Index Card Literature Guide

2014 Update

Dr. Matthew S. Detar

Contributions by: Drs. Richard D. Archer and Tareq Al-Ali

Original Guide by: Drs. Randy Todd, Colleen Shull, and Steven Tsoucaris

History of Endodontics


1943 AAE begins (Clyde Davis-1st president)

1963 Endodontic specialty recognized by ADA

1956 ABE begins

1965 1st ABE board exam

1st in Endodontics:

Hermann (1930): Introduced Ca(OH)2 - vital pulp cap; Frank: Apexification

Coolidge (1919): Introduced NaOCl as tissue solvent (Dakin’s Solution)

Nygaard Ostby (1957): Introduced EDTA for dentin softening

Imperial Chemical Industries (1940s).: Introduced CHX

Barnum (1864): Introduced concept of Rubber dam

Bowman: Introduced GP for obturation, Rubber dam forceps

Koller: Proposed Cocaine as anesthetic

Einhorn (1906): Procaine (novocaine) introduced

Maynard: Developed broach

Arthur: Introduced barbed broach

1st in Endodontics:

Harry B. Johnston: Created term “Endodontia”; 1st Endodontic Office

Clyde Davis: 1st president of AAE

Otto Walkhoff: 1st dental radiograph, CMCP as pulpal antiseptic

Ingle (1961): Standardization of GP and instruments

Miller; Hunter: Introduced Focal Infection Theory, Billings: Introduced Focal Infection Theory to USA

Pfaff: Introduced pulp capping

Codman: Concept of secondary dentin in pulp cap healing

Buckley: Developed Formocresol for pulpal antiseptic (“Buckley’s solution”)

Jasper: Silver points

Hudson: 1st to obturate canal (gold)

Hill: Introduced Hill’s stopping (GP, carbonated lime, quartz) for obturation

Perry: 1st carrier based obturation (Goldwire/GP for obturation), see also Wm Ben Johnson: Thermafil

Callahan: Introduced chloropercha technique for obturation


AAE Terminology


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 (sensibility) 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 than 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).

NOTE: See AAE Glossary of Endodontic Terms for further definitions


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/or percussion or palpation. 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.

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.

Radiological Exam

A.  Vital case w/ AP – Stashenko; Yamasaki; Byers (CGRP sprouting)

a.  Torbijork – C fibers resistant to hypoxia/necrosis

B.  Bone loss & AP – Avg 7.1% MBL, 12.5% CBL – Bender 1982

C.  Digital Comparison studies

a.  Film vs digital – root length – NSD – Pitt Ford

b.  Film vs digital – PARL det. – NSD – Mistak/Loushine

c.  Digital (filtered) > D speed – Cortical lesion – Hadley/Replogle

d.  Film vs digital – WL measurement – NSD – Lamus/Katz

e.  Digital (Kodak) > Film – WL (10,15 k) – Goodell/McClanahan

f.  80 – 90% radiation reduction w/ digital – Soh

D.  Lamina dura – Most consistent feature aiding dx of PAP – Kaffe

a.  Strindberg – PDL width/shape, Lamina dura aids dx of PAP

E.  Radiographic Interpretation accuracy –

a.  Brynolf - accuracy increases with added films, 1=74%, 3=87%

b.  Goldman – 47% interobserver, 75% intraobserver (6-8 mo later)

c.  Tewary/Hartwell – digital PAs – 35% interobserver agreement

F.  Technique - Paralleling > Bisecting Angle – WL – Forsberg


-Coneshaped beam captures variable size cylindrical/spherical volume data (FOV)

-Isotropic cubic Voxels (3-D pixels) comprise the image

-3 Orthogonal planes: Axial, Coronal, and Sagittal; Multiplanar reconstruction

-Spatial Resolution is less (2 line pairs/mm) than digital PA (7-25 line pairs/mm)

Diagnosis: Hassan – Axial view best for VRF detection

1.  Patel 2007 – Applications for CBCT & Endo:

·  Detection of PA changes & Diagnosis (PRE-OP)

·  Anatomical anomalies (i.e.: Dens), Resorptive lesions

·  Treatment complications – Perforations, VRFs, sep instruments

·  Pre-surgical planning

·  Healing/Treatment Outcomes (POST-OP)

2.  Simon 2006 – Large PARL, Granuloma vs. Cyst; CBCT (grey scale) >Biopsy

3.  Bernardes/Azevedo 2009; Ozer 2010 – VRF detection: CBCT > Digital PA

4.  Ozuk 2011 – Accumoto 93% accuracy VRF (confirmed via Sx/RETX)

5.  Ee/Johnson 2014 – CBCT>Digital PA Diagnosis: VRFs, Resorption, Perforations, PARLs- 83% vs 36%. CBCT changed recomm. tx 60% of time

6.  Blattner 2010 – MB2 detection: CBCT = Sectioning (gold standard)



1.  Ludlow 2006/AAE 2011 – Kodak: Effective dose (mSv): Max Ant: 4.7, Max Post: 9.8, Mand Post: 38.3; 1 dig. PA: 6, FMX: 171, Background (day): 7-8

