAL
ANOMALOUS TUBERCLE OR CUSP LOCATED IN THE CENTER OF THE OCCLUSAL
SURFACE
Oehlers-recommended DPC (30% of tubercles not have pulp horns)
Levitan-tx recommendations: Normal pulp (mature and immature teeth/apex)reduce opposing occl, flowable cmpst to tubercle; Inflamed pulp: Mature-RCT,
restore; Immature: MTA potomy; Necrotic pulp: Mature-RCT, restore; ImmatureImmediate MTA apexification or Revascularization (Banchs & Trope)
Yip-2.2% incidence, 3.6% Chinese (PMs only-84% man, 16% max); 90% bilateral;
26% pulpally involved
TAURODONTISM
TEETH THAT HAVE ELONGATED CROWNS OR APICALLY DISPLACED FURCATIONS
PULP CHAMBERS HAVE INCREASED APICAL-OCCLUSAL HEIGHT
ASSOCIATED WITH SYNDROMES SUCH AS DOWN AND KLINEFELTERS
HIGH PREVELANCE IN ESKIMOS AND 11% IN MIDDLE EAST
SUBERNUMERARY ROOTS
ACCESSORY ROOTS MOST COMMONLY SEEN IN MANDIBULAR CANINES,
PREMOLARS AND MOLARS

ENAMEL PEARLS
DROPLETS OF ECTOPIC ENAMEL
COMMONLY SEEN IN THE BIFURCATION OR TRIFURCATION AREA OF TEETH
MAX MOLARS MOR COMMON
ANODONTIA
ABSENCE OF TEETH
MOST COMMON ARE 3RD MOLARS THEN MAX LAT INCISSORS AND SECOND
PREMOLARS
COMPLETE ANODONTIA ASSOCIATED WITH ECTODERMAL DYSPLASIA- X-LINKED
RECESSIVE DISORDER
SUPERNUMERARY
EXTRA TEETH
ASSOCIATED WITH GARDNERS SYNDROME AND CLEIDOCRANIAL DYSPLASIA
THE ANTERIOR MIDLINE OF THE MAXILLA IS THE MOST COMMON SITE FOLLOWED
BY MAXILLARY MOLAR AREA
AMELOGENESIS IMPERFECTA
HERIDITARY DISORDER OF ENAMEL FORMATION IN BOTH DENTITIONS
1. HYPOPLASTIC INSUFFICIENT AMOUNT OF ENAMEL
2. HYPOCALCIFIED QUANTITY OF ENAMEL IS NORMAL BUT SOFT AND FRIABLE
3. HYPOMATURATION
COLOR RANGE FROM WHITE OPAQUE TO YELLOW TO BROWN
RADIOGRAPHICALLY DENTIN THIN ROOTS NORMAL
DEFECTS OF DENTIN
DENTINOGENESIS IMPERFECTA (HEREDITARY) OPALESCENT DENTIN
AUTOSOMAL DOMINANT
1. TYPE 1 OCCURS IN PATIENTS WITH OSTEOGENESIS IMPERFECTA
2. TYPE 2 PATIENTS HAVE ONLY DENTAL ABNORMALITIES NO BONE DISEASE
3. TYPE 3 OR BRANDYWINE TYPE SIMILAR TO TYPE 2 BUT INCLUDE FEATURES
SUCH AS MULTIPLE PULP EXPOSURES AND PERIAPICAL RADIOLUCIENCIES
(Shell teeth w enlarged pulp chambers)

CLINICALLY ALL THREE TYPES SHARE NUMEROUS FEATURES

1. TEETH EXHIBIT AN UNUSUAL TRANSLUCENT, OPALESCENT APPEARANCE
2. COLOR RANGES FROM YELLOW BROWN TO GRAY
3. ENAMEL NORMAL BUT FRACTURES EASILY
4. ABNORMAL MORPHOLOGY TEETH TULIP OR BELL SHAPED DUE TO
CONSTRICTION OF CEJ
5. ROOTS ARE SHORT AND BLUNTED

RADIOGRAPHICALLY
1. TYPES 1 AND 2 PULP SPACE OPACIFIED
2. TYPE 3 PULP CHAMBERS AND ROOT CANALS EXTREMELY LARGE

DENTIN DYSPLASIA

AUTOSOMAL DOMINANT TRAIT

TYPE 1 RADICULAR
1. CROWNS NORMAL
2. TEETH SHOW GREATER RESISTANCE TO CARIES
3. ROOTS EXTREMELY SHORT
4. PULPS OBLITERATED
5. PERIAPICAL LEUCENCIES

TYPE 2 CORONAL
1. CROWNS NORMAL
2. PULPS LARGE (THISLE TUBE)
3. ROOTS EXTREMELY SHORT

Radiographic Exam Overview

Can a PARL be seen with irreversible pulpitis?
Yes Yamasaki Rat study demonstrating PARL prior to pulp necrosis
Jordon, Suzuki & Skinner PARL with IP; 11/24 healed with IDPC
Bergenholtz- 16% of vital teeth had lesions (nerves more resistant to
necrosis)
Lin-structurally intact & functioning nerve fibers found in teeth with PA
lesions
Abella- CBCT detected addl 10% (13 vs 3) of PA lesion in IP teeth, Sig more AP
lesions in sym vs asym IP
How much bone loss before a PARL is noted radiographically?
Bender Avg 7.1% MBL & at least 12.5% CBL; lesion must penetrate endosteum
Lee & Messer Lesions in cancellous bone detected if lamina dura is affected
What radiographic features are important when evaluating PA pathology?
Kaffe & Gratt continuity & shape of lamina dura; width & shape of PDL
Strindberg-PDL width and contours nml, lamina dura intact
How many films should be taken for diagnosis?
Brynolf 73% accurate with 1 film; 87% accuracy with 3 films
How accurate is our radiographic assessment?
Goldman, Pearson & Darzenta - 6 examiners agreed 47%; 6-8mo later they
agreed approx. 80% with their first interpretation
Tewary: with digital found similar numbers; 25% inter-observer and 68% intraobserver agreement
What is the most accurate technique?
Forsberg paralleling is more accurate in length determination vs. bisecting angle
What type of conventional film (speed) is the most diagnostic?
Eleazer & Farman NSD in WL measurements or image preference
Compare conventional radiography to digital:
Evaluating for PARL

Mistak & Loushine NSD between digital, transmitted digital & conventional
radiography for PARL identification
Folk NSD between shick (cmos) & trophy RVG ui (ccd)
Nair conv. film displayed the highest % of PARL detection (vs. ccd & storage
phos.)
Arkdeniz-enhanced digital superior than original digital, E or F speed film
Comparing WL measurements
Lamus & Katz NSD between shick & conv.
Goodell & McClanahan Kodak > schick or conv. for size 10 & 15 files
Lozano Conv. was more precise with any size file (digital ok with size 15 file)
How much radiation reduction is there between digital and conventional
radiography?
Soh Used only 22% of radiation dose compared to conv. film
White/Pharoah oral radiology text- 75% reduction

CBCT and Endodontics overview

Is 3-D imaging better than conventional radiography?
Patel improved detection of PA lesions with CBCT (28% more lesions vs digital
xray)
Bornstein sinus membrane was sig thicker near roots with AP vs w/out AP
Maillet- 50% sinusitis associate with AP lesion? check on data
Abella- CBCT detected addl 10% (13 vs 3) of PA lesion in IP teeth, Sig more AP
lesions in sym vs asym IP
What uses does CBCT have in endo?
Cotton & Schindler: Endo appications: 1) Dx endo path, 2) assess pathosis of
non-endo origin, 3) root fx, 4) Resorption, 5) pre-surgical planning. Cons: 1) incr
radiation, 2) cost, 3) availability, 4) medico-legal
What is the approximate equivalent dosage to conventional digital PA xrays?
Patel- NSD in 180 vs 360 scans using Acciutomo 3D in detecting artificial AP lesions
& less radiation
Ludlow Small FOV unit scans (Accuitomo/Kodak) equivalent to about 3 digital PAs
Can CBCTs reliability detect root fx better than conventional PA?
Hassan- axial slice is best view to diagnosis
Ozuk- Accuitomo 93% accurate in identifying VRFs, confirmed via retx or surg

Edlund- clinical study on limited CBCT and VRFs, CBCT has relatively high
accuracy in detecting
Costa- presence of metallic post sig inhibits accuracy of fx diagnosis w/
CBCT (beam hardening

Subjective / Objective Overview

9

Can pts. determine which tooth hurts?

Friend & Glenwright - No, only 37% accurate; usually tooth to either side; 3.4%
referral to opposite jaw; 1.5% referral across midline
Mumford-142 pts with pain, NO correlation betw histology and clinical symptoms
Seltzer no correlation b/w clinical signs/symptoms and histo status of pulp
McCarthy/McClanahan- pt w/o PA symptoms 30% can identify tooth; w PA symp
-89% can identify
Discuss cold testing? (Endo Ice -15 deg F, CO2 Snow -119 deg F)
Trowbridge & Franks response sooner than temp change @ PDJ supports
Branstom
Walton / Miller response quicker with endo ice on #2 pellet; use with crowns
Jones use large cotton pellet; spray better than dip technique
Cooley-nml: respond w/i 5-8 secs, returns w/i 15 secs; Reversible: immed, sharp,
subsides w/i 15 secs; Irreversible-severe, long-lasting > 1min
Who discussed heat testing?
Cooley hot water test
Does temp testing harm the tooth?
Peters CO2 does not harm the enamel
Rickoff & Trowbridge heated GP or CO2 showed no pulpal injury if used for
clinically relevant duration
Discuss EPT?
Nahri stimulates A-beta and A-delta fibers; not C-fibers
Abdel Wahab & Kennedy slow increase in current 2uA/sec
Mumford no relationship with value and pulp pathology; density important: incr
surface area requires incr current to produce sensation (all or none response)
Where do you place the probe tip?
Bender incisal-edge of incisors (or incisal 1/3)
Jacobson occlusal two-thirds of the buccal surfaces of max incisors and premolars
Is EPT safe on pts. with pacemakers?
Yes Baumgartner
Wilson-apex locators and EPT not interfere with cardiac pacemakers or
defibrillators
Can you tell the histologic dx from clinical test?
Seltzer & Bender No, only correlation exists, but not extent of pathology
How reliable are our pulp tests?
Petersson & Soderstrom overall accuracy: Cold 86%, EPT 81%, Heat 71%
probability the neg.=necrosis: cold 89%; EPT 88%; hot 48%
probability the pos.=vital: cold 90%; EPT 84%; hot 83%
Fulling & Andreasen cold test are more reliable in kids
Texiera- use both cold and EPT to incr accuracy
Do any other pulp tests have potential?
Ingolfsson & Tronstad Laser dolpler flowmetry is more accurate than EPT
Wilcox & Johnson pulse oximetry
What causes pain while flying / diving?

10

Ferjentsik Barodontalgia - Navy study found 86% with faulty restorations

Senia inflamed vital pulp tissue major cause
Kollman 0.26% incidence in German soldiers

American Board of Endodontics Pulpal & Periapical Diagnostic

Terminology:
PULPAL:
Normal pulp A clinical diagnostic category in which the pulp is symptom free and
normally responsive to vitality testing.
Reversible pulpitis A clinical diagnosis based upon subjective and objective
findings indicating that the inflammation should resolve and the pulp return to
normal.
Irreversible pulpitis A clinical diagnosis based on subjective and objective
findings indicating that the vital inflamed pulp is incapable of healing.
Additional descriptions:
Symptomatic Lingering thermal pain, spontaneous pain, referred pain
Asymptomatic No clinical symptoms but inflammation produced by caries,
caries excavation, trauma, etc.
Pulp necrosis A clinical diagnostic category indicating death of the dental pulp.
The pulp is non-responsive to vitality testing.
Previously Treated A clinical diagnostic category indicating that the tooth has
been endodontically treated and the canals are obturated with various filling
materials, other that intracanal medicaments.
Previously Initiated Therapy A clinical diagnostic category indicating that the
tooth has been previously treated by partial endodontic therapy (e.g. pulpotomy,
pulpectomy).
APICAL (PERIAPICAL):
Normal apical tissues Teeth with normal periradicular tissues that will not be
abnormally sensitive to percussion or palpation testing. The lamina dura
surrounding the root is intact and the periodontal ligament space is uniform.
Symptomatic apical periodontitis Inflammation, usually of the apical
periodontium, producing clinical symptoms including painful response to biting and
percussion. It may or may not be associated with an apical radiolucent area.
Asymptomatic apical periodontitis Inflammation and destruction of apical
periodontium that is of pulpal origin, appears as an apical radiolucent area and does
not produce clinical symptoms.
Acute apical abscess An inflammatory reaction to pulpal infection and necrosis
characterized by rapid onset, spontaneous pain, tenderness of the tooth to
pressure, pus formation and swelling of associated tissues.

11

Chronic apical abscess An inflammatory reaction to pulpal infection and

necrosis characterized by gradual onset, little or no discomfort and the intermittent
discharge of pus through an associated sinus tract.

