100+ Free ABOMP Oral Pathology Practice Questions

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Question 1

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Bilateral bony exostoses on the lingual aspect of the mandible in the premolar region are most consistent with which developmental anomaly?

Torus palatinus

Osteoma

Torus mandibularis

Buccal exostosis

to track

2026 Statistics

Key Facts: ABOMP Oral Pathology Exam

100

FREE Practice Questions

OpenExamPrep ABOMP question bank (2026)

3 components

Exam Format

Written + Practical (microscopic slides) + Oral

~15%

Odontogenic Tumors Weight

Largest single domain on 2026 ABOMP content outline

~$2,500-$3,500

2026 Combined Exam Fee

ABOMP Written + Practical + Oral (verify current schedule)

3 yr

Required Residency

CODA-accredited Oral and Maxillofacial Pathology residency

~80-90%

First-Time Pass Rate

ABOMP annual statistics (CODA residency graduates)

The ABOMP Certification is a multi-component examination (Written, Practical microscopic slide session, and Oral) administered by the American Board of Oral and Maxillofacial Pathology for Diplomate status. Content spans odontogenic tumors (~15%), developmental anomalies (~10%), odontogenic cysts (~10%), bone lesions (~10%), salivary gland pathology (~10%), squamous cell carcinoma (~8%), viral infections (~8%), ulcerative/immune-mediated disease (~8%), premalignant lesions (~6%), fungal (~5%), bacterial/periodontal (~5%), reactive soft tissue (~5%), pigmented lesions (~3%), miscellaneous/syndromic (~4%), and diagnostic techniques (~3%). Total fees ~$2,500-$3,500; requires a CODA-accredited OMP residency (3 years) following DDS/DMD.

Sample ABOMP Oral Pathology Practice Questions

Try these sample questions to test your ABOMP Oral Pathology exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1Bilateral bony exostoses on the lingual aspect of the mandible in the premolar region are most consistent with which developmental anomaly?

A.Torus palatinus

B.Osteoma

C.Torus mandibularis

D.Buccal exostosis

Explanation: Torus mandibularis presents as bilateral bony protuberances on the lingual surface of the mandible, typically in the premolar region. Torus palatinus occurs at the midline of the hard palate. These are developmental, non-neoplastic hyperostoses composed of dense cortical and lamellar bone.

2A well-defined radiolucency below the mandibular canal near the angle of the mandible, containing ectopic salivary gland tissue, is called:

A.Simple bone cyst

B.Stafne defect

C.Traumatic bone cyst

D.Lingual mandibular salivary gland depression cyst

Explanation: Stafne defect (static bone cavity / lingual mandibular bone concavity) is a developmental depression on the lingual surface of the mandible below the inferior alveolar canal that often contains ectopic submandibular salivary gland tissue. It is asymptomatic and requires no treatment.

3Small, asymptomatic yellow-white papules on the buccal mucosa or vermilion representing ectopic sebaceous glands are called:

A.Fordyce granules

B.Koplik spots

C.Lichen planus papules

D.Leukoedema

Explanation: Fordyce granules are heterotopic sebaceous glands of the oral mucosa, most commonly on the buccal mucosa and upper lip vermilion. They are a normal variant present in up to 80% of adults. No treatment is needed.

4Multiple osteomas of the jaws, intestinal polyps, and epidermoid cysts are characteristic of which syndrome?

A.Peutz-Jeghers syndrome

B.Gorlin syndrome

C.Gardner syndrome

D.Cowden syndrome

Explanation: Gardner syndrome is an autosomal dominant condition caused by APC gene mutation on chromosome 5q21. Features include multiple osteomas (often of the jaws), colorectal adenomatous polyps with near 100% malignant transformation, epidermoid cysts, fibromas, desmoid tumors, and supernumerary/unerupted teeth.

5A red, atrophic, rhomboid-shaped lesion on the midline dorsum of the tongue anterior to the circumvallate papillae most likely represents:

A.Geographic tongue

B.Median rhomboid glossitis

C.Hairy tongue

D.Fissured tongue

Explanation: Median rhomboid glossitis is a well-demarcated erythematous patch at the midline dorsal tongue anterior to the circumvallate papillae, with loss of filiform papillae. It was once thought to be developmental (failure of tuberculum impar fusion) but is now recognized as a chronic Candida infection in most cases.