CBCT vs. PA Radiograph (PARL detection):

1.  Velvart 2001 – Mand. Molars, CBCT 100%, E speed PA 78%

2.  Lofthag-Hansen 2007 – CBCT 100%, F speed PA 62%

3.  Bornstein/Von Arx 2011 – Mand. Molars, CBCT 100%, F speed PA 75%

4.  Tsai/Torabinejad 2012 – Simulated lesions (0-1.4 mm), CBCT > Digital PA

CBCT vs. PA Radiograph (Mandibular canal detection):

1.  Velvart 2001 – Mand. Molars, CBCT 100%, E Speed PA 61%

2.  Bornstein/Von Arx 2011 – Mand. Molars, CBCT 100%, F speed PA 35.3%

Working length:

1.  Jeger/Bornstein 2012 – NSD using CBCT and Digital PAs for FWL

Subjective & Objective Examination

A.  Reeves/Stanley – Irrev. pulpitis - caries w/in 0.5mm of pulp or reparative dentin

B.  Tronstad – direct pulp cap is only 50% successful (= Irrev. Pulpitis)

C.  Barthel – direct pulp cap (CaOH2) – 5 yrs: 40% fail, 10 yrs: 80% fail

D.  Cvek – Cvek (partial) pulpotomy (trauma/2 mm/7 days) = 96% success

E.  Kretzschmar – referred pain may come from Max. sinus (Rhinosinusitis)

F.  Cold test

a.  Rickoff/Trowbridge – no pulp injury Cold CO2 5 min, Heat 10s

b.  Miller – RS(TFE) > CO2 Pulp temp red; PFM/All Ceram/Gold Crns

c.  Jones/Rivera/Walton – RS Faster response than CO2 snow

d.  Petersson – Overall accuracy: Cold 86%, EPT 81%, Heat 71%

i.  Sensitivity (test identifies disease): 83%, 71%, 86%

ii. Specificity (test identifies healthy): 93%, 93%, 41%

iii.  Pos. Predictive Value (given test states diseased, probability subject is diseased): 89%, 88%, 48%

iv.  Neg. Predictive Value (given test states healthy, probability subject is healthy): 90%, 84%, 83%

e.  Villa-Chavez 2013 – Cold>Heat>EPT – Accuracy, Reproducibility

f.  Trowbridge – mode of action Cold test – hydrodynamic theory

G.  Cold + EPT

a.  Peters/Baumgartner - Cold neg + EPT neg = True Necrotic

b.  Weisleder/Trope - RS + CO2 + EPT: All 3 tests positive (NPP): 97% vital, All 3 tests negative (PPP): 90% necrotic; Cold + EPT ­ accuracy

H.  Barodontalgia –pain caused by change in pressure (flying/diving)

a.  Senia/Cunningham – inflammed vital pulp tissue

b.  Fenjensick – 86% faulty restorations

I.  Histopathologic correlation with testing & clinical symptoms

a.  Seltzer/Bender; Dummer – no correlation btw diagnostic tests (except PN) & histo pulp status and clinical signs/symptoms & histo pulp status

J.  Localization of Pain:

a.  Friend/Glenwright –37% patients could localize symptoms to offending tooth, to 3 teeth 80% (EPT stimulation – Vital teeth)

b.  McCarthy/McClannahan –73% patients could localize symptoms to the offending tooth (Irreversible Pulpitis); 90% Perc + patients, 30% Perc - patients; 100% No midline cross; ­pain (VAS) = ¯ localization

K.  Mechanical Allodynia (percussion sensitivity):

a.  Khan/Hargreaves – 67% Irrev. Pulpitis, 57% Pulp Necrosis

b.  Owatz/Hargreaves – 57% Irreversible Pulpitis

Vitality testing = Sensibility testing = pulpal nerve status only

*** Does not evaluate blood/vascular supply***


a.  Fulling/Andreasen; Fuss/Trowbridge – immature developing teeth, unreliable response to EPT, use CO2 snow/RS (Higher EPT thresholds/late innervation of plexus of rashkow)

b.  Bhaskar – trauma cases - EPT, cold and heat tests – unreliable (due to nerve damage w/out altering blood supply)

c.  Fuss/Trowbridge –EPT unreliable w/ large restoration


a.  Narhi- Mode of action – low threshold Aδ fibers (prepain sensation) – ionic fluid shift

b.  Abdel Wahab- Technique - slowly increased current- more accurate

c.  Mumford – No relationship between EPT value and pulp histopathology

d.  Bender – test Incisal Edge in Anterior teeth

e.  Jacobson – test Middle 1/3rd F -Incisors, Occlusal 1/3rd B -Premolars

Heat test:

a.  Schindler – used on refractory (persistent AP) cases to identify missed canals or late stage of irreversible pulpitis

Laser Doppler

LDF = Use of infared beam of light – scatters by Doppler principle when interacting with moving RBCs – photodetector reads this Doppler shifted backscattered light = Index of pulpal blood flow