NS RCT Overview
Apex Locators
Who was instrumental in developing the apex locator / Root ZX?
Suzuki electrical resistance between periodontium & oral mucous membrane was
6500 ohms in dogs
Sunada found same results in human (basis for resistance type EALs)
Kobayashi developed the Root ZX base on a ratio of impedance at 8 and .4 kHz
frequencies
How accurate is the Root ZX?
Shabahang 96.2% +/- .5mm of the apical foramen, 65% exact apex
Welk and Marshall-91% accurate locating minor constriction
Does the pulp status affect EAL readings?
Dunlap NSD between vital and necrotic pulps
Does the irrigant solution affect the reading?
Jenkins No; NSD in function with 7 irrigants tested
Does apical resorption or an open apex affect the reading?
Goldberg accurate with resorption
Katz preferable method to determine WL in primary dentition
Are EALs safe for use in pts with pacemakers?
Garofalo & Dorn In vitro Root ZX safe Bingo caused interference
Baumgartner In vivo study found EALs and EPTs safe in 27 pts
Wilson-apex locators and EPT not interfere with cardiac pacemakers or
defibrillators
Canal Preparation
Why is the ideal working length .5 1mm short of the apex
Burch and Hulen avg. .59mm from occlusal aspect of maj diameter to apex
Kuttler - .525mm (18-25yr olds) - .659mm (.55yr olds) from major to minor
diameter
Discuss historical preparation techniques?
Coffae and Brilliant Serial step back
Torabinejad Passive Step back
Marshall Crown Down Pressureless
Abou Ross Anticurvature Filing
Roane Balanced Force
Goerig-Crown down
Do you preflare the canal and why?
Stabholz better tactile sense of the apical constriction (WL); more accurate
obturation length

12

Ibarrola preflaring allowed more consistent EAL readings (allowed access to

apical foramen)
Roland - .04 taper NiTi files were far less likely to separate in preflared canals
Can patency filing cause problems?
Goldberg cause apical transportation (61% #25, 25% #10) use small files
Why do you create a guide path?
Peters No Protaper instrument fractured is guide path was created
What are the advantages of the balanced force technique?
Wu & Wesselink produced cleaner apical portion of canals vs other hand techn.
McKendry extruded less debris
Sepic less apical canal alteration in curved canals vs step back techn.
Southard- up to size 40 able to maintain canal curve 80% of time
Why would you choose to use NiTi rotary files over SS hand files?
Short, Baumgartner NiTi rotaries were faster and stayed more centered
What are the properties of NiTi files?
Haikel 55% Nickel / 45% Titanium; 2 phases: Austentite & Martensite cycling
between the two phases allows for superelasticity and shape memory; radius of
curvature is most important factor for cyclic fatigue, causing failure
Do NiTi files remove more bacteria?
Trope Not any more effected than SS hand files
Peters all type of NiTi rotaries left 35% or more of canal surface area unchanged
At what speed should NiTi rotaries be run at?
Gabel & Hoen Profiles at 333 rpm separated 4x more often as files at 167 rpm
Gambarini recommended electric low torque or right torque motors
K3 and ProTaper 300 rpms
How many times can NiTi files be used
Yared Up to 10 canals (2-3 cases)
Does sterilization affect NiTi files
Hicks 10 cycles through heat sterilization did not increase chance of fracture
Mize-sterilization not affect # of cycles to failure of rotary NiTi files
Irrigation
How large should the apical preparation be for irrigation?
Ram size 40
Brunson 40/04 best; #35 to #40 = 44% incr of irrigant at apex; #40 to #45:
4%; .02 to .04 taper: 74%, .04 to .06: 5%
Card/Trope: larger apical prep size showed incr reduction in CFU counts
What makes sodium hypochlorite antibacterial?
Hurst pH 11; hypochlorus acid is the active antibacterial property of sodium
hypochlorite; disrupts oxidative phosphorylation and other membrane activities
Why use full strength sodium hypochlorite?
Dissolves tissue, bactericidal, bleaching agt, lubricant, deodorizer, inexpensive

13

Hand, Smith & Harrison dilution of 5.25% significantly decreases the ability to
dissolve necrotic tissue
Siqueira Increased concentration (4%) most effective against gram anaerobes
and facultative anaerobes
Harrison & Baumgartner 5.25% is safe for clinical use and does not increase
postop pain
Carpio-Perenchena- full strength NaOCl able to dissolve imm. biofilm sig faster
than if diluted (in vitro)
When should chlorhexidine be considered as an irrigant?
Jeansonne 2% chlorhexidine & 5.25% NaOCl showed NSD in antibacterial activity;
CHX does not dissolve tissue; Consider with NaOCl allergies, perfs and open apicies
Haapasalo CHX activity is reduced by dentine
Dametto & Gomes- 2% CHX better than 5.25% NaOCl in reducing CFU of E.
faecalis for 7 days
Ng and Gulabivala Never use, in prospective study of factors = success, non-use
of CHX adjunct = more success
What about MTAD?
Torabinejad Doxycycline, citric acid & Tween-80; use with NaOCl and
recommended for smear layer removal did not cause dentinal erosion seen with
EDTA; kills E. faecalis more effectively than NaOCl
Who discussed smear layer removal?
McComb & Smith 1st to describe; used NaOCl & REDTA
Sen made up of organic & inorganic debris (pulp, bacteria and byproducts)
Baumgartner, Mader & Peters 2 layers: 1-2 microns thin layer on canal wall; up
to 40 microns in tubules
Yamada-17% EDTA followed by NaOCl
Should the smear layer be removed?
Torabinejad Yes - in infected cases it allows more thorough disinfection of canal &
tubules; allows better adaptation of obturation material (Foster-allow CaOH, Salehallow sealer)
Jeansonne less coronal leakage with smear layer removal (AH 26)
Walton & Drake No blocks bacterial entry into tubules
Ng and Gulabivala Yes- in prospective study removal of smear layer = more
success
How do you remove the smear layer?
Calt - > 1min EDTA caused excessive peritubular and intertubular erosin
Crumpton & McClanahan 1mL 17 % EDTA for 1 min, followed by 3mL NaOCl
Yamada-17% EDTA followed by NaOCl
What is EDTA & how does it work?
Ethylendiamine tetraacetic acid Chelating agent collects Ca ions in dentin
making it softer; removes inorgranic portion of smear layer; no antibacterial effect
Schilder self limiting after 7hrs
Ultrasonics
How do ultrasonics work?
Ahmad, Pitt Ford & Crum acoustic streaming & not cavitation

14

Do ultrasonic remove more bacteria?

Sjogren & Sundqvist ultrasonics were better than hand instrumentation
Cunningham and Martin-combo US and high vol irrigation better than traditional
methods
Are ultrasonics effective in cleaning canals?
Jensen & Hutter 3min passive sonic or ultrasonic following hand
instrumentation produced cleaner canals
Gutarts US = cleaner canals and isthmuses than after hand/rotary
instrumentation alone
Haidet- US improved canal debridement at 1 mm level and isthmuses
Klyn NSD if get needle deep irrigation (w/in 1 mm of WL)
Intracanal Medicaments
Discuss Calcium hydroxide and how it works?
Hermann introduced
Siqueira Hydroxyl ions create free radicals destroying components of bacteria
cell membranes.
Free radicals (hydroxyl ions) react with bacterial DNA inhibiting DNA replication
and cell activity.
Increased pH (12.5) alters enzyme activity disrupting cellular metabolism and
structural proteins.
Ca(OH)2 effective when in direct contact with bacteria which may not always be
possible such as bacteria located in dentinal tubules or in the center of bacterial
colonies. pH in tubules is increased, but only up to 8-11 (Tronstad).
Certain bacteria such as enterococci tolerate high pH levels of 9-11.
Vehicle used to deliver Ca(OH)2 must not alter the pH significantly.
Safavi & Nichols inactivates LPS in vitro (also Buck)
How long do you keep Ca(OH)2 in the canal?
Sjogren & Sundqvist 7 day dressing eliminated bacteria that survived
instrumentation
Bystrom- C&S: 20%-40% reduction in bacteria, C&S + 0.5% NaOCl 40-60%, + 24
hrs CaOH 90%, 7 days CaOH almost 100% (also Shuping)
Nerwich, Figdor & Messer 2-3wks before increase in outer root dentin pH (9.3)
Andreasen use < 1mo (sheep teeth)
Doyon-no change in fx resistance of human teeth at 30 days, at 180 days =
decreases strength
Sathorn- Sys Rev saying at least 7 days
How do you place Ca(OH)2 in the canal?
Sigurdsson & Madison lentulo>injection>K-file
Deveaux-paste inject or lentulo improved placement
Estrella-CaOH not effective unless touch canal walls (also Chamberlain)
How do you remove Ca(OH)2 from the canal?
Tasdemir ultrasonics with NaOCl better than needle with EDTA/NaOCl (none
completely removed)
Calt & Serper- NaOCl and EDTA to remove CaOH
Margelos- CaOH in presence of Roth sealer makes it set immediately lead to poor
apical seal
Obturation
Discuss the hollow tube theory?

15

Richert & Dixon introduced; inserted metal needles in CT of rabbits; canal must
filled to the end to prevent outward diffusion of circulatory elements which cause
inflammation; body not like empty spaces; circulatory elements seeped into tube,
stagnated and broke down and released toxins causing inflammation
Torneck sterile empty polyethylene tubes healed in rat ct disputes HTT
Goldman no evidence of inflammation at the open ends of Teflon rods implanted
in guinea pigs disputes HTT
Wenger Polyethylene tubes sealed 1mm short with GP/Grossmans cement
elicited little or no inflammation in rat bone disputes HTT
What is gutta percha made of and what are its properties?
Friedman 65% Zinc oxide; 20% GP; 10% metal sulfates (radiopacity); 5% waxes
and resins
Schilder GP exists in beta-semicrystalline state; undergoes change to alpha
phase upon heating (42-29 C); compactable not compressable
Sorin-heating GP and quenching restores to Beta form (rejuvinate)
Is latex allergy a concern for gutta percha? Is it biocompatible?
Trans-isomer of polyisoprene (rubber)
Costa & Johnson no cross reactivity but slight concern with gutta balata additive
Nair large pieces were encapsulated and free of inflammation; fine particles
evoked inflammatory reponse (macrophages and multi-nucleated giant cells)
How do you sterilize gutta percha points?
Senia 1min immersion in 5.25% sodium hypochlorite
Ludlow-1 sec exposure to NaOCl
How do you place sealer?
Wilcox NSD found between file, lentulo, ultrasonics or coated MC
Hall- NSD in method (file, lentulo, MC) after obturation (none exceeded 62%
coverage)
Does extrude material cause problems?
Augsburger & Peters did not prevent healing; removed over 6 yr period
Baumgartner - extruded GP or sealer was associated with postop pain (teeth w/o
lesions)
What type of spreader should be used for lateral compaction? How far should it
penetrate?
Joyce NiTi induce less stress and decrease risk of VRF
Allison & Walton less leakage with deep spreader penetration (within 1-2mm)
Berry- NiTi spreader penetrated sig greater depth than SS in curved canals
Dang & Walton- D11 more damage than finger spreader
Discuss the custom cone technique?
Keane 1 sec dip gave best adaptation and less leakage; less chloroform = less
leakage
Knapp & Marshall- Master apical impression technique, use cone a couple sizes
larger
Compare lateral compaction and warm vertical technique?
Baumgartner NSD in bacterial leakage (continuous wave vs cold lat)
Reader NSD in fill quality; more lateral canals obturated with warm techniques
Wong- warm vertical placed larger mass of GP into canal than lat con

16

Peng SR w/ M/A of lat con vs Warm vert, NSD in post op pain, obt quality or
success
Can warm techniques damage the periodontium?
Eriksson & Albrektsson - > 10 deg C is threshold level for bony necrosis
Sweatman & Baumgartner System B, obtura and ultrasonic delivery of GP < 10
deg change at external root surface
Romero- System B at 200C only produced 1C incr on ext root surface at apex and
2 at 5mm from apex
Does the Thermafil system work well?
Lee- Thermafils with out GP leaked most vs all other materials
Walton Thermafil leaked most possibly due to stripping of GP off carrier; at 1 mm
from apex only 5% were completely covered with GP complete encasement of
carrier over entire canal was never seen
Is Resilon a better obturation material?
Trope teeth were more resistant to fx
Pashley NSD in leakage compared to GP/AH plus
Cotton- NSD in clinical trial between GP and Resilon
Is there a problem with Sargenti Paste?
Newton demonstrated 6m & 1 yr cytotoxicity; contains paraformaldehyde; leads
to destruction of tissues, intractable pain and parastesia of nerves
What about quality of SimpliFil?
Shipper and Trope- best w respect to bacterial leakage (Warm vert, lat con)

Procedural Errors Overview

How are perforations classified?
Fuss & Trope Old or Fresh (better prognosis); Large or small (<size 20=good
prognosis); Cervical (unfavorable), Coronal/middle (fair), Apical (favorable)
--Time, size and location
How can they be detected?
Fuss apex locators
Also: radiographs, blood on paper points, microscope, perio probings
What criteria are important for successful management?
Time, size & location
Pitt Ford and Torabinejad immediate repair better than delayed (MTA)
Benenati delay ok if aseptic (only article)
Sinai- time, size, location, and accessibility
Fuss and Trope-location of perforation most important level of crestal bone and
epith attachment
How would you manage a perforation?
If larger, consider an internal matrix as proposed by Lemon: (used HA)
Rosenberg Collacote
Alhadainey Calcium sulfate (Capset); Vitrebond
Frank Ca(OH)2
Also: hydroxyapatite, DFDBA, Gelfoam, Calcium phosphate

17

Repair with MTA as proposed by Main & Torabinejad (no matrix required) 16/16
success X1 yr; Biocompatible and caused cementum formation; less leakage than
amal & IRM
Nakata & Baumgartner less bacterial leakage than amal
Daoudi less dye leakage than Vitrebond
Whats the prognosis of perforation repairs?
Harris 88% with Cavit
Main- 100% success with MTA
Mente 86% at aver 3 yr recall, perfs bigger than 3mm had less success
Whats the incidence of separated instruments & does it affect prognosis?
Crump & Natkin NSD in failure rate; 53 match pairs, success depends on location
and amt of debridement prior to separation
Spilli and Messer- 3-5% incidence; NSD in success (pre-op lesion only factor: 98%
vs 86%); 146 pairs
Sathorn/Messer did Sys Review which contained only these studies
How would you manage a separated instrument?
Attempt removal, bypass or obturate to fx; platforming (Iqbal)
Ruddle staging platform with modified gates; ultrasonic with SOM; IRS
Other methods: Endo extractor tubs with cyanoacrylate; braiding headstroms; wire
loop and tube
Alomairy-80% success with ultrasonics, 60% success with IRS (NSD in time-40min)
Suter-87% of separated instruments were removed successfully (41% were in
apical third)
Souter-files removed in apical and middle thirds weakened teeth; if can see/not
beyond curveremove
How do you manage a sodium hypochlorite accident?
Signs: immediate severe pain, sig swelling, bleeding in canals instantly, hematoma,
tissue necrosis
Gluskin long acting LA, irrigation w saline to dilute, Amox, analgesics, steroids,
cold compresses/recalls
Kleier diplomate survey did not affect prognosis; women > men, necrotic with
PARL more common
Sabala: 1) reassure pt, 2) pain control-LA blk and analgesics, 3) saline irrigation, 4)
Abx, 5) cold compresses 4-6h, then warm, 6) Medrol dose pack

