Abe oral Board Study Guide Topic List

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Fabricius - # of obligate anaerobes increase with time & nearer the apex

Gram - Anaerobic rods: Porphyromonas, Prevotella, Fusobacterium, Bacteroides

Also Candida (Waltimo) & HIV (Trope) found
What bacteria are more likely to infect a previously treated case?

Usually 1 or a few species, generally treatment resistant gram + facultative cocci

Sundqvist – Avg. 1.3 species; E. faecalis frequently isolate 38%

Nair – Yeast / Candida involve in treatment failures

Gram + facultative cocci: Enterococcus, Streptococcus, Staphylococcus

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
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
Discuss the bacterial flora found in acute PA abscesses?

Siqueira – Polymicrobial – similar to primary infections – BPB

Sundqvist – BPB associated with purulent infections
Are bacteria found in PA lesions? Controversy?

Yes: Tronstad – found extraradicular (anaerobes) in 8 refractory lesions

Siqueira – SEM study; only 1/24 cases or 4%

No: Walton – histo study; confined to canal space

Nair – histo study; criticized Tronstad for contamination
Does RCT cause bacteriemia?

Baumgartner – very low incidence if confined to RC system – 3.3%
Are bacteria present in traumatized teeth with intact crowns?

Bergenholtz – Yes – 64% mixed flora with necrotic pulp; remaining had aseptic necrosis; proposed bacterial entry through tubules and cracks
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

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.

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 / Infectionbacteria, PMNs

Contamination – bacterial toxins, lymphocytes, macrophages

Irritation – osteoclasts, lymphocytes, macrophages

Stimulation – osteoblasts, fibroblasts
What is the role of neuropeptides?

Cause neurogenic inflammation

Byers – demonstrated “sprouting” of CGRP nerve fibers after dental injury

Wakisaka – neurpeptides found in pulp – regulate PBF and precipitate pain; neuropeptides include SP, CGRP, NKA, 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
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: IL-1beta, TNF alpha & PGE2

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 Rxn – IgE mediated; binds to basophils & mast cells which release inflammatory mediators (allergic rhinitis & asthma)

Type IICytotoxic Rxn – IgG & IgM mediated; triggers complement or phagocytosis (autoimmune hemolytic anemia, some organ rejection & idiopathic thrombocytopenic purpura)

Type IIIImmune 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 IVDelayed-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; Dentritic 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

Pulver – Igs (see below)

Stashenko – cytokines
Which antibodies predominate in a periapical lesion?

Pulver – IgG>A>E>M for cysts and granulomas; IgE cells had degranulated mast cells nearby
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
Noxious stimuli → A-delta / C-fibers (primary afferent fibers with cell bodies located in the trigeminal ganglion) → subnucleus caudalis (medullary dorsal horn) → second order projection neuron → cross midline to the thalamus via the trigeminothalamic tract → third order neuron → cerebral cortex via the thalamocortical tract (pain perception)
Define Allodynia & Hyperalgesia:

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)
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.
Discuss referred pain:


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.

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%

Are antibiotics a concern with birth control pills?

Hersch – Rifampin is only known antibiotic to inihibit bcp; discuss possibility with pt
Discuss non-opiod analgesics:

NSAIDS – Non-selective COX inhibitors – inhibits synthesis of prostaglandins

Acetominophen – COX 3 inhibitor centrally; peripherally blocks pain impulse; produces antipyresis by inhibition of hypothalamic heat-regulating center
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

Lundgren & Hutter - .25mg Triazolam better than 5mg Diazepam
Prognosis / Outcomes Overview
When should pts be recalled?

Orstavik – 1 yr; peak incidence of healing / CAP occurred @ 1 yr; may take 4 yrs

Andreasen – 1 yr; wait 4 yrs for uncertain healing cases
How long doe 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): Perforation, Obturation; Overfill, Root canal missed, Perio disease, Another tooth, Split tooth, Trauma

Friedman – Toronto study: NSRCT – Pre-op lesion

RETX – Pre-op lesion, perforation, fill quality, restoration

S RCT – lesion > 5mm quadrupled risk
Do the radiographic healing correlate to histologic healing?

Byrnolf – No; only 7% demonstrated no inflammation

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

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
Does the level of root canal fill influence success/failure?

Seltzer & Bender – Overfill decreased success; underfill had no influence

Ng – meta-anaylsis shows w/in 2mm of apex improved success
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






Toronto (Friedman)

85% healed; 95% functional

Washington Study (Ingle)


Perforation Repair




Toronto (Friedman)

81% healed; 93% functional (with Perforation - 42%)

Allen, Newton , Brown


2nd RE-TX

Allen, Newton , Brown



Toronto (Friedman)

74% healed; 91% functional

Rubinstein, Kim

97% (3-12 mo.); 92% (5-7yrs.)

Allen, Newton , Brown


2nd S RCT

Peterson & Gutmann

36% healed; 26% uncertain

Root AMP



Int Replant

Bender & Rossman



Jordan, Suzuki & Skinner

<50% (11/24 cases)



80% (uninflammed pulps)


<50% (carious exposure - consider IP)

Cvek Pulpotomy


96% (young incisors)


91% (young molars)



96% -Ca(OH)2 long term


91-94% -MTA

Pulpotomy (primary teeth)


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

Implants vs. RCT


NSD - 94%


Meta analysis - NSD

Internal Bleaching


98% -pt. subjective success

Regenerative Endodontics Overview
What cells are potentially utilized for endo regeneration?

Huang – stem cells located in the apical papilla are viable following necrosis
Discuss how regenerative endo may be achieved?


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
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