1.  Yanpiset/Trope 2001 – dog study, avulsion/reimplantation - detect return of pulpal blood flow by 4 wks

2.  Gazelius 1988 – case report, Lateral luxation 4 lower incisors – detected blood flow 6 wks (partially), 9 mos (complete)

3.  Chandler/Sundquist 1999 – case report: LDF – Dx: Periapical COD

4.  Mesaros/Trope 1997 – case report: 8 yr old, luxation #8,9 – LDF- vital

5.  Tronstad 1994 - LDF 91% accurate, more accurate than EPT (64%)

Pulse Oximeter

Pulse Ox = 2 light emiting diodes at 2 wavelengths (red, infared) transmit light through vascular tissue, absorbed selectively by oxygenated and deoxygenated hemoglobin, photodetector reads unabsorbed light = Oxyhemoglobin (HgO2) Saturation of Arterial blood

1.  Gopikrishna 2007 – Compared Pulse Ox to EPT and Cold tests for recently traumatized (uncomplicated crown fractures, concussions, subluxations only) maxillary incisors (day 0 to 6 months post trauma); Pulse Ox signficantly improved ability to detect pulp vitality (intact vascular supply) day 0 – 1 month

2.  Setzer 2012 – Evaluated Pulse Ox for determining pulpal conditions: Normal pulp, Reversible pulpitis, Irreversible pulpitis, and Pulp necrosis. Statistically significant differences in mean pulp oxygenation levels for each pulpal condition – possible method to determine pathological process within pulp

ASA Classification

I.  A normal healthy patient

II.  A patient with mild to moderate systemic disease

III.  A patient with severe systemic disease that limits activity but is not incapacitating

IV.  A patient with severe systemic disease and is a constant threat to life

V.  A moribund patient not expected to survive 24 hours with or without an operation.

Glickman – Classification of furcation involvement

Class I – Incipient lesion

Class II – Bone destroyed on one or more aspects of furca, partial penetration of probe into furcation

Class III – Interradicular bone absent but orifice of furca is occluded by gingival tissue, complete penetration of probe through furcation

Class IV – Furca opening visible

Mobility – Miller Index Classification

Class I - barely perceptible

Class II - < 1 mm movement

Class III - > 1 mm movement/depressible in socket

Does periodontal disease cause pulpal disease?


1.  Seltzer – Yes, bacteria can pass through lateral/accessory canals

2.  Rubach/Mitchell – Yes, bacteria can pass through lateral/accessory canals

3.  Wong – Pulpitis adjacent to areas of scaling/root planing (Perio tx)


1.  Langeland – Only when Apical Foramen involved

2.  Bergenholtz - No

3.  Mazur/Massler – found no relationship between pulpal & periodontal disease

Gutmann – 28% Molars – Furcation Canals (see also de Deus - 27% accessory)

AAE definitions:

Accessory Canal – Any branch of the main pulp canal or chamber that communicates with the external surface of the root

Lateral Canal – Accessory canal located in the coronal or middle third of the root

Simon’s Classifications for Endo-Perio Lesions

1.  Primary Endo: Necrotic pulp, CAA drains into sulcus/furca = Narrow isolated PD; mimics VRF, Perio Abscess

2.  Primary Perio: Vital pulp, Wide PD defect, Angular/may involve several teeth; Prognosis depends on Perio Tx

3.  Primary Endo + Secondary Perio: Necrotic pulp, CAA drains into sulcus/furca + Plaque/calculus at gingival margin = solitary, wider PD

4.  Primary Perio + Secondary Endo: (Controversial) Wide PD defect extending to AF ® IP/PN; Prognosis depends on Perio Tx

5.  True Combined: PN + Perio = Endo lesion (apically) meets perio lesion (cervically); Extensive bony destruction, Wide defects, May involve multiple teeth; Prognosis depends on Perio Tx

6.  Concomittant Endo Perio Lesion (added later): Separate and Distinct Endo and Perio lesions w/ no influence on either; Prognosis depends on Perio Tx

Biologic Width

Gargiulo – 1. sulcus depth ~ 1mm

2.  epithelial attachment ~ 1mm

3.  connective tissue attachment ~ 1mm

Calcific Metamorphosis (aka PCO)

1.  Trowbridge/Kim – caused by luxation injury, obliteration of pulp by mineralized tissue. Occurs in immature teeth, pulpal infarct, connective tissue from PDL proliferates and replaces pulp.

2.  Gutmann –1-16% CM cases develop pulpal necrosis, do not treat cases of calcific metamorphosis unless AP or nonvital

3.  Andreasen – 22% trauma cases ® Calcific metamorphosis

4.  Jacobsen – 70-90% horiztonal root fractures develop Calcific Metamorphosis

5.  Walton – No visible canal radiographically but ALWAYS present histologically

Calcific Metamorphosis (aka PCO)

1.  Trope – caused by luxation injury, uncontrolled reparative dentin or hemorrhage and clot formation act as a nidus for calcification, occurs in immature teeth.