Emergency / Flare-up Overview

What is the incidence of a Flare-up and are there any predictable indicators?
Walton 3%; Female 2X more than males; Pre-op pain or swelling, necrosis before
initial apt, painful AP, pts on analgesics, large PARL are at greater risk; overall
3.17%, necrotic 6.5%, vital 1.3%
Torabinejad Pre-op pain was an excellent predictor; Females age 40-59; no or
small PA lesions, man PM or anteriors, pts w/ allergies, retreatments, increased the
frequency of interappointment emergency
Tsesis- meta-analysis: 8.4%
What causes flare-ups?
Seltzer & Naidorf Overinstrumentation, overmedication, extruded debris,
incomplete pulp removal, over-irrigation, hyperocclusion, root fx, or another tooth

18

Walton- immunological response, secondary intraradicular infection, physical tissue

damage
Siqueria- extruded infec debris, changes in microbiota, 2 intraradicular infection,
incr in redox potential
Is it okay to leave tooth open for drainage?
Weine-increased exacerbations and more appts needed to tx
Torres-increased concentration of secretory IgA; triggers alternate pathway of
complement
Is it ok to close a tooth previously left open?
August only minimal flare-ups seen 5% (Weine initially said if you file, dont
close)
Do prophylactic antibiotics help decrease flare-up rate?
Reader Pen VK did not decrease flare-ups with IP
Amox did not help decrease flare-ups with necrotic, asymptomatic teeth
Pen VK did not decrease flare-ups with necrotic, symptomatic teeth
Walton Pen VK had no sig effect on incidence of flare-up pain
Brennan-no difference in infection, pain, adverse events following use of PCN
When are Antibiotics indicated?
Baumgartner Antibiotics are recommended in conjunction with appropriate endo
tx for progressive infections with systemic signs and symptoms such as fever (100
deg F), malaise, cellulits, unexplained trismus, and progressive or persistent
swelling. I & D is indicated for any infection marked by cellulites (fluctuant or
indurated). (systemic involv, immunocompromised (dz or drugs) & rapidly
progressing)
What are other tx considerations for a flare-up?
Occlusal Adjustment Rosenberg works for IP pre-op pain (perc. sens)
Re-enter for complete debridement
Establish Drainage I & D; Trephination is ineffective (Moos as adjunct to
pulpectomy alone, Reader on post-op pain in necrotic teeth)
Evaluate for Analgesics Hargreaves 3D pain control (diagnosis, definitive tx,
drugs )
Flexible prescription plan 1) max nonnarcotic (aceto or
NSAID) or 2) add aceto (w or w/out opiod) to NSAID
Match the pts needs
Evaluate for Antibiotics systemic involvement or immunocompromised
Evaluate for Steroids Reader Oral (48mg methylPN) or IO (IP pts asymp for 7
days no other tx done)
Marshall Intraoral IM dexamethasone .07-.09mg/kg
usually 6-8mg total
When are steroids indicated?
Marshall- moderate/severe pain with dx of necrosis and PARL, Reader- IP if cant do
pulpectomy
Nobuhara- buccal vestibule
What is a Medrol Dose Pack?
21 tabs of 4mg methylprednisolone; taken for 6 days, start with 6 tabs and reduce
by 1 ea day
What is incidence of pain following RCT?
Pak and White: Systematic review: Pain prevalence: Pre-op- 81%, 24hr-40%, 1 wkless than 10%

19

Pain severity (100pt scale): Pre-op- 54, 24hr- 24, 1 wk5

Pain dropped substantially after 2 days and continued to decrease to
day 7
Torabinejad- maximal pain relief in first 24-48 hours
Polycarpou-12% long term pain (chronic pain 8.6x, pre-op pain 7.8, perc
tenderness 7.8, inter apt pain 3.9)
Nixdorf- 5% have pain more than 6 months post endo, 3.4% of which is likely nonodontogenic

Infections Overview
Discuss the infections of the Mandibular area:
Fascial Space
Buccal Vestibule

Body of the Mandible

Mental Space
Submental Space

Sublingual Space

Submandibular Space
(mild trismus)

Pterygomandibular
Space
(Mdr/severe trismus)

Source
Any Mand tooth exudates
breaks through B cort. plate
and apicies lie above
attachment of Buccinator or
Mentalis muscle
Any Mand tooth exudate
has not perforated the
periosteum
subperiosteal abscess
Mand anterior tooth
exudate breaks through the B
cort. plate and apex lies
below attachment of Mentalis
Mand anterior tooth
exudate breaks through L
cort. plate and apex lies
below attachment of
Mylohyoid
Any Mand tooth exudates
breaks through L cort. plate
and apex lies above
attachment of Mylohyoid
Mand posterior tooth
exudates breaks through the
L cort. plate and apicies lie
below attachment of the
Mylohyoid
Mand second or third Molars
exudates drains directly into
the space or contaminated
IAN block

Borders

Buccal cortical plate

Alveolar mucosa
Buccinator (post)
Mentalis (ant)

Buccal or lingual
cortical plate
Periosteum

Mentalis (superiorly)
Platysma (inferiorly)

Mylohyoid
(superiorly)
Platysma (inferiorly)

Mucosa of floor of the

mouth (superiorly)
Mylohyoid (inferiorly)
Mandible (lateral)
Mylohyoid
(superiorly)
Platysma (inferiorly)
Mandible (lateral)
Medial Pterygoid
(medial)
Ramus (lateral)
Lateral Pterygoid
(superior)

What 3 spaces are involved in Ludwigs angina?

Submental, Submandibular & Sublingual - life threatening cellulites
which can advance to the pharyngeal and cervical spaces, resulting in airway
obstruction
20

Discuss the infections of the lateral face and cheek:

Fascial Space
Buccal Vestibule

Buccal Space

Source
Max posterior tooth
exudates breaks through the
B cort plate and apicies lie
below attachment of the
Buccinator
Any Mand or Max posterior
tooth exudates breaks
through B cort plate and
apicies lie above/below the
attachment of the Buccinator
respectively

Borders

Buccal cortical plate

Alveolar mucosa
Buccinator
(superiorly)

Buccinator (medial)
Skin of Cheek (lateral)
Zygomatic
arch/Buccinator
attachment
(superiorly)
Mandible/Masseter
attachment
(inferiorly)
Ramus (medial)
Masseter (lateral)

Submasseteric Space

Impacted 3rd Molar

Temporal Space

Involved indirectly if an
infection spreads superiorly
from the inferior
pterygomandibular or
submasseteric spaces

(severe trismus)

Deep Temporal:

Skull (medial)

Temporalis (lateral)
Superficial Temporal:

Temporalis (medial)

Fascia

Discuss the infections of the midface:

Fascial Space
Palate
Base of the Upper Lip

Canine Space
(Infraorbital)
Periorbital Space

Source
Any Maxillary tooth with apex
near palate
Maxillary Central Incisor with
apex close to B cort plate &
above attachment of
Obicularis Oris
Maxillary Canine or 1st
Premolar exudates breaks
through B cort plate and apex
lies above the attachment of
the Levator Anguli Oris
Spread of infection from the
Canine or Buccal Spaces

Borders

Palate (superiorly)
Periosteum (inferior)
Mucosa of the Base of
the Upper Lip
Obicularis Oris
(inferior)
Levator Anguli Oris
(inferior)
Levator Labii
Superioris (superiorly)
Lies deep to the
Orbicularis Oculi

Why are infections of the midface dangerous?

Cavernous sinus thrombosis life threatening infection in which a
thrombus formed in the cavernous sinus breaks free, resulting in a blockage
of an artery or the spread of infection. Infections in the midface initiate an
inflammatory response. Increased pressure can reverse the direction of
venous blood flow (due to lace of valves) causing stasis in the cavernous
sinus this may initiate thrombus formation.

Retreatment Overview
Are Silver points a concern?
21

Seltzer corrosion products of silver sulfides, silver sulfates, silver

carbonates, and silver amine sulfate amide hydrates which are cytotoxic;
sulfur comes from sulfur containg amino acids cysteine, methionine
Goldberg- no correlation of corrosion and failure; poor chemomechanical
debridement
What are some techniques to remove Silver points?
Krell ultrasonics with hedstroms
Ruddle ultrasonics with IRS
How do you remove posts?
Johnson 16 min ultrasonic vibration
Baumgartner Gonan produced less cracks than ultrasonics and was
quicker
Can ultrasonic post removal cause any problems?
Dominici & Eleazer - > 15 sec caused high root surface temps
Huttula & McClanahan irrigate with ultrasonics reduced temps
Davis 20 sec dry U/S to post can cause 10C or more incr in root surface
temp
What solvent is most effective at gutta percha removal?
Kaplowitz tested 5 solvents; only chloroform dissolved GP completely
Wilcox- no technique removed all GP/sealer; chloroform has limited effect on
AH 26
Edgar-chloroform kills E.faecalis
Is chloroform safe for the patient and the dental staff?
Chutich no health risk to the pt; .32mg extruded 49mg is permissible
toxic dose
McDondald safe for staff; air vapors well below OSHA standards
How are Thermafil carriers removed?
Bertrand chloroform and endo files/Hedtroms
Baratto Profiles at 300 rpm
Wolcott & Hicks System B 225 deg & hand instruments
What is Red Russian paste and how do you remove it?
Gound Resorcinol-formaldehyde resin; 10% sodium hydroxide causes
polymerization
Krell use ultrasonics
Hartwell no solvent works; NaOCl works best
Technique to remove separated files?
Ward & Messer- staging platform, #3 or #4 GG with tip cut off
Ruddle- ultrasonics after access with staging platform; IRS

Surgery Overview
22

What are the indications for surgery?

Gutmann & Harrison- 1) strong possibility of failure with NS retx, 2) failure of
NSRCT and retx not possible or not achieve a better result, 3) need for biopsy
1) Failure to heal, 2) anatomic considerations (complex apical curvature),
3) iatrogenic considerations (transportation, ledges, overfilled canal,
broken instruments in apical third) 4) establish drainage, 5) NSRCT not
practical (large post.crn, calcified canals), 6) persistent post-oper pain
What are the anatomical concerns during periapical surgery?
Maxillary:
Eberhardt & Torabinejad MB root of 2nd molar is closest to the sinus
(0.8mm) and furthest from buccal cort plate (4.5mm); buccal root of 1st
premolar is closest to buccal cort plate (1.6mm) and furthest from sinus
(7mm); 5% of roots protrude into the sinus
Mandibular:
Phillips & Weller mental foramen located 60% the distance from the
buccal cusp tip of the 2nd premolar to the inferior border of the mandible;
exits posterior-superiorly; radiographically 3mm below and slightly mesial of
apex of 2nd premolar; 20%/60%/20% in relation to 2nd PM
Denio & Torabinejad IAN S shaped buccal to the D root of 2nd molar;
crosses to L below the M root of 2nd molar; L to 1st molar; crosses to buccal
below 2nd PM; 2M (3.7mm), 2PM (4.7mm)
Moiseiwitsch-90% between 1st and 2nd PM
Littner-3.5-5.4mm below apices 1st/2nd Molars; B to 2nd M, L to 1st M
(radiographic study)
How would you manage a sinus exposure?
Lin & Langeland prescribe decongestants (.5% neosynephrine); abx only
if sinusitis develops
Ericson- sinus exposure (13%) no bearing on successful healing: no nose
blowing, decongestant, abx (amox)
How do you avoid the mental foramen and nerve?
Moiseiwitsch take vertical PA radiograph; triangular incision w/ D vert
release; notch bone superiorly for retractor; 90% between 1st and 2nd PM
Discuss hemostasis during surgery?
Kim Recommends racellet epi pellets; other hemostasis measures include:
Bone wax may act as foreign body if any remains (Ibarolla-bone wax bad,
surgical okay, gelfoam best))
Chemical vasoconstrictors epi pellets placed 2-4min little systemic
absorption (Vickers)
Ferric sulfate must be completely curetted or healing will be delayed
(Jeansonne)
Calcium sulfate acts via tamponade effect; biocompatible and resorbs
Collagen causes platelet aggregation
Buckley: 1:50k epi bleeding of 1:100k
Are epi pellets a concern systemically?
23

Vickers/Baumgartner epi racellets produce no significant cardiovascular

effects
How much blood is typically lost during endodontic surgery?
Messer Avg 9.5mL; similar to tooth extraction; time is biggest factor
Buckley use 1:50,000 epi the blood loss as 1:100k epi
How much of the root end should be resected? Bevel?
Kim 3mm resection = 98% of apical ramifications and 93% of lateral canals
removed
Weller, Niemczk & Kim 4mm root resection of MB root of Max 1st molar
will expose a complete or partial isthmus 100% of the time; so we prep all
roots betw two canals
Gilheany & Figdor aim for 0 deg bevel for decreased leakage; 0 degree
bevel 1 mm resection, 30 deg 2.1 mm, 45 deg 2.5 mm resection to get
no leakage thru dentinal tubules
DO you always perform a root-end resection?
Gutmann and Harrison-YES. 1) Remove pathology, 2) remove anatomic
variations, 3) remove operator error, 4) enhance soft tissue removal, 5) gain
access to canal system
Why use ultrasonics (US) for the retro-prep? Do ultrasonics cause cracks?
Baumgartner 3mm prep with diamond coated ultrasonics; no crack seen
and minimal bony crypt required
Torabinejad/Wuchenich- more parallel walls, deeper preps, followed canals
better, cleaner walls than burs
Waplington- US not cause cracks but marginal chips
Calzonetti- not cause microfxs since impact dampaned by supporting
tissues
Do you always prep between two canals?
Weller-100% of MB root had full or partial isthmus at 4 mm level
Cambruzzi and Marshall-isthmus presence: MB 30%, M 60%, D 15%
Von Arx: MB 76%, M 83%, D 36%
Does the entire lesion need to be curetted and removed for healing to occur?
Lin & Langland No, but must remove all foreign objects; lesion will be
incorporated into new granulation tissue
Is it necessary to remove the apical smear layer?
Jeansonne no difference in healing noted (used tetracyc. & citric acid)
Abeti removing smear layer inhibited cementogenesis over MTA
Is a retro-fill required? What do you use and why?
Christiansen rand clin trial of success of smoothing GP vs MTA retro fill at
1yr f/u: 52% vs 96% for MTA
Kim Super EBA showed success rates 91% at 5-7yrs
24

Chong/Pitt Ford- success at 2 yrs 92% for MTA, 87% IRM

Setzer contemporary tech with EBA, IRM or MTA was 94% at 1 yr
Discuss MTA as a retro-fill material?
Torabinejad biocompatible; demonstrates the least leakage; substrate for
osseous and cementum growth, sets in presence of moisture/blood
Baek MTA promoted better PA tissue healing vs. Super EBA or am
Why use MTA?
1) Successful (Chong-92%), 2) Biocompatible (Kaiser-less toxic to PDL cells
than EBA, Baek and Torabinejad-substrate for osseous and cementum), 3)
Least leakage (Torabinejad), dry or in blood
Would you consider guided tissue regeneration?
Pecora & Kim If > 10mm; through & through; endo-perio defect
Tsesis M/A showing GTR sig better for through & through lesions and
trending better for > 10 mm diameter lesions
Suda Calcium sulfate was effective in bone regeneration
Sotosanti-80/20 mix of DFDBA/CaSO4
Von Arx- membrane NOT enhance new bone formation compared to flap
readaptation alone
What type of sutures do you use and why?
Becker Vicryl (polyglactin) produced little inflammatory response
compared to polypropylene, silk or gut
Discuss incision and wound healing following endodontic surgery?
Harrison & Jurosky
Healing of the incisional wound:
First 24 hrs:
clotting and inflammation: fibrin clot/PMNs, then
macrophages
2.3 Days: epithelial healing: 4d for intrasulcular incision vs 2-3 d for vertical
incision
3.5 Days: CT healing: fibroblasts
5.7 Days: Maturation and remodeling: collagen
Healing of the osseous wound:
Day 1-3 Coagulum fills defect (macrophages, PMNs, fibroblast-like cells)
Day 2-4- Outgrowth of granulation tissue from PDL (PMNs, macrophages
replaced w fibroblasts)
Day 4Endosteal tissue proliferates into coagulum (macrophages/PMNs
replaced c fibroblasts)
Day 14 new periosteum forms; osteoblastic activity; new woven bone
trabeculae occupy 80%
Day 28 lesion fills in with maturing new trabecular bone (and a functioning
periosteum was active in repair of cortical plate
4-5 months- maturation/remodeling complete

25

Periosteum does not survive flap reflection; dont curette cortical retained
tissue; crestal bone levels will reduce following sx
When should sutures be removed?
Kim 2-3 days (after epithelial healing occurs)
Harrison and Jurosky: epithelial seal at 2 days, epithelial healing occurs 4
days for intrasulcular incisions, 2-3 d for vertical
Selvig-rapid increase of collagen content of granulation tissue at day 4
When would decompression be considered and discuss different approaches?
Neaverth and Burg-Large lesions in order to avoid: devitalizing adjacent
teeth, damage anatomical structures, parasthesia or risky surgery (elderly)
Freedland used polyvinyl tubing and daily irrigation
Hoen Aspiration & irrigation
What is the rebound phenomena?
Gutmann and Harrison-concentration of vasoconstrictor decreases to a
level that no longer produces alpha-adrenergic effects. Blood flow increases
not due to Beta-adrenergic effects of epi, but from localized tissue hypoxia
and acidosis caused by prolonged vasoconstriction

Trauma Overview
How do you classify crown fractures?
Andreasen: Crown infraction (craze line); Uncomplicated crown fx (enamel
and/or dentin with no pulp exposure); Complicated crown fx (pulp exposed)
What is the probability of pulp necrosis following crown fx?
Ravn 6% with uncomplicated crown fx; if concussion & mobility, then 30%;
80% success with DPC and uninflammed pulps
Andreasen-1-13% with uncomplicated fxs
Cvek 96% success cvek pulpotomy ( remove 2mm pulp up to 7days after
fx)
What is the tx for a crown fx?
Uncomplicated Restore with GI or composite resin; attempt bonding fxd
segment
Complicated Cvek pulpotomy with Ca(OH)2 or RCT (if mature root)
What is the tx for a root fx?
Michanowicz- 3 XRs; Reposition coronal segment & physiologic splint X3
wks; relieve occl
-if fx is coronal, remove coronal segment; consider gingivectomy or ortho
extrusion
(also Andreasen)
IADT- splint up to 4 weeks with flexible split, if cervical fx up to 4 months
What is probability of pulp necrosis with root fxs?
Cvek & Andreasen 22% of the coronal segment (534 teeth), less than 1%
in apical segment
26

What are the methods of healing for a root fx?

Andreasen Calcified tissue; connective tissue; bone & CT; granulation
tissue w/out healing
What is the tx for a luxation injury?
Take multiple angled radiographs to discern root fx or not;
Reposition tooth in normal position (consider ortho reposition with intrusion);
physiologic splint X 2 wks (4 weeks for intrusive/lateral luxation); relieve
occlusion; monitor for pulpal necrosis/pathology (3-4w, 6-8w, 6mo, 1 yr for
5y)
-If intrusion of fully formed root apex, initiate RCT in 3wks (2 weeks
Andreasen)
What is tx for intruded tooth?
Andreasen-immature root development-await re-eruption, mature root dev
(12-17 yro)-await re-eruption, mature toot dev (> 17 yro)-ortho or surgical
re-eruption
What is the probability of pulp necrosis following luxation injuries?
Andreasen Concussion 4% (0% in immature teeth) ; Subluxation 15%;
(0%) Extrusion 55% (9%); Lateral Luxation 77% (9%); Intrusion 100% (62%)
How do you manage an avulsed tooth with an open apex (<1 hr dry)?
Clean root and socket with saline; Soak tooth in doxycycline 1mg/20mL for 5
min (Cvek- less ankylosis or inflammation, Yanpiset-dbl revasc rate to
47%); examine for alveolar fx & replant; physiologic splint X1-2 wk
(Andreasen); monitor for necrosis/PA pathology; systemic Abx (Trope),
tetanus booster (Rothstein)
How do you manage an avulsed tooth with an open apex (>1 hr dry)?
IADT- either no replant or replant with eventual decoronation, systemic
antibiotics, check Tetanus, clean root surface (soak in 2% NAF solution to
delay resorption), replant and stabilize with flexible splint for 4 weeks, RCT at
2 weeks or prior to replantation, prepare for decoronation at infraposition of
1-3mm
How do you manage an avulsed tooth with a closed apex (<1 hr dry)?
Clean root and socket with saline/place in HBSS (Matsson); examine for
alveolar fx & replant; physiologic splint X1 wk (Andreasen); systemic abx
(Hammarstrom), initiate RCT X7-10 days
How do you manage an avulsed tooth with a closed apex (>1 hr dry)?
Clean root surface/remove PDL (Lindskog), and soak in NaF- X5min
(Krasner); clean socket with saline; examine for alveolar fx and replant;
physiologic splint X4-6 wks; systemic abx (Hammarstrom), initiate RCT X710 days
What type of healing can you expect with an avulsed tooth?
27

Andreasen normal, surface resorption, replacement resorption, &

inflammatory resorption; <30min before replanted, 90% no resorption;
>90min = resorption
Discuss storage media for avulsed teeth?
Trope: Best to worst: HBSS > Milk > Saline > Saliva > Water
Blomlof Milk gives you 6 extra hrs, saran wrap as good as milk
Harkacz-skim milk
Discuss splinting of avulsed teeth?
Nasjeleti splinting X7 days recovered uneventfully; 30 days induced
resorption & ankylosis
Antrim-20-30 ib monofilament nylon line
Andreasen-functional splint to reduce replacement resorption
Berude-type of splint not a factor as long as time of splinting is short
IADT guidelines say flexible splint
What are some general adjuncts for trauma tx?
Tetanus booster (Rotsein); chlorhexidine rinses; analgesics
Antibiotics Pen VK 500mg or doxycycline 100mg (Trope) X1wk for
avulsions
What is the role of Ca(OH)2 in replanted teeth?
Trope decrease incidence of inflammatory resorption; 1wk = 8wks
Dumsha NSD in inflammatory resorption with GP or 5mo tx with Ca(OH)2;
recommends obturating immediately
AAE-CaOH until intact lamina dura traced around root surface, usually 1
month
What is the role of fluorides in replanted teeth?
Klinge SnF2 delays replacement resorption
Trope-make teeth more resistant to resorption
What is the recommended follow-up for traumatic dental injuries?
Pathways after tx 3, 6, 12 mo and yearly thereafter
Hinckfuss/Messer RCT within 10-14 days if indicated
Adequacy of pulp testing following trauma?
Andreasen-if complete rupture, takes 36 days before positive response
Bhaskar-due to resiliency and coiled nature of pulp vessels, blood supply
may remain intact
Zadik-if no response in 6 mo, RCT indicated

Anesthesia Overview
What properties of local anesthetics determine the onset of action, potency,
and duration of action?
Malamed
28

pKa determines the onset of action the lower the pKa the more rapid the
onset
Lipid solubility determines the potency permits anesthetic to penetrate
the membrane more easily
Protein binding is responsible for the duration of action. Duration also
increased with vasoconstrictor which decreases blood flow and systemic
absorption
Amide LAs are metabolized in the Liver, excreted by kidney (Arti in both
kidney & plasma)
What is the mechanism of action for local anesthetics?
Blockage of sodium channels by partitioning into 2 types, the charged acid
(RNH+) and the uncharged basic form (RN), which penetrates the nerve
membrane, ionizes, binds to voltage-gated Na channel and blocks the influx
of Na ions preventing depolarization (-70 mV 40 mV)
What are some explanations for anesthetic failure?
Hargreaves - 1) lower pH of inflamed tissue reduces the amount of base
form of anesthetic that penetrates the nerve membrane (ion trapping)
2) Unsuccessful technique, anatomy
3) Inflamed nerves have altered resting potentials & decr excitability
thresholds (hyperalgesia)
4) TTX-R sodium channel (1.8 and 1.9) which are resistant to LAs (increased
expression in IP cases)
5) Apprehensive pts have decreased pain thresholds
6) Acute tachyphylaxis
Fouad 6 fold increase in TTX-resistant sodium channels in IP cases
Does accessory nerve innervation affect anesthesia?
Frommer mylohyoid nerve may supply accessory innervation
Pogrel cross innervation of Mand incisors
Clark, Reader-mylohyoid injection not sig enhance pulpal anesthesia
What are some supplemental anesthesia techniques and how do they work?
PDL IO anesthesia (Walton) 63% effective after 1st attempt, 90% 2nd
attempt
Stabident / X-tip IO anesthesia
Intrapulpal pressure anesthesia (Birchfield and Rosenberg)
What are alternative injection techniques to the IAN block? Are they more
successful?
Gow-Gates & Vazirani-Akinosi
Malmed Gow-Gates is superior to IAN block
Goldberg, Reader failed to show either GG or V-A is better than IAN block
Compare the efficacy of different anesthetics?
Reader NSD in 4% prilocaine, 3% mepivicaine & 2% lidocaine with IAN
block
29

Claffey- Articaine 24%, Lid 23%: NSD in irrev pitis for IAN blks
Brandt sys rev w/ M/A showing arti sig better for infiltration anes vs lido
(Kanaa showed same thing in a RCT)
Is Articaine the solution?
Claffey & Reader NSD between 4% articaine & 2% lidocaine with IAN
block & IP (24%/23%)
Kanaa-Articaine did show increased success if given as a buccal infiltration
injection
following IAN block in symptomatic pts
Brandt -sys rev and M/A articaine sig better for infiltration anesthesia
Hillerup Articaine has a 5 fold higher incidence of paresthesias compared
to lidocaine
Haas articaine 3.6x more incidence of parathesia, based on usage/sales
percentage
Pogrel- 15% prolonged paresthesia after IAN, of this 81% spont heal w/in 2
wks, addl 10-15% heal w/in 8 wks. If paresthesia lasts more than 8 wks,
unlikely to completely heal, but might get better, surgery not a good option
for injection paresthesia, good for overfills (compress injury)
Discuss Intraosseous anesthesia success and side effects?
Replogle & Reader 67% had an increase in heart rate ok with healthy
pts; consider mepivicaine (28.8 BPM vs 4 BPM); normal within 4 minutes;
most perceived incr w/ lido, none with Mepivicaine
Nusstein - Stabident with 2% lidocaine 88% effective for IP
Reisman- Stabident with 3% mepivicaine for IP 80% successful x1
injection; 98% x2
What are the anesthetic and epinephrine concentrations in common
anesthetics?
2% lidocaine w/ 1:100,000 epi = 34mg lido w/ .017mg epi
3% mepivacaine (Carbocaine, Polocaine) = 51 mg mepivacaine
4% articaine w/ 1:100,000 epi = 68 mg articaine w/ .017mg epi
0.5% bupivacaine (Marcaine) w/ 1:200,000 epi = 9mg bupivacaine w/ .
009mg epi
What drug interactions are a concern with epinephrine?
Tricyclic antidepressants amitriptyline, doxepin
Nonselective beta blockers nadolol, propranolol
Recreational drugs - cocaine
Nonselective alpha adrenergic blockers chropromazine, clozapine,
haloperidol
Digitalis - Digoxin
Thyroid hormones Levothyroxine
MAO inhibitors
Do pre-oper NSAIDs help success of anesthesia?
Parirokh-600 mg ibuprofen 1 hr pre-oper in pts w/irrev pulpitis incr anes
successs (32% to 78%)
30

