Radiological Exam

1. Vital case w/ AP – Stashenko / Yamasaki
2. Bone loss & AP – S/B 7.1 MBL / Root position to bone
3. Digital Comparison studies
1. Film to digital – root length – NSD – Pitt Ford
2. Film to digital – PARL – NSD – Newton
3. D, E, F – film for measurement – NSD – Eleazer
4. Film to digital – NSD – Lamus
5. 80 – 90% radiation reduction – Soh
4. Lamina dura – consistent feature aiding dx – Kaffe
5. Interpretation accuracy –
1. Brynholf – accuracy increases with added films, 3=87%
2. Olsen – one film accuracy = 86%
3. Goldman/Darzenta – 46% agreement on interpretation
6. Technique – best view, paralleling – Forsberg

Subjective & Objective Examination

1. Reeves – Irreversible pulpitis develops when caries is w/in 0.5mm of pulp
2. Tronstat – pulp cap is only 50% successful
3. Cvek – Vital pulp therapy 95% successful
4. Kretzchmar – referred pain may come from sinusitis
5. Cold test –
1. Peters – no damage to tooth from CO2 snow or endo ice
2. Jones & Miller 2004 – use large cotton pellet, CO2 snow = endo ice
3. Peterson – cold test 90% accurate
4. Trowbridge – mode of action – hydrodynamics
6. Heat test –Schindler – used on refractory cases to identify missed canals or late stage of an irreversible pulpitis
7. Barodontalgia – sensitivity or pain caused by change in pressure – Cunningham
8. Seltzer/Bender – no histologic correlation w/diagnostic tests
9. Friend – patient accuracy of etiology only 37%

Pulp Tests – vitality tests give information about pulpal nerve status only

Does not evaluate blood supply

Reliability –

1. Andreasen – immature developing teeth, unreliable response to EPT, use CO2 snow
2. Bhaskar – trauma cases, EPT, cold and heat tests – unreliable (due to nerve damage w/out altering blood supply)
3. Fuss – unreliable EPT response in presence of large restoration, endo ice, CO2 and EPT equally reliable in adult teeth.

EPT –

a. Mode of action – stimulate Aδ fibers

b. Technique – Wahab – slowly increased current is more accurate

c. Bender – test incisal edge in anterior teeth

d. Jacobson – test middle-third of incisors, occlusal-third premolars

Laser Doppler

A) Sundquist 99 Dx: pcd

B) Trope ’97- #8,9 dx’d w/ dopler revealed vital

C) Trondstad ’94: LD 91% accurate, more accurate than EPT (64%)

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 common threat to life

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

Mobility – Modified Miller Classification

Class I - barely perceptible

Class II - < 1 mm movement

Class III - > 1 mm movement

Does periodontal disease cause pulpal disease?

Langeland – yes when all main apical foramina are involve by bact. Plaque

Seltzer/Bender – yes, bacteria can pass through lateral/accessory canals

Massler – found no relationship between pulpal & periodontal disease

Glickman system to classify 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

Class IV – Furca opening visible

Simon Classified Endo-Perio Lesions

Primary endo, primary perio, primary endo w/ secondary perio, primary perio w/ secondary endo, or true combined.

Biologic width

Gargiulo – 1. sulcus depth ~ 1mm

2. epithelial attachment ~ 1mm

3. connective tissue attachment ~ 1mm

Calcific metamorphosis

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

Gutmann – trauma causes 1-16% to develop pulpal necrosis, therefore do not automatically treat cases of calcific metamorphosis unless AP or nonvital.

Andreasen – 22% of traumatized teeth undergo calcific metamorphosis

Walton – no visible canal but always present histologically

Pulp canal obliteration

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

Dystrophic Calcification

Diffuse foci of calcification frequently found in the aging pulp; usually described as being perivascular or perineural.

Cracked tooth syndrome

Cameron – coined term, most commonly found in the mandibular second molar

Rivera – Classified longitudinal tooth fracture

1. craze lines

2. cuspal fracture

3. cracked tooth

4. split tooth

5. vertical root fracture

Guthrie – treat with cast crown, banding and operative procedures do not protect against interocclusal forces.

Pashley 2004 JOE – Best method to identify cracks is transillumination and methylene blue dye.

Vertical Root Fracture

Pitts – identification requires direct visualization, transillumination, is a endo-perio lesion. Consider root resection, amputation and extrusion.

Testori – in endodontically treated teeth, occurs most often in premolars, usually observe narrow periodontal defect.

Cause of Apical Periodontitis

Microorganisms colonizing the root canal system play an essential role in the pathogenesis of periradicular lesion.

Kakehashi – germ free rat study directly linked AP to bacteria

Moller – monkey study repeated findings of Kakehashi

Sundqvist – human study further confirmed findings of Kakehashi

Host immunological mechanisms mediate tissue destruction and bone resorption in response to bacterial infection. IL 1,2,6 TNFά

In previously treated cases, bacteria may be present due to missed canal or coronal leakage.