6Migrating erythematous patches with white serpiginous borders on the dorsum of the tongue that change location over days best describes:

A.Hairy tongue

B.Median rhomboid glossitis

C.Geographic tongue (benign migratory glossitis)

D.Erythroplakia

Explanation: Geographic tongue (benign migratory glossitis) shows areas of desquamated filiform papillae with a raised white serpiginous border. Lesions heal and reappear elsewhere, producing the characteristic migratory pattern. It is a benign inflammatory condition associated with psoriasis and atopy.

7Elongation of filiform papillae on the dorsal tongue producing a hair-like appearance, often with brown-black discoloration, is known as:

A.Oral hairy leukoplakia

B.Hairy tongue

C.Black hairy nevus

D.Acanthosis nigricans

Explanation: Hairy tongue (lingua villosa) results from defective desquamation of filiform papillae that may reach several millimeters in length. Bacterial or fungal pigments and extrinsic stains (tobacco, coffee, chromogenic bacteria) give the brown-black color. It is distinct from oral hairy leukoplakia (EBV, lateral tongue).

8A short or thick lingual frenum that restricts tongue movement is called:

A.Ankyloglossia

B.Macroglossia

C.Microglossia

D.Glossoptosis

Explanation: Ankyloglossia (tongue-tie) is a developmental anomaly characterized by a short, thickened lingual frenum that restricts tongue mobility. It may cause difficulty with breastfeeding, speech articulation, or oral hygiene and is managed by frenectomy when clinically indicated.

9Failure of fusion of the median nasal process with the maxillary processes produces which anomaly?

A.Cleft lip

B.Cleft palate

C.Pierre Robin sequence

D.Macrostomia

Explanation: Cleft lip results from failure of fusion between the median nasal process and the maxillary process during the 6th-7th week of embryonic development. It may be unilateral or bilateral and is more common on the left side and in males. Cleft palate arises from failure of palatal shelf fusion.

10Hypodontia, conical teeth, sparse hair, and hypohidrosis are features of:

A.Cleidocranial dysplasia

B.Ectodermal dysplasia

C.Osteogenesis imperfecta

D.Dentinogenesis imperfecta

Explanation: Hypohidrotic ectodermal dysplasia (X-linked, EDA gene) features hypodontia with conical/peg-shaped teeth, fine sparse hair, reduced sweating (heat intolerance), and frontal bossing. Cleidocranial dysplasia features numerous supernumerary teeth and absent/hypoplastic clavicles but not these ectodermal changes.

About the ABOMP Oral Pathology Exam

The American Board of Oral and Maxillofacial Pathology (ABOMP) Certification establishes Diplomate status in the diagnosis of diseases of the oral cavity, jaws, and adjacent structures. The multi-component examination (Written, Practical microscopic slide session, and Oral examiner interview) spans odontogenic tumors (ameloblastoma BRAF V600E, AOT, CEOT, odontogenic myxoma, ghost cell lesions), odontogenic cysts (radicular, dentigerous, OKC with PTCH1 and Gorlin syndrome, calcifying odontogenic cyst), developmental anomalies (amelogenesis/dentinogenesis imperfecta, cleft, tongue anomalies), bone and fibro-osseous lesions (fibrous dysplasia GNAS, ossifying fibroma, cemento-osseous dysplasia, cherubism, CGCG, ABC, Paget), salivary pathology (pleomorphic adenoma PLAG1, Warthin, mucoepidermoid carcinoma MAML2, adenoid cystic MYB-NFIB, acinic cell NR4A3, secretory ETV6-NTRK3, salivary duct AR/HER2), oral SCC and HPV+ oropharyngeal SCC (p16 IHC, AJCC 8), viral/fungal/bacterial infections, immune-mediated disease (pemphigus vulgaris with Nikolsky sign, mucous membrane pemphigoid, lichen planus, TUGSE, Behçet), premalignant lesions (leukoplakia, erythroplakia, PVL, submucous fibrosis, actinic cheilