ABE Endodontics cheat sheet

Reversible pulpitis: provoked, sharp pain of brief duration with no spontaneous pain and a vital pulp. Irreversible pulpitis: spontaneous or lingering pain, including pain that persists after cold removal.

A-delta fibers are myelinated and located at the pulp-dentin junction, mediating sharp, localizable pain. C fibers are unmyelinated, lie deeper, and mediate dull, poorly localizable pain.

Tertiary dentin: reactionary dentin is formed by surviving primary odontoblasts; reparative dentin is formed by odontoblast-like cells recruited after odontoblast death.

The pulp sits in a rigid, low-compliance chamber; inflammatory edema raises tissue pressure, collapses venules, produces ischemia, and drives necrosis.

Apical periodontitis is a host defense response to microbial colonization of the necrotic canal; bone loss results from osteoclast activation driven by RANKL.

Radiographs cannot distinguish a periapical granuloma from a radicular cyst; histopathology is required. Cysts account for roughly 15 percent of periapical lesions in biopsy series.

Internal resorption requires vital pulp tissue and appears as a ballooning canal enlargement. External inflammatory resorption requires a necrotic infected pulp plus a root surface defect.

Kakehashi's experiment: exposed pulps in germ-free rats developed no periapical lesions, whereas conventionally housed rats did, establishing bacteria as the essential cause.

Cold test: brief response means vital; lingering response means irreversible pulpitis; no response means necrosis or previous treatment. False negatives occur with calcification, immature apices, trauma, and crowns.

The electric pulp test assesses sensory nerve conduction, not blood supply; it may be positive in a partially necrotic pulp and negative in a vital tooth with an obstructed conductive path.

Percussion and palpation tenderness indicate apical periodontitis; a sinus tract should be traced with gutta-percha and radiographed to identify the source tooth.

AAE diagnostic terms: normal pulp, reversible pulpitis, symptomatic irreversible pulpitis, asymptomatic irreversible pulpitis, pulp necrosis, previously treated, previously initiated.

A cracked tooth is suggested by pain on release from biting, a localized narrow pocket, or a visible crack line; transillumination and staining help, and CBCT often misses incomplete cracks.

Treatment planning requires restorability, periodontal status, strategic value, crown-to-root ratio, and the patient's medical and behavioral factors.

CBCT detects periapical lesions, missed canals, fractures, and resorption earlier than periapical radiographs, but is used selectively because of radiation dose.

Irreversible pulpitis remains a clinical diagnosis based on prolonged cold response and spontaneous pain; the pulp may still be vital and responsive to testing.

Primary endodontic infections are polymicrobial, dominated by gram-negative anaerobes such as Porphyromonas, Prevotella, Fusobacterium, and Treponema, plus gram-positive cocci and rods.

Enterococcus faecalis is linked to secondary and persistent infections; it forms biofilm, tolerates high pH, and can survive calcium hydroxide medication.

Microorganisms colonize canal walls as biofilm and invade dentinal tubules, isthmuses, lateral canals, and the apical delta, where instruments and irrigants may not reach.

Lipopolysaccharide from gram-negative cell walls activates Toll-like receptor 4, inducing IL-1, TNF-alpha, and IL-6, which drive inflammation and osteoclastic resorption.

RANKL from lymphocytes and stromal cells promotes osteoclast differentiation; osteoprotegerin is a decoy receptor; the RANKL-to-OPG ratio determines net bone loss.

Neutrophils dominate acute periapical inflammation and abscess formation, while macrophages, plasma cells, and lymphocytes predominate in chronic lesions.

Culture-independent sequencing reveals hundreds of taxa per canal, many uncultivable, so culture sampling substantially underestimates community diversity.

Bacteria protected within dentinal tubules survive mechanical instrumentation, and residual bacteria are a major cause of post-treatment apical periodontitis.

Working length is set 0.5 to 1.0 mm short of the apical foramen near the apical constriction, verified with an apex locator and confirmed radiographically.

Sodium hypochlorite (0.5 to 5.25 percent) dissolves necrotic tissue and is broadly antimicrobial; both tissue dissolution and cytotoxicity rise with concentration and temperature.

EDTA 17 percent is a final chelating rinse of about one minute that removes the smear layer and opens dentinal tubules; it is not antimicrobial on its own.

Chlorhexidine 2 percent has substantivity but does not dissolve tissue, and it must not be mixed directly with sodium hypochlorite because a precipitate forms.

Irrigants are delivered with side-vented needles placed 1 to 2 mm short of working length using gentle expression; apical negative-pressure systems reduce extrusion risk.

Calcium hydroxide at pH near 12.5 is the most common intracanal medicament, typically placed for one to two weeks; alone it is unreliable against Enterococcus faecalis.

Crown-down preparation and glide path creation reduce torsional stress on nickel-titanium instruments; torque limits, speed, and reuse must follow manufacturer instructions.

Single-visit and multiple-visit treatment show no consistent outcome difference; multiple visits are favored when infection control is difficult or the patient is symptomatic.

Obturation aims to fill the canal system three-dimensionally and block coronal-to-apical leakage; gutta-percha with sealer is the standard core material.

Accepted techniques include warm vertical compaction, carrier-based systems, and single-cone placement with calcium silicate sealers; sealer extrusion should be minimized.

Coronal restoration quality strongly influences healing of apical periodontitis; a defective coronal seal can cause failure despite acceptable obturation.

When preparing a post space, leave at least 4 to 5 mm of apical gutta-percha to preserve the apical seal and avoid root weakening.