Bacteria involved in initial necrotic case – Gram -, anaerobes

Provotella Lactobacillus

Porphyromonas

Fusobacterium Peptostreptococci

Veillonella Streptococci

Eubaterium *mixed infection, polymicrobial

Propionibacter 3-17 species, symbiotic relationship

Actinomyces

Sundqvist – redirected understanding of canal flora – predominantly anaerobic but mixed with facultative anaerobes.

Baumgartner – apical 5 mm, predominantly anaerobic, BPB found in both coronal and apical area, most common found was P. nigrescens.

Fabricus – number of anaerobes increases with time and apical position

Bacteria involved in previously treated cases – Gram+, facultative anaerobes – treatment resistant

Moller – high incidence of Enterococcus Faecalis (Gr+, facultative) – few or mono species infection

Sundqvist – also found E. Faecalis, frequently as a single species microorganism.

Retreatment success rate ~74%

Nair – found yeast-like microorganisms, therapy resistant

Waltimo – Candida (resistant to many medicaments)

Gomes – Predominantly found same bacteria but also noted that symptomatic cases had anaerobes (pepto, porph., provet, fusos)

Haapasalo – unsealed cases during treatment or multiple appts reveal higher frequency of E. Faecalis.

Species associated with refractory cases

Strep

Enterococci

Staph

Lactobacillus

Proprionibacter

Eubacterium

Actinomyces

Prevotella, Fusobaterium

Causes of E. Faecalis Resistance

Love – because the hide in the tubules

Distel – because they form biofilms

Evans – because the have a proton pump

Haapasalo – Ca(OH)2 – does not kill E. Faecalis / smear layer removal facilitates bacterial invasion into dentinal tubules.

Orstavik – dentin buffers Ca(OH)2

Baumgartner – 2% CHX kills E. Faecalis

Bacteroides Melanogenicus – new nomenclature

Bacteroides – ferment carbs

Porphyromas: asacrolytic

Prevotella: sacrolytic

Is HIV found in the root canal or apical lesion ?

Torabinejad 1994 JOE – found HIV in the periradicular lesion w/ PCR

Trope 1991 OOO – found HIV in pulp tissue fibroblasts w/ DNA hybridization

Sebeti 2004 JOE – found Herpes simplex, Epstein-Barr & human Cytomegalovirus in periapical lesions. Large lesions showed higher levels.

Are Bacteria associated with symptoms?

YES

1. Newton – Bacteroides Melanogenicus are associated with pain, sinus tract and odor

2. Hahn – Gr+ cocci & Gr- rods = cold sensitivity

3. Sundqvist - >6 species = pain, 5 or less = no pain

NO

1. Baumgartner – no relationship of BPB w/ symptoms

Are bacteria found in periapical lesions? Controversy

YES

1. Iwu – homogenized study

2. Siqueira – Biofilm colonys

3. Sunde –

NO

1. Walton – inflammation resists spread of bacteria, confined to root

2. Nair – bacteria confined to root except

a. Abscess

b. Therapy resistant – actinomyces

c. Infected cysts

3. Holland – bacteria are present when pushed out during RCT

Sjogren – isolated P. propionicum extraradicularly

Waltimo – no candida in AP and is resistant to Ca(OH)2

Torabinejad & Trope – found HIV in AP

Discuss bacterial flora in acute PA abscesses

Langeland – found facultative and anaerobic bacteria/ fuso & streptococcus

Siqueira – described flora as polymicrobial

Sundqvist – BPB’s in abscess – associated with purulence

Bacteremia from RCT

Baumgartner – very low incidence (3.3%) / none if inst. kept w/in canal

Tronstat - ~25% even when instrument is confined to canal

Antibiotic Susceptibility

Baumgartner –

1. Pen VK 1^st choice – 85% effective
2. Amoxicillin – 91% effective
3. Amox + Clavulanic acid 100% effective
4. Clindamycin 96% effective
5. Metronidazole – 45%*

*due to effect only on anaerobic bacteria

Antibiotic effect on Oral Contraceptives

Hersch – only effected by Rifampin, but still advise patient to use alternate BC due to legal issues.

Are bacteria present in traumatized teeth with intact crowns?

YES – Bergenholtz found bacteria 64% of the time/ mixed anaerobic infection, got in through tubules or cracks.

Do Bacteria grow into the tubules?

YES –

Haapasalo – E. Faecalis survived in tubules 10days w/out nutrients

Sen – bacteria penetrate 10-150 microns into the tubules

Oguntebi – bacteria in tubules is a reservoir for future infections

Does anachoresis occur?

YES

1. Robinson – 2 requirement – inflammation