(MOA: decr inflammation, decr inflammatory mediators (PGE2), decrease

TTX-r channels)
Reader-OSU and Aggarwahl both say 600-800 mg pre-op ibuprofen had
no sig effect on IAN success in pts with IP; Aggarwahl says Ketorlac no
benefit either
What is the max dosage of anesthetic?
Moore rule of 25 = 1 carp for every 25 pounds of pt weight
Adults 4.4mg /kg or 2mg/lb
Malamed:
Manufacturer:
Malamed: 2% Lido
4.4mg/kg or 2mg/lb, 300 mg max
7.0mg/kg,
500mg
3% Mepiv plain
4.4mg/kg, 300 mg max
6.6mg/kg, 400
mg
4% Articaine 7mg/kg or 3mg/lb, 500 mg max
same
0.5% Marcaine 1.3mg/kg, 90 mg max
same

ENDO-PERIO Overview
Can Endo pathosis create perio pathology?
Sinai & Soltanoff rat study showed pulpal disease affects the
periodontium quickly with inflammation; perio disease affects the pulp slowly
with degenerative changes
Seltzer and Sinai-perio lesions may be initiated by inflamed or necrotic
pulp thru lat canals
Does perio disease cause endo pathosis?
Yes: Seltzer disease caused through lateral/accessory canals and viceversa
Langeland, Rodregues & Dowden if all main apical foramina are
involved
Kipioti & Kobayashi (2 sep. studies) caries free teeth with endo path
showed similar microorganisms in perio pockets and root canals
No: Mazur & Massler / Torabinejad/ Czarnecki & Schilder histo
studies showed no correlation
Who discussed endo-perio terminology?
Simon, Glick & Frank Primary endo; Primary endo with 2nd perio; Primary
perio; Primary perio wth 2nd endo; true combined lesions (ie root fx)
Does perio tx affect the pulp?
Wong & Hirsch pulpitis was noted adjacent to areas of root
planning/scaling
Bergenholtz-only 3% of 417 advanced-perio dz teeth required RCT
Does endo tx affect future perio tx?
Dunlap in vitro study found RCT does not interfere with growth of
fibroblasts on planed dentin surfaces
Cortellini RCT has no neg effect on GTR and GTR no neg effect on pulp
31

What is the biologic width?

Gargiulo, Wentz & Orban sulcus depth - 0.69mm
epithelial attachment 0.97mm
CT attachment 1.07mm
What are common perio pathogens?
Red complex Bacteria: P. gingivalis, T. forsythensis & T. denticola
Other bacteria linked to perio disease: Actinobacillus
actinomycetemcomitans, B. forsythus & P. intermedia.
Trope spirochetes common in perio abscesses but less likely in endo
abscesses
Success of vital root amps?
Flipowicz: 13% success at 5 yrs
Smukler & Tagger: vital root amp okay if do RCT w/i 2 weeks
Success of root resection?
Langer: 62% success at 10 yrs (85% success at 5 yrs)
Fugazzoto NSD in survival of root resected molars vs molar implants at 13
yr f/u (both 97% overall); D roots of man molar were sig worse though -75%
survival

ENDO-PEDO Overview
Discuss Primary tooth anatomy:
Hibbard: Mand incisors 2 canals 10%
Max 1st molar 2 MB canals 75%
Max 2nd molar 2MB canals 85-95%
Mand 1st molar 2 mesial canals 75%; 2 distal canals 25%
Mand 2nd molar 2 mesial canals 85%
Discuss formocresol pulpotomies: technique, formulation & concerns?
Sweet: Technique remove coronal pulp, moist cotton pellet until heme control,
place formocresol X5 min, ZOE cement & SSC
Law & Lewis: FC 93% success at 2 yrs
Ranly recommends 1/5 concentration
Pashley found formocresol systemically (spleen, liver & kidney) after placing in
dogs teeth
Pruhs-enamel defects noted on F and O surfaces of perm successors
*WHO declared formaldehyde a human carcinogen (FC=19% Formaldehyde, 35%
cresol, dissolved in 17.5% glcerine and water))
Are there any other options & compare success rates?
Fuks FC - 84%; Glutaraldehyde - 72%; FeSO4 - 93%, MTA 97%
Peng & Li: meta-analysis- Ferric sulfate 92% success (74% on XR); NSD than FC but
safer
Maroto-gray MTA 98.5% success at 42 months
Hoshino-Triple abx paste into canals 2 mm: 95% of teeth had symptoms resolved at
1 yr
Doyle: FC 94% success, CaOH 64% but 25% exhibited internal resorption (Dont use
CaOH)

32

How would you obturate primary teeth?

ZOE or Ca(OH)2 paste, (Vitapex: 30% CaOH, 40% Iodoform in a silicone lubricant)
Coll 78% success with ZOE pulpectomies (long=58%, short=87%, at apex 89%;
no resorption 92%, min pre-op resorption 83%, excessive pre-op resorption 23%)
Who decribed Apexification & what types of repair are seen?
Frank long term tx with Ca(OH)2
4 types of repair/closure: periapex closes with recession of the root canal
obliterated apex w/o any change of canal space
no radiographic evidence of closure / apparent clinically
calcified bridge coronal to the apex (detected
radiographically)
How long does this take?
Kleirer 1yr +/- 7months
Cvek Avg 18 months; check q 3-6 months
Are there concerns about long term use of Ca(OH)2?
Andreasen >30 day use will weaken dentin; strength in 1 yr
Doyon- strength not decrease until 180 days
Are there other options to manage an open apex? (Immature permanent teeth)
Apical Bariers: Dentin Chips Holland; Ca(OH)2 Weisenseel, Hicks & Pelleu;
MTA Torabinejad
Witherspoon- MTA/cmpst 93% success in 1 visit, CaOH, then MTA/cmpst 90.5% (2
visits)
Holden- MTA/GP 85% healed, 100% functional success
Knapp and Marshall-master apical impression
Banchs and Trope-regeneration
Is RCT needed after a pulpotomy procedure?
Cvek-No, 16/21 teeth had normal pulp tissue so pctmy not justified just because
tooth calcifying

ENDOORTHO Overview
Can orthodontics cause pulp necrosis?
Butcher extreme ortho forces can cause circulatory interruptions leading
to necrosis
Hamilton and Gutmann- ortho can cause degenerative and/or inflamm
responses
deSorza- healing of AP is faster w/o ortho, but ortho does not stop healing
process
Can ortho cause resorption?
Reitan ortho movement too quickly = resorption
Hamilton and Gutmann- endo teeth dev apical resorption less than vital
teeth
Can you orthodontically move an endo treated tooth?
33

Wickwire ok to move endo teeth no signs of pathologic changes

Who first discussed ortho extrusion?
Simon-immature bone in 2 wks, mature bone in 4 wks; PDL not tear, need
CL (1.5mm/wk)
Heithersay indicated for transverse root fx 1-4mm subcreastal; 6 wk
stabilization
How long should you stabilize an extruded tooth?
Lemon 1 mo stabilization for every 1mm of movement (Benenati also)
Can anything else be done to prevent a relapse?
Malmgren fiberotomy may help before retention to avoid relapse
Pontorriero- supracrestal fiberotomy: weekly, extrude faster in 3 weeks,
stabilize 8-12 weeks

Resorption Overview
How is resorption classified?
Tronstad transient inflammatory (surface), progressive inflammatory,
internal & external (progressive external, cervical, and replacement)
How do you differentiate internal from external resorption?
Gartner & Mack radiographic differences: internal symmetrical, cannot
trace canal through lesion, stays centered in shift shots; external irregular,
can trace the canal through the lesion, moves on shift shots
What causes resorption?
Trope Two things must happen: 1) the loss or alteration of the protective
layer (pre-cementum or pre-dentin); 2) inflammation must occur to the
unprotected root surface
Osteoclasts will not adhere to or resorb unmineralized matrix; if the cemental
layer is lost or damaged, the inflammatory stimulators can pass from an
infected pulp space through the dentinal tubules into the PDL resulting in
both bone resorption and root resorption
Discuss internal resorption and tx approach?
Wedenberg normal pulp is replaced with periodontal-like connective tissue
Turkun - >90% success with non-perforating using 1 wk CaOH2 and warm
GP; 25% success with perforating defect
Stamos ultrasonics & warm GP
Frank-without perf: pctmy, obturate w GP; with perf/no communication w
sulcus: pctmy, CaOH, obturate w GP; with perf/communication w sulcus:
pctmy, obturate with GP, surgical repair or ortho extrusion
Discuss external inflammatory resorption and tx approach?
Johnson Necrotic teeth with AP had more apical resorption than those with
a normal periapex or IP
34

Trope Long term (12 wk) CaOH2 tx may be more effective than 1wk for
established inflammatory root resorption
Discuss external cervical resorption and tx approach?
Heithersay strong association with ortho, trauma, bleaching, trauma &
bleaching; distinguished class 1-4 defects; recommended surgical access,
topical 90% trichloracetic acid, curettage & GI restoration (endo tx) (ICR)
Frank Tx and prognosis based on complete debridement of the defect (EIR)
Heithersay-class 1 small cervical lesion, class 2-well-defined coronal lesion
not extending into root, class 3-deeper invasion of coronal dentin with
extension into coronal 1/3 of root, class 4-extends beyond coronal 1/3 of root
Can ortho tx cause resorption?
Reitan ortho movement too quickly = resorption
Heithersay showed 24% association of ICR and ortho

Bleaching Overview
Who described internal bleaching?
Spasser described Na perborate walking bleach/water
Nutting & Poe recommended Superoxol + Na Perborate for greater
efficacy; change every week; coined term walking bleach
Rotstein- Na Perborate and water just as effective as 30% hydrogen
peroxide (superoxol)
Holmstrup Na Perborate/water very effective at 3 yrs, no case of
resorption
Can bleaching cause resorption?
Madison & Walton bleaching factors associated with resorption were heat
with 30% hydrogen peroxide
Rotstein-heating, diffusion of hydrogen peroxide thru patent dentinal
tubules
What is incidence of post-bleaching cervical resorption?
Friedman- 7%
Abou-Rass 0%
Heithersay- 2%
What can you do to prevent resorption?
Rotstein use a 2mm base material at the CEJ; also recommends water
instead of superoxol
How do you treat post-bleaching cervical resorption?
Gimlin, Schindler-remove 2mm of GP, CaOH long-term
Can tetracycline stained teeth be bleached?
Walton only internal bleaching is effective
Abou-Rass- recommended intentional RCT/internal bleaching
35

Leonard & Haywood- nightguard vital bleaching for 6 months effective,

stable for 90 months
Does bleaching affect bonding of composite restorations?
Titley & Torneck H2O2 may inhibit resin polymerization
Demarco short term use of Ca(OH)2 restores bonding capabilities
Is internal bleaching effective?
Glockner - 5 yrs later; pts are 98% satisfied; 80% subjective success for
dentists
Abou-Rass-7% darker at 3-15 yr follow-up
Is vital tooth bleaching effective?
Haywood 92% experience some lightening; 66% experienced transient
side effects
Ritter safe for the pulp up to 10 yrs post-op; bleaching effectiveness may
decline
Cohen-no harm to pulp (histo)

Endodontic Materials Overview

RC Prep: EDTA, Urea Peroxide, Cetyl Alcohol
Gutta Percha: 65% Zinc Oxide; 20% GP; 10% metal sulfites; 5% waxes and
resins, trace pigments
GP 19-22%, ZnO 59-75%, waxes & resins 1-4%, metal sulfates 1-17%,
pigments 0.1-0.3% - Friedman
AH Plus: epoxy-amine resin (Bisphenol paste A / Amine paste B)
Roth 801 Sealer: ZOE: ZnO 42%, stabelite resin 27%, BaSO4 15%, Bi
subnitrate 15%, Na Borous anhydrous 1% - Friedman
Cavit: Zinc oxide; calcium sulfate, zinc sulfate, glycoacetate,
polyvinylchloroacetate, triethanolamine, red pigment
MTA: 75% Portland Cement, 20% bismuth oxide, 5% gypsum
-White MTA has less iron, aluminum and magnesium
(Portland cement: tricalcium silicate, tricalcium aluminate, dicalcium
silicate, tetracalcium aluminoferrite)
Super EBA: Powder 60% Zinc Oxide, 34% Silicate dioxide, 6% resins
Liquid 62.5% Ethylene Benzoic Acid, 37.5% Eugenol

Restorative Overview
Are endodontically treated teeth more brittle?
Helfer-9% less moisture content in pulpless teeth vs vital teeth
36

Papa, Messer NSD in moisture content

Sedgley Vital dentin 3.5% harder; biomechanical properties are not
significantly altered
Reeh, Messer & Douglas RCT reduces cuspal stiffness by 5%; Occl cavity
prep. 20%; MOD 63%
Gutmann-shear strength of endo tx teeth lower than vital tth (14%); altered
collagen structure
Is the seal of the coronal restoration important?
Swanson & Madison loss of coronal seal = bacterial contamination in as
little as 3d
Ray & Trope Quality of coronal seal more important than quality of endo
tx
Ricucci, Bergenholtz GP exposed for up to 3 months showed lesions did
not worsen, in histo study 96% bacteria limited to coronal third
Khayat-10 mm of contaminated GP with saliva leaked full length by 30 days
(4-48d range)
Alves-LPS 23 days, bacteria 62 days
Gillen Sys rev & m/a show GE/GR is sig better success (3x) than GE/PR or
PE/GR; NSD b/w GE/PR or PE/GR
What type of temporary restorations do you use?
Cavit, Glass ionomer:
Weber use 3.5mm thickness of Cavit
Beach & Hutter 3 wk bacterial leakage test: no leakage w/ Cavit clinical
study
Pashley Cavit, Term & GI provided leakproof seals for 8wks
Is cuspal coverage important for endodontically treated teeth?
Aquilino teeth without crown lost at 6X higher rate
Salehrabi & Rotstein- 97% functional success of RCT, of the 3% failed 85%
not have cuspal cov
When should post space be made? What technique and dimensions?
Immediately due to familiarity to canal anatomy & setting of sealer
Lemon NSD with immediate or delay
Kwan NSD with heat or rotary removal of GP
Sorensen & Martinoff post = crown length
Portell, Solano, Fan (diff papers)-all recommended immediate post space
Johnson max post width is 1/3 root width
Karapanou- Roth sealer: less leakage with immediate, AH-26 no diff in
immed or delayed
Goodacre-NSD between immed and delayed; leave 4-5 mm GP (3mm
minimum)
Does Eugenol affect post cementation?
Yes Nemetz with panavia (resin) cement
No Boone; NSD in post retentive strength when using Roth or AH26
(Panavia); Schwartz-NSD
37

Can posts cause root fractures?