A 1.5 to 2 mm circumferential ferrule of dentin above the restoration margin improves fracture resistance and retention of the restoration.

Calcium silicate sealers set in the presence of moisture, are biocompatible, release calcium hydroxide, and bond chemically to dentin.

Posterior endodontically treated teeth generally require cuspal coverage; anterior teeth with minimal structural loss can be restored with composite.

Mineral trioxide aggregate or calcium silicate apical plugs of 4 to 5 mm manage open apices and perforations and provide an apical barrier for subsequent obturation.

Retreatment indications: persistent symptoms, new or enlarging apical periodontitis, inadequate obturation, untreated canals, coronal leakage, or need to replace the restoration.

Nonsurgical retreatment is usually attempted before apical surgery; reported success is somewhat lower than for initial treatment, roughly 70 to 85 percent.

Gutta-percha removal uses rotary retreatment files, heat, solvents such as chloroform or eucalyptol, and ultrasonic instruments; solvent residue is removed before reobturation.

A separated instrument is managed by bypassing it with a fine file; if the canal can be cleaned and the fragment is not infected, it may be retained and monitored.

Torsional fracture occurs when a file binds and exceeds its elastic limit; flexural fatigue results from repeated cyclic bending within curved canals.

Sodium hypochlorite accident causes severe pain, rapid swelling, ecchymosis, and possible nerve injury; manage with reassurance, cold compresses, analgesia, and monitoring for necrosis.

Perforations are sealed promptly with mineral trioxide aggregate or calcium silicate cement; prognosis depends on location, time to repair, and infection status.

Procedural errors include ledging, transportation, zipping, elbow formation, and strip perforation in the danger zone of the mesiobuccal root of mandibular molars.

Periradicular surgery is indicated when nonsurgical treatment fails or cannot be performed, such as with calcification, posts, perforation, anatomical obstacles, or need for biopsy.

Microsurgical principles: operating microscope, minimal osteotomy, roughly 3 mm root-end resection with minimal bevel, ultrasonic retropreparation, and calcium silicate retrofill.

Success criteria for apical surgery are absence of symptoms, a functional tooth, and radiographic evidence of healing by regeneration, repair, or scar formation.

Intentional replantation involves extraction, extraoral endodontic treatment, and replantation; extraoral time under about 15 minutes limits ankylosis and root resorption.

Flap options include sulcular full-thickness, papilla-preserving, and Ochsenbein-Luebke designs; papilla preservation reduces esthetic and periodontal complications.

Local anesthetic with a vasoconstrictor aids hemostasis, which is essential for visibility during retropreparation and retrofilling.

Guided tissue regeneration may benefit large through-and-through lesions, but evidence for routine use remains limited.

Nerve injury risk includes the mental nerve in mandibular premolar surgery and the greater palatine nerve and maxillary sinus in posterior maxillary surgery.

Avulsion: replant immediately if possible; dry time under 60 minutes improves prognosis; store in milk, saline, or Hank's balanced salt solution and handle by the crown.

Avulsed teeth are splinted flexibly for about two weeks, with antibiotics and tetanus prophylaxis considered; closed-apex teeth receive root canal treatment within two weeks.

Root fractures are repositioned if displaced and splinted flexibly, about four weeks for cervical and four months for midroot fractures, with vitality monitoring.

Luxation injuries include concussion, subluxation, extrusive, lateral, and intrusive injuries; intrusive and severely displaced teeth carry higher risk of necrosis and resorption.

External inflammatory resorption occurs with an infected necrotic pulp and damaged root surface; treatment is pulp extirpation with calcium hydroxide medication and radiographic follow-up.

Replacement resorption by ankylosis follows periodontal ligament loss, is progressive, and is managed by decoronation in growing patients rather than by endodontic treatment.

Regenerative endodontic procedure for immature necrotic teeth: minimal instrumentation, low-concentration sodium hypochlorite, EDTA rinse, induced blood clot, coronal seal, and serial follow-up.

Cervical invasive resorption occurs in vital teeth below the epithelial attachment and is treated by curettage, 90 percent trichloroacetic acid application, and restoration.

Inferior alveolar nerve block success in irreversible pulpitis is only about 50 to 80 percent; supplemental intraligamentary, intraosseous, or articaine buccal infiltration improves anesthesia.

Articaine 4 percent has higher lipid solubility and bone diffusion than lidocaine 2 percent, and maxillary infiltration provides predictable pulpal anesthesia.

Maximum doses in a healthy adult: lidocaine 4.4 mg/kg (300 mg), articaine 7 mg/kg (500 mg), mepivacaine 6.6 mg/kg (400 mg), bupivacaine 1.3 mg/kg; epinephrine limit about 0.2 mg.

Epinephrine 1:100,000 equals 0.01 mg/mL, and a 1.8 mL cartridge contains 0.018 mg; 1:50,000 equals 0.02 mg/mL.

Antibiotics are not indicated for irreversible pulpitis or a localized abscess without systemic signs; indications include fever, cellulitis, spreading infection, or immunocompromise.

Amoxicillin 500 mg three times daily for about seven days is first-line; penicillin allergy alternatives include clindamycin 300 mg four times daily or azithromycin.

Ibuprofen 400 to 600 mg is a first-line analgesic, and combining ibuprofen with acetaminophen improves analgesia; aspirin is avoided when bleeding is a concern.

Non-selective beta-blockers blunt epinephrine effects and can cause hypertension through unopposed alpha stimulation; caution is also needed with tricyclic antidepressants and cocaine.