Akin Stress patterns are a result of post insertion
Randow pts detect pressure earlier in vital teeth
How do you improve the fracture resistance of immature teeth following
endo treatment?
Lawley-bonded cmpst
Wilkinson and Kirkpatrick- self-cured hybrid cmpst
Schmoldt-fiber post with fiber reinforced cmpst was best vs MTA or cmpst
only
Mannocci-fiber post and cmpst more fx resistant than cuspal coverage
Amalgam (Premolars)
Discuss incomplete crn-root fractures
Cameron-coined term cracked tooth syndrome; 1) man 2nd M 2) max 1st M,
3) man 1st M; classic symptoms of biting sensitivity/cold sensitivity
Krell-20% will need RCT w/i 6 mo after cuspal coverage; if last 6 mo
probably wont need RCT
How do you diagnose vertical root fractures?
Pitts and Natkin-hx of RCT, diffuse RL, isolated narrow probable defect,
minimal pain, perio abscess, dual sinus tracts (pathognomonic)
Walton-VRF in F-L direction; crn-root fx in M-D direction
Dang and Walton-D11 spreader > finger spreaders
Tamse-deep pocket, sinus tract close to marginal gingiva, PA and lateral RL,
CC of pain or abscess; max 2nd PM most common followed by M root of man
molar

Pulpal Histology/Pathology Overview

What are the cellular elements of the pulp?
TenCate Odontoblasts, fibroblasts, undifferentiated mesenchymal cells,
macrophages, Lymphocytes & Dendritic cells
Farnoush found mast cells in both inflamed and normal pulps
Reader mylenated A-delta fibers 28%; unmylenated C fibers 72% of total
How far do the odontoblastic processes extend into the tubules?
Pashley 1/3 the length of the tubule
What types of collagen are found in the dental tissues & what cells
synthesize collegen?
Pulp type I & III; Dentin type I (90% of organic component)
Synthesized by mainly fibroblasts, but also odontoblasts, osteoblasts &
cementoblasts
Are lymphatics found in the pulp?
Bernick demonstrated lymphatics in the pulp Bishop also showed this
38

Jontell- dendritic cells in pulp

Discuss the pulp vasculature and regulation of blood flow?
Takahashi & Kim SEM showed AV anastomosis, VVanastomosis, U-shaped
arterioles
Kim PBF increased with C-fiber activation (A-delta insignificant); C-fibers
release substance P which increases PBF; the increase in tissue pressure
excites both A-delta & C fibers
Describe the strangulation theory & does it occur?
As pulpal inflammation , pulpal pressure . With this increased pressure,
veins and lymphatics collapse at the apex and strangle the pulp necrosis
results
Tonder cat study disproved this theory; localized increase in pressure to
site of injury with no strangulation
Discuss calcific metamorphosis? Is RCT indicated?
Pathways - Pulp canal obliteration due to trauma resembles cememtum or
bone
Andreasen 22% of traumatized teeth undergo CM; only 8.5% developed
pulp necrosis
Walton canal present histologically, although absent radiographically
Holcomb & Gregory RCT if PARL develops; only 7% require RCT
Cvek histo wise, most pulps had a rel normal appearance, no bacterial
found, able to negotiate 53/54 radiographically calcified canals, so RCT can
be done if needed
Discuss the pulpal rxn to caries?
Reeves & Stanley if caries is < .5mm from the pulp or if it invades
reparative dentin, there is irreversible damage; if >1.1mm then little
pathosis is seen
Trowbridge chronic inflammation occurs long before bacteria penetrates
the pulp
What is the effect of restorative dentistry on the pulp?
Stanley, White & McCray tertiary dentin begins to form @ 19 days at
1.49 um/day
Abou-Rass consider RCT for teeth with stressed pulps
Zach heat is capable of causing pulp necrosiz
How does age affect the pulp?
Bernick decreased vascularity, nerves & pulp chamber size; increased
calcifications
Describe the hydrodynamic theory of dentinal hypersensitivity. Any
solutions?
Brannstrom heat causes inward fluid movement; cold outward;
distortion of odontoblastic processes stimulates nerve response
Pashley occlude tubules with unfilled resins or oxalate salts
39

Kim K+ ions desensitize nerve ending

Three theories on dentinal sensitivity:
1) Dentin innervation-nerve fibers penetrate tubules and are stimulated upon
mechanical injury
2) Dentinoblastic receptor-injury to odontoblastic process cause changes in
odontoblast which lead to activity in approximating nerve fibers
3) Hydrodynamic-pain caused by pressure changes w/I or outside pulp; fluid
movement in tubules cause stimulation of nerve endings in odontoblastic or
subodontoblastic areas of pulp
How does vital bleaching affect the pulp?
Ritter safe for the pulp up to 10 yrs post-op; bleaching effectiveness may
decline

Periapical Pathology Overview

Define:
Granulation tissue: healing tissue w fibroblasts, collagen, proliferating
capillaries & leukocytes
Granuloma: chronic inflammatory tissue primarily infiltrated with
lymphocytes, plasma cells & macrophages
True cyst (bay cyst Simon): inflammatory lesion with a distinct
pathological cavity completely enclosed in an epithelial lining
Pocket cyst: lined with epithelium, but communicates with the root canal
Abscess: acute inflammation consisting primarily of PMNs
What are causes of persistent apical disease?
Nair- intraradicular infection, cholesteroal crystals, true cyst, extradicular,
foreign body rxn
Ricucci/Siquiera - 6% incidence of extradicular biofilm (100% in PARL
10mm or more diameter)
Is it possible to differentiate between a granuloma or cyst?
Priebe No, cant determine from a radiograph
Bhaskar-no correlation betw size or shape
Lalonde-lesions > 200mm2 were cysts (0-100mm2=30% cysts, 100200mm2=60% cysts)
Simon-CBCT 76.5% accurate
Morse-electrophoresis 100% accurate (based on albumin production)
Rosenberg no reliable correlation b/w CBCT and histo
What is the incidence of a granuloma, cyst & abscess?
Lalonde-44% cysts, 56% granuloma (1097 cases)
Bhaskar-42% cysts, 48% granuloma, 10% other (2308 cases)
Nair 50% granuloma; 35% abscess; 15% cyst (distinguishes 6%pocket / 9%
true); lesion removed in toto
Koivisto over 9000 lesions; 40% granuloma, 33% cyst, 27% other
What is the composition of a PA granuloma?
40

Stern- 40% fibroblasts, 24% macrophages, 16% lymphocytes, 7% plasma

cells, 6% vascular elements, 5% epithelial cells, 4% neutrophils
What are the theories of cyst formation?
1. Nutritional Deficiency or Breakdown (Toller, TenCate) central cells
of proliferating epithelium get removed from their nutritional supply and
undergo degeneration and liquefaction necrosis; PMNs attracted,
microcavities containing degenerating epith cells, PMNs and tissue exudates
coalesce and form cyst
2. Merging of Epithelial Strands (Lin)-as epith strands grow, they merge
to form 3-D ball mass; when CT trapped inside, ball degenerates and cyst
formed
3. Abscess Cavity Theory (Nair/Summers)-tissue necrosis and lysis takes
place in PA inflamm tissues and abscess formed; epith proliferates around
abscess (an inherent property of epith)
4. Immunologic Theory (Torabinejad)- immune PA rxns stimulate epith
rests of Malessez to proliferate resulting in cystic lined lumen formation
Do cysts heal following RCT?
Nair pocket cysts should heal; true cysts, particularly large ones with cholesterol
crystals are less likely
What are the histologic features of a sinus tract?
Baumgartner lined with either epithelium or granulomatous tissue; 100% lined
with stratified squamous epithelium to level of mucosal rete ridges; 33% were
completely lined with epithelium to the PA lesion, 67% lined with granulomatous
tissue
Is condensing osteitis a LEO?
rxn to chronically inflamed pulp
Eliasson, Halvarsson & Ljungheimer tx successfully and resolved with RCT
85%
Provide a differential diagnosis for the following:
Unilocular Periradicular Radiolucency:
PA Granuloma
PA Cyst
(Spatafore: 96% are lesion of endo origin)
PA Abscess
PA Fibrous Scar more frequent with thru & thru lesions or S RCT
Nasopalatine Duct Cyst max midline; > 6mm between central incisor roots
Traumatic Bone Cyst (IBC) not a true cyst; trauma etiology; mand teeth
Benign Fibro-osseous lesions (early stages) periapical cemental dysplasia,
focal cement-osseous dysplasia; central ossifying fibroma
Lateral Periodontal Cyst man premolar area (75-80%), max lateral
OKC, CGCG, Metastatic carcinoma
Mutiloculary Periapical Radiolucency: MACHO
Myxoma
Ameloblastoma aggressive neoplasm; any tooth-bearing area, but man most
common; peak age 30-40

41

Central Giant Cell Granuloma multinucleated giant cells; rule out

hyperparathyroidism
Hemangioma
Odontogenic Keratocyst post mand most common but may occur in any tooth
bearing area; multiple OKCs associated with Basal cell nevus syndrome
Periradicular Radiopacities
Condensing Osteitis LEO, PM or M in man, no RL border
Idiopathic Osteosclerosis idiopathic dense bone; vital pulps, man molar, no RL
rim
Benign Fibro-osseous lensions mixed RL/RO; centroal ossifying fibroma, focal
cemento-osseous dysplasia (post), PA Cemental Dysplasia (ant); vital pulps
Cementoblastoma attached to root with RL rim; neoplasm of cementoblasts
(Man 1st M)
Osteoblastoma neoplasm of osteoblasts; large osteoma (>2 cm); not attached to
root
Odontoma - compound (tooth like) or complex
Osteoma-root divergence, resorption, circumscribed sclerotic mass in body of man
Incidence of oral cancer?
4% of all cancers in US; 29,000 new case/yr
Most common sites: lat and ventral tongue, floor of mouth, oropharynx, lower lip
Leukoplakia-3% invasive SCC, Erythroplakia 50% invasive SCC

Anatomy Overview
Describe the Nerve supply to the teeth?
The Anatomic Basis of Dentistry
Brain stem Trigeminal nerve (cranial nerve V) 3 Divisions (I Opthalmic;
II Maxillary; III Mandibular)
Nerve supply to the Maxillary teeth:
Trigeminal nerve 2nd Div Maxillary nerve (foramen rotundum)
PSA Maxillary Molars
MSA Maxillary Premolars (MB root Max. Molar)
ASA Maxillary Anteriors
Nerve supply to the Mandibular teeth:
Trigeminal nerve 3rd Div Mandibular branch (foramen ovale)
IAN Mandibular Molars / Premolars Incisive branches Canines /
Incisors
Describe the blood supply to the teeth?
The Anatomic Basis of Dentistry
Arterial supply:
R atrium/R ventricle Pulmonary artery Lungs Pulmonary vein L
atrium/L ventricle Aorta Common Carotid artery External Carotid
artery Maxillary artery
Maxillary Posterior teeth: Pterygopalatine artery PSA artery
Maxillary Anterior teeth: Pterygopalatine artery PSA artery ASA artery
42

Mandibular Posterior teeth: Mandibular artery Inferior Alveolar artery

Mandibular Anterior teeth: Mandibular artery Inferior Alveolar artery
Incisive artery
Venous supply:
Veins from the Mandibular teeth Inferior Alveolar vein
Veins from the Maxillary anterior teeth Infraorbital vein
Veins from the Maxillary posterior teeth
Maxillary Vein Pterygoid venous plexus retromandibular vein Internal
Jugular vein Brachiocephalic vein Superior vena cava Heart (r. atrium)

Microbiology Overview
What causes periapical pathology?
Bacteria: Kakahashi lesions developed with exposed pulp in conv. rats &
not
germ-free
Moller lesions only developed in infected devitalized pulps in
monkeys
Sundqvist bacteria were necessary to cause lesions in human
teeth
*Host immune response mediates tissue and bone destruction in response to
bacteria (see inflammation section)
Lin- bacterial needed for development of PA lesions (dogs)
What is the general distribution of bacteria within the tooth?
Crown = Aerobes associated with caries: Strep mutans, lactobacillus,
facultative anaerobes - Moller
Mid-root = Mixed, Facultative species (Gram + rods/cocci): Staph aureus,
Actinomyces,
Lactobacillus
Apex = Anaerobes (Gram rods/Gram + cocci), Fusobacterium,
Porphyromonas, Prevotella, Eubactium, Peptostreptococcus
(Baumgartner, Sundquist)
What specific bacteria are involved the pathogenesis of a primary root canal
infection?
Siqueira polymicrobial w/ 10-30 species/canal, predominately gram
anaerobic rods (Porphyromonas species, T. denticola, Tannerella forysthius,
Prevotella, Fusobacterium nucleatum)
Ribiero- 66% species uncultivable in primary lesions, Siquiera says around
50%
Baumgartner Prevotella nigrescens most common BPB isolated
Fabricius - # of obligate anaerobes increase with time & nearer the apex
43

Gram - Anaerobic rods: Porphyromonas, Prevotella, Fusobacterium,

Treponema
Also Candida (Baumgartner) & HIV (Glick &Trope) found
What bacteria are more likely to infect a previously treated case?
Usually 1 -5 species, generally treatment resistant gram + facultative cocci
Sundqvist Avg. 1.3 species; E. faecalis frequently isolate according to
Gomes, Rocas, Sedgley
Nair Yeast / Candida involve in treatment failures
Gram + facultative cocci: Enterococcus, Streptococcus, Staphylococcus
Molander- gram + facultative anaerobes 69%; 32% E. faecalis
Gomes- E. faecalis 78% with PA lesions
Kaufman/Fouad-12% w/PCR; assoc more with normal periapex than lesion
Why are Enterococcus species resistant?
Love- able to invade dentinal tubules and adhere to collegen in the presense
of serum
Distal forms biofilm resistant to defense cells and antibiotics
Evans proton pump resists high pH of calcium hydroxide
Sedgley-entombed in tubules; can survive a long time without nutrition
Are any bacteria associated with symptoms?
No: Baumgartner No relationship between BPB and symptoms & signs
Yes: Gomes Association between Prevotella & Peptostreptococcus and pain
Sundqvist BPB associated with purulent infections
Nakamura Bacteroides and Poryphmonas more pain/odor
Griffee B melanonginacus to foul odor, pain, sinus tracts
Discuss the bacterial flora found in acute PA abscesses?
Siqueira Polymicrobial similar to primary infections BPB, Treponema,
Tannerella
Sundqvist BPB associated with purulent infections
Ferreira/Siqueira- HHV present in 67% of AAA aspirates (role of virus unclear)
Are bacteria found in PA lesions? Controversy?
Yes: Tronstad found extraradicular (anaerobes) in 8 refractory lesions
Wayman/Fowler (83%), Sunde/Tronstad (97%), Nair, Ricucci
cysts and abscesses but no PA granuloma
No: Walton histo study; confined to canal space
Nair histo study; criticized Tronstad for contamination
Siqueira SEM study; only 1/24 cases or 4%
Shindell (5%), Langland (14%), Walton (11%), Siquera (4%)
Does RCT cause bacteriemia?
Baumgartner very low incidence if confined to RC system 3.3% (3%/20%
if long)
Baumgartner-100% ext, 83% flap, 33% osseous resection (implied
bacteremia short-lived)
Bender- 0% in canal/31% if long; NONE after 10 min
44

Debelian-connected bacteremia with NSRCT (4/13 short, 7/13 long)

Are bacteria present in traumatized teeth with intact crowns?
Sundqvist Yes mixed flora with necrotic pulp; remaining had aseptic
necrosis; proposed bacterial entry through tubules and cracks (sterile
necrosis)
Does anachoresis occur?
Yes: Robinson & Boling cat study; inflammation & bacteria required
Gier bacteria attracted to inflamed pulps (IV injection of bacteria)
No: Doyle not demonstrated through IV injection of bacteria; cat study
Moller non-infected pulp did not induce PA inflammation; monkeys
Delivanis-need tissue in canals, unfilled canals didnt become infected
from bloodstream
What is prevalence of Actinomyces periapically. How treat?
Siqueira-up to 50% in primary infection, 3-24% in secondary infection
Happonen- PA surgery w/ complete curettage is definitive tx (suspect actino
if persistent sinus tracts after sound NSRCT)
Rush-86% healed with apical surgery alone (no abx)
Barnard-2-6 weeks abx; NaOCl and CaOH were effective
Discuss the methods used to study endo microbioloby?
Histology-limited to observing morphology, cant use alone to ID species
Culturing-not all species can be cultured, minor diff in culturing/exam can
influence results
Molecular method (PCR, DNA-DNA Hybridzation)-cant distinguish betw live
and dead bacteria, very technique sensitive (contamination problems);
HOWEVER can ID microbes that are not cultivable
PCR-(mid 80s)-amplifies nucleic acid sequences
DNA-DNA (mid 90s)-hybridizes DNA samples against DNA probes; no
amplification so minor contaminates not likely detected but not as good
detecting species in low numbers
Sedgley-molecular methods are more sensitive than culturing

Inflammation Overview
Discuss the focal Infection theory.
A localized or generalized infection resulting from a dissemination of bacteria
or toxic products from a foci of infection (necrotic pulp or dental abscess).
WD Miller(1890) introduced focal infection
William Hunter (1900) ignited the theory; multitude of diseases attributed
to focal infection
Frank Billings(1912) introduced focal infection to American physicians
(started era)
Reimann & Havens (1940) critique of theory unproven
Torabinejad - chronic periapical lesions cannot act as a focus to cause
systemic diseases via immune complexes.
45

Siqueira (2002) no clear evidence that microorganisms from the RC can

cause disease in remote sites of the body
Describe the Zones of Fish.
Necrosis / Infection bacteria, PMNs
Contamination bacterial toxins, lymphocytes, macrophages
Irritation osteoclasts, lymphocytes, macrophages
Stimulation osteoblasts, fibroblasts
What is the role of neuropeptides?
Cause neurogenic inflammation, regulate pulpal blood flow
Byers demonstrated sprouting of CGRP nerve fibers after dental injury
Caviedes-Bucheli-SP, CGRP, NKA, NPY, VIP found in pulp; neuropeptides
regulate pulpal blood flow and involved in development of neurogenic
inflammation/pain; NPY(sympathetic/vasoconstrictive) &
VIP(parasympathetic/vasodilation)
Who studied LPS and what is its role in PA pathology?
Schein & Schilder pulpless teeth endotoxin (LPS) than vital pulps;
symptomatic teeth and those with PARL have LPS than asymptomatic teeth
Martino-chemomech prep reduced bacterial load 99.8%, but only 60% LPS,
if remove smear layer than 98% reduction in LPS
Schonfeld-LPS found outside canalcan account for PA dz even if viable
bacteria not present
Martinho - 1 infect had 2x more endotoxin vs 2; more endotoxin = more
pain & bigger PARLs
Horiba- LPS can penetrate up to 800 um into tubules but usually only 3-400
-- why removing smear layer is important before CaOH fill
Diogenes- LPS can sensitize TRPV1 via TLR-4 receptors in TG neurons
causing nociceptive sensitization and inflammation
What are cytokines and which are involved in bone resorption? Any other
factors involved?
Polypeptide products of immune cells. They modify behavior of other cells,
produce systemic effects & act as growth factors
Stashenko (rat studies) bone resorbing activity is due to cytokines rather
than LPS
Cytokine involved in bone resorption alone or in synergistic combination: IL1beta, TNF alpha & PGE2;
Wang&Stashenko-OAF: IL-1a, IL-1B, TNFa, TNFB, IL-6, IL-11 (IL-1B (60%)
TNFB most responsible)
Torabinejad - arachidonic metabolites and the complement system play an
important role in bone resorption

Immunology Overview
Discuss the 4 types of immune rxns?

Type I Anaphylactic (Immediate-Type) Rxn IgE mediated; binds to basophils & mast
cells which release inflammatory mediators (allergic rhinitis & asthma)

46

Type II Cytotoxic Rxn IgG & IgM mediated; triggers complement or phagocytosis
(autoimmune hemolytic anemia, some organ rejection & idiopathic thrombocytopenic
purpura)
Type III Immune Complex (Ag-Ab) Rxn Ag-Ab complexes activate complement; (Arthus
type large complexes within blood vessel; serum sickness-type small & soluble
complexes which pass into the tissues)
Type IV Delayed-Type Hypersensitivity no Ab required; cell mediated immunity;
macrophages and Killer T cells recognize Ag bearing cells; Involves memory T cells;
4
types: 1) chronic infection of intracellular bacteria, viruses & fungi
2) contact dermatitis
3) graft rejections
4) autoimmune diseases
Torabinejad Ag-Ab complexes & IgE mediated rxns can initiate changes in PA tissues; type
IV rxns may be involved in PA lesion progression

Discuss the complement cascade.

C consists of some 20 interactive plasma and cell membrane proteins. Once

activated:
1. Mediate vascular responses (histamine release via C3a and C5a
anaphylatoxins)
2. Recruiting phagocytic leukocytes
3. Opsonizing targets of phagocytic cells (C3b)
4. Directly damaging target cells (C5-9 MAC)
Most important step is cleavage of C3.
Classical pathway is activated by Ab coated targets or Ag-Ab complexes (IgM, IgG)
Alternate pathway is activated by LPS, aggregated IgM or IgG, Ag-IgA complexes,
plasmin
Which immune components are found in the dental pulp?
Jontell T & B lymphocytes; Plasma cells; Macrophages; Dendritic cells; Cytokines
& Prostaglandins
Are antibodies found in the pulp?
Nakanishi levels of IgG, IgA, IgM, elastase & PGE2 were higher in inflamed pulps
than in normal pulps
Which immune components are found in the periapical tissues?
Nilsen Lymphocytes, Macrophages, plasma cells Mast cells, NK cells
Schein Lymphocytes, macrophages, PMNs, plasma cells
Pulver Igs (see below)
Stashenko Lymphocytes (T,B,NK cells), macrophages, PMNs, plasma cells,
eosinophils, mast cells, antibodies (IgG, IgA, IgE, IgM)
Which antibodies predominate in a periapical lesion?
Pulver IgG (70%)>A(14%)>E(10%)>M (4%) for cysts and granulomas; IgE cells
had degranulated mast cells nearby
Discuss immune system
Innate immune system provides immediate, but non-specific response (Neutrophils,
macrophages, DCs). If pathogens successfully evade innate response, the adaptive
immune system is activated to improve recognition of pathogens (T and B cells
lymphocytes)

47

Antigen (Bacteria/virus)Ag presenting cellIL 12Th1cell mediated (PMN,

macrophages)
CD4+ T cellIL 4Th2humoral immunity (B cellsPlasma
cellsAbs)

Pain Overview
Trace the pain perception originating from a tooth?
Narhi - A-fibers are responsible for sharp pain (direct dentin stimulation,
osmotic, temperature changes). C-fibers are activated only if the external
stimuli reach the pulp proper and may be responsible for dull, diffuse pain
(intrapulpal pressure, increase in pulpal temperature, inflammatory
mediators). Prepain sensations induced by electrical stimulation result from
activation of the lowest threshold A-fibers
SessleNoxious stimuli nociceptors in pulp A-delta / C-fibers (primary
afferent fibers) inferior alveolar n (man)/max n via PSA, MSA or ASA n
(max) trigeminal ganglion nucleus caudalis in medullary dorsal
horn of spinal trigeminal nucleus (second order projection neuron- wide
dynamic range neurons) cross midline to the thalamus via the
spinothalamic tract (third order neuron) cerebral cortex via the
thalamocortical tract (pain perception)
Neurotransmitters: glutamate, SP, CGRP
Define Allodynia, Hyperalgesia, and Central Sensitization:
Hargreaves Allodynia reduction in pain threshold so that non-noxious stimuli are painful
(cold sensitivity & chewing discomfort)
Hyperalgesia the response to noxious stimuli produces more pain than it
would normally (exaggerated response to endo ice)
Central sensitization-increased excitability of central neurons (2nd/ 3rd order)
from a barrage of impulses from C nociceptors so that normal inputs produce
abnormal responses also neurogenic inflammation can cause spontaneous
depolarization of central neurons, also incr size of receptive fields)
Owatz- 57% pt w/ IP have mech allodynia, Pacheco showed 67%-IP, 56%necrosis (unpub)
What is neural sprouting?
Byers - Changes in neural structures occur after most dental injuries.
Analysis of the progressive stages of pulpal abscess and necrosis showed
sprouting CGRP nerve fibers (a) at the retreating interface between abscess
and vital pulp; (b) in periapical areas during onset of lesions; and (c) around
chronic abscesses in granulomatous periodontal tissues.
(Sprouting incr density of innervation in inflamed tissue and leads to incr
pain sensitivity)
Discuss referred pain:
Sessle
48

Convergence Referred pain caused by afferent input from cutaneous and

visceral nociceptors onto the same projection N (i.e., nociceptors from the
max sinus and max molar projecting to the same projector N in nucleus
caudalis).
Travell - Myofascial pain & Trigger zones:
Superior belly of masseter referred to maxillary posterior teeth.
Inferior border of masseter referred to mandibular posterior teeth.
Wright- 3% of TMD pts had acute pulpalgia; 12% TMD pts had referred pain
to teeth
What are some nonodontogenic causes of tooth pain?
Hargreaves: musculoskeletal (MFP, TMD), neuropathic (TN, AO),
neurovascular (migraine, cluster HA), inflammatory (sinusitis), systemic d/o
(cardiac, Herpes, tumors, DM), psychogenic

Pharmacology Overview
Discuss the mechanisms of commonly prescribed antibiotics:
Cell wall inhibitors:
Penicillins bactericidal; inhibits bacterial cell wall synthesis
Augmentin (Amox + Clavulanic acid): clavulanic acid binds and inhibits
beta-lactamases (produced by some bacteria) that inactivates amox
resulting in expanded spectrum of activity
Cephalosporins may have cross reactivity with Pen allergic pts
Anti-ribosomal Inhibit protein synthesis:
Clindamycin bacteristatic/cidal (based on dosage); inhibits protein
synthesis by binding to 50S ribosomal subunit; strong bone penetration
(Vacek)
Azithromycin, Erythromycin - inhibits protein synthesis by binding to 50S
ribosomal subunit
Tetracyclines inhibits protein synthesis by binding to 30S ribosomal
subunit
Inhibitors of Nucleic Acid Synthesis:
Metronidazole inhibits nucleic acid synthesis; ineffective against
facultative anaerobes; added to penicillins if ineffective
Discuss antibiotic susceptibility:
Baumgartner susceptibility from isolated endo infections (98 bacterial
species):
Pen V 85%; Amox 91%; Augmentin 100%;
Metronidazole 45%; Pen + Metro 93%; Amox + Metro 99%
Clindamycin 96%
What is first choice of abx in dental infection?
PCN-narrow spectrum, effective against RC bacteria, efficacy in polymicrobial
infection
49

PCN- effective against g(-) anaerobes, g(+) aerobes and facultative

anaerobes
+Metronidazole if ineffective after 48-72hrs: MTN affective against g(+)
anaerobes, no aerobes
Are antibiotics a concern with birth control pills?
Hersch Rifampin is only known antibiotic to inihibit bcp; discuss possibility
with pt
Bainton-effect of bacterial flora in gut (PCN)
Discuss non-opiod analgesics:
flexible prescription plan
NSAIDS Non-selective COX inhibitors inhibits synthesis of prostaglandins
and thromboxane
Acetominophen cannabinoid receptor agonist centrally; peripherally blocks
pain impulse; produces antipyresis by inhibition of hypothalamic heatregulating center
Menhinick combining APAP w/ NSAID better than ibuprofen alone in post
op pain
Wells/Reader- NSD of NSAID/APAP vs NSAID alone is post-op pain in
necrotic cases
Discuss opiod analgesics:
Potency: Codiene < Hydrocodone < Oxycodone
Activate opiate receptors in the CNS & inhibit release of excitatory pain
transmitters
Side effects: nausea, dizziness, drowsiness, respiratory depression &
constipation
Discuss anxiolytic therapy:
Hargreaves & Dionne Triazolam safe & effective for dental outpatients,
equal to 19 mg Diazepam in sedation quality
Berthold- greater anxiety reduction with sublingual route of admin; 28%
more bioavailability

Prognosis / Outcomes Overview

When should pts be recalled?

Orstavik 1 yr; peak incidence of healing / CAP occurred @ 1 yr; may take 4 yrs
Rud/Andreasen 1 yr; wait 4 yrs for uncertain healing cases
How long does it take a lesion to heal?
Murphy Avg. rate is 3.2mm/mo.; >70% require >12mo
What factors may be detrimental to a successful outcome?
Crump (POOR PAST AM): Perforation, Obturation; Overfill, Root canal missed, Perio
disease, Another tooth, Split tooth, Trauma, Anatomy complex, Microleakage
Friedman Toronto study: NSRCT Pre-op lesion
RETX Pre-op lesion, perforation, fill quality, restoration
S RCT lesion > 5mm quadrupled risk
What are reasons for continued thermal pain following RCT?
Keir-missed canals

50

Tidwell-1) inadequate C&S, obturation, 2) missed canals, 3) sliver cones in contact

with coronal restoration, 4) metallic GP carriers in contact with
oral/pulpal/periradicular tissue, 5) broken metallic instrument in contact with apical
vital tissue, 6) Defective coronal restoration, 7) Referred pain from another tooth
Do the radiographic healing correlate to histologic healing?
Byrnolf No; only 7% demonstrated no inflammation
Green, Walton Yes; 74%
Is bacterial culturing indicated? Does it influence healing?
Sjogren & Sundqvist 94% success w/ -culture; 68% w/ +culture; regardless, they
state modern anaerobic culturing techniques are not readily available, nor are they
required
Seltzer and Bender- no diff: 84% (- culture) vs 81% (+ culture)
Molander-80% vs 49%; removal of bacteria important but not # of appts
Peters & Wesselink found NSD between 1 or 2 visit, or between + and cultures
What are reasons for failure of NS RCT?
Intraradicular infection Nair main reason for failure is microbes persist in canals
Extraradicular infection Siqueira rare / Nair Actinomycosis
Foreign body rxn Nair root filling materials
Cysts Nair possibly with cholesterol crystals
Nair-1) intraradicular infection persisting (fungus, E. faecalis), 2) Extraradicular
infection (Actino, viruses), 3) Extruded RC filling or other exogenous material that
cause foreign body rxn, 4) Accumulation of cholesterol crystals (18-44%), 5) True
cysts, 6) scar tissue
Crump POOR PAST (Perf, obturation inadequate, overextended, root canal
missed, perio dz, another tooth, split/fx tooth, trauma) also microleakage
Does the level of root canal fill influence success/failure?
Seltzer & Bender Overfill decreased success (71%); flush/underfill had no
influence (87%,87%)
Ng meta-anaylsis shows w/in 2mm of apex improved success
Schaefer and Walton-meta analysis: 0-1mm best, >1-3 mm; both better than long
Sjogren-0-2mm 94%, > 2mm 68%, long 76%
Is 1 or 2-visit treatment more successful?
Peters & Wesselink NSD
Weiger, Rosendahl & Lost NSD for teeth with AP treated in 1 visit or with 1 wk
Ca(OH)2
Figini-meta analysis: NSD; 1 appt more post-oper pain meds and swelling
Sathorn/Messer-sys rev w/ ma: NSD; 1 appt had 6% more success
Success differences between GPs and Endodontists?
Alley-endodontists had 10% higher success rates
Lazarski similar success rates, but endodontists had sig harder cases, GPs had sig
more failure of surg RCT
What may affect prognosis of NS RCT?
Fouad-DM decreases success, more flare-ups
Polycarpou-chronic pain 8.6X risk factor for post endo pain
Marending-conditions affecting immune response (DM, renal insufficiency, breast
cancer), pre-oper lesion (PAI score), quality of fill all factors leading to decreased
success

51

Ng, Gulabivala- Age assoc with decreased healing; Improved outcome of NSRCT:
absence of pre-op PARL, root fill with no voids, root fill w/i 2 mm of apex, good
coronal seal (ie crown), M/D contacts
Chen-HTN decreases healing
Nasstrom-high doses of corticosteroids lead to significant PCO and pulp
calcifications
Galili-PCO assoc with hemodialysis
Eleazor-pulp stones assoc with atherosclerosis
Gillen Sys Review on coronal restoration, GE/GR has 3x more success

OUTCOME
STUDIES
TX

STUDY

FAVORABLE PROGNOSIS RATE

NSRCT

Friedman
Washington Study
(Ingle)
Sjogren
Seltzer and Bender

92-98% (74-86% w AP)

Epidemiological Studies

Salehrabi & Rotstein

Lasarski
Chen

97% functional success @ 8 yrs (1.5 million)

94% @ 3.5 yrs (110,000)
93% (1.6 million)

Length of obturation

Seltzer and Bender

Sjogren
Schaefer and Walton

Flush 86.5%, underfill 87%, overfill 71%

<2mm short 94%, overfill 76%, >2mm short 68%
0-1mm better than 1-3 mm short; both > long

Perforation Repair

Mente
Main

86% at aver 3yr

100% with MTA

RE-TX

Friedman
Salehrabi
Torabinejad
Gorni and Gagliani

No AP: 92%; AP : 80-85%

89% survival at 5 yrs
83% at 4-6 yrs, sys rev and M/A
87% if RC morph respected, 47% if not

S RCT

Setzer (SR w/ m/a)

Rubinstein, Kim
Torabinejad
Frank
Kim/Song

94% using contemporary tech, 59% using historical

SuperEBA 91.5% (5-7yrs.)
73% at 4-6 yrs (sys rev & M/A include hist tech studies)
58% w/ Am at 10 yrs (of those initially successful)
90% with SOM and IRM, EBA or MTA at 6-10 yrs

2nd S RCT

Gagliani and Gorni

59% (86% 1st surgery) at 5 yrs (complete healing)

Song/Kim

93% (1st surg failure assoc with history tech/materials

Root AMP
Root resection

Fugazatto
Langland

97% surv at 13 yrs, D root of man molar was worst-75%

62% at 10 yrs

Int Replant

Bender, Grossman

81%, 80%

IPC

Mertz-Fairhurst

70% at 10 years

92%
96%/86% w AP
92% (76% w AP)

52

Marchi
Thompson

89% with Dycal/SBMP/cmpst; 93% w/ Vitremer

Meta-analysis: advocated IPC

Barthel
Haskel and Stanley
Bogen
Aguilar (metaanalysis)

55% at 5yrs, 21% at 10 yrs (carious exposure)

87% at 11.7 yrs
98% w/MTA at 9 yrs

Cvek
Fuks
Witherspoon
Aguilar (metaanalysis)

96% (young incisors)

94% success - CaOH
95% w MTA

Cvek
Witherspoon

96% -Ca(OH)2 long term

93.5% 1 visit, 90.5% 2 visit -MTA

Fuks

FC -84%; FeSO4 -93%; MTA -97%

Coll

78% ZOE: no resorption 92%, min resorption 83%, excessive

Doyle
Iqbal and Kim

Woodmansey

NSD - 94%, implants 5X more post-oper interventions

Meta analysis NSD implant/crn 96%, RCT/crn 94%
NSD survival or success; implants more surg intervention (1
vs 1.4%)
Implants less max biting force, chewing efficiency, and smal
areas of contact than RCT/crn

Internal Bleaching

Glockner
Abou-Rass

98% -pt. subjective success

93% at 3-15 yr follow-up

Systemic Disease

Morsani

IL-1 beta polymorphism 7x incr risk of persistent AP

Pre op lesion (12x), poor RCT quality (12x), and innate immu
deficiency (8x) sig assoc with persistent AP
No decreased success in AIDS pts taking HAART
Diabetes is sig risk factor for persis AP

DPC

Cvek Pulpotomy

Apexification

Pulpotomy (primary
teeth)

MTA-90%, CaOH 71% (SS); open apex 94%, closed 69%

CaOH 94%, MTA 87% (SS)

Pulpectomy

Implants vs. RCT

Hannahan & Eleazor

Marending
Quesnell
Fouad

Regenerative Endodontics Overview

History - based on the trauma lit of avulsion (open apex without
contamination = contd root development
Nygaard-Ostby role of the blood clot in wound healing
Iwaya 2001 dens evag case report using DAP (found root development by
accident, pt never came for completion of tx)
Banchs & Trope 2004 dens evag (1st case report of intentional regen)
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Discuss how regenerative endo may be achieved?

Hargreaves
1. Achieved most predictably in teeth with open apices
2. Instrumentation with NaOCl irrigation is not sufficient to reliably create
the conditions necessary for revascularization of the necrotic tooth
3. Ca(OH)2 placement prevents revascularization coronal to paste
4. The use of (3 mix-MP triple antibiotic paste, developed by Hoshino
(consisting of cipro, metronidazole & minocycline) is effective for disinfection
of the necrotic tooth, setting the conditions for subsequent revascularization
3 major components of tissue engineering:
1. Cell source i.e. apical papilla
2. Physical scaffold i.e. blood clot or PRP
3. Signaling molecules
What is the technique for regeneration?
Banchs & Trope- 1st to described technique
1. Flush canal with 20ml NaOCl, 10 ml CHX (no filing) Can use saline in
between
2. Triple abx paste: 200 mg cipro, 500 mg metronidazole, 100 mg
minocycline (3-4 weeks); combine with sterile water for creamy mix;
place in canal (lentulo)
3. Flush canal with 10ml NaOCl
4. Initiate bleeding into canal (endo explorer, large file) 3 mm below CEJ,
allow blood clot to form (15 min)
5. MTA, wet cotton pellet, tem access restoration
6. Permanent access restoration
Do irrigants affect stem cells?
Trevino EDTA best, CHX worst
Galler final irrigation with 17% EDTA is best
What are the current recommended concentrations for NaOCl and TAP/DAP in
regen?
AAE recommendations 2013 1.5% NaOCl (lowest concentration for

antibact and tissue dissolution properties) Harrison & Hand

Ruparel TAP or DAP @ 0.01-0.1 mg/ml or Ca(OH)2 **Ca(OH)2 promotes
survival and potentiates proliferation**
Hoshino showed antibact against endo bugs at 0.001mg/ml
What can we do to minimize or treat staining in regen?
Akbari apply dentin adhesive to chamber walls prior to MTAplacement
Kim adhesive reduces TAP staining, but does not prevent it completely
Ilya case report of internal bleaching after staining w/white MTA
What else can be used besides triple antibiotic paste?
Cheuh-used CaOH instead of trip abx paste
Shah-used Formocresol cotton pellet instead of trip abx paste
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Bose & Hargreaves-Regen with Trip abx paste and CaOH produced sig
greater increases in root length than MTA apexification or NSRCT; Trip abx
produced greater wall thickness than CaOH or formocresol; depth of CaOH
placement correlated to dentinal wall thickness (54% increase if restricted to
coronal half vs 3% if beyond coronal half)
Shin-case report of successful revascularization without use of CaOH or
triple abx paste, just MTA seal
What are we looking for in success Regen?
Law - Clinical and Radiographic exam:
No pain or soft tissue swelling (often observed between first and
second appointments)
Resolution of apical radiolucency (often observed 6-12 months after
treatment)
Increased width of root walls (this is generally observed before
apparent increase in root length and often occurs 12-24 months
after treatment)
Increased root length
apical closure?
Who talked about the tissue engineering triad and what are the components?
Nakashima stem cells, growth factors and scaffold
What is the source of stem cells in regendo?
Huang stem cells located in the apical papilla are viable following necrosis
Sonoyama identified SCAP as mesenchymal stem cells (STRO1) and
demonstrated ability to differentiate into odontoblast-like cells
Lovelace recruitment of stem cells with evoked bleeding
What has been proposed as a scaffold?
Thibodeau blood clot
Torabinejad - PRP
Where are the growth factors and how do we access them?
Anthony Smiths work TGFbeta is present in dentin, acid etching can
expose TGF beta on surface
Galler dentin conditioning with EDTA promoted adhesion and odontoblastlike differentiation
What is the characteristic of the tissue formed with regenerative Tx?
Wang cellular cementum-like tissue
Yamuchi- dog study, 2 mineralized tissues formed in canal, 1 cementoid, 1
osteoid
Shimizu 2012 (human histo) - odontoblast-like cells lining predentin with
blood vessels and loose connective tissue with collagen fibers in the canal
3.5 weeks after regenerative
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Iohara 2011 - Removed the pulp tissue of fully formed teeth, enlarged the
apex and implants stem cells with growth factors. By day 14, there was
complete pulpal regeneration. Used RT-PCR and histology to evaluate the
tissue formed. (SDF-1 is growth factor used to promote neovascularization)
**highlights importance of tissue engineering to promote desired tissue**
Do we have any outcome studies for prognosis of regen?
Mahidol first outcome study 14-27 months compares survival of regen
(100%) to MTA apexification (94%) and Ca(OH)2 apexification (77%). Succes
of Tx (healed/healing/failed) regen (80% / 20% / 0) MTA (68% / 26% / 6)
Calcium hydroxide (77% / 0 / 23%). Also confirmed Bose findings that
increase in width with regen is 2x increase in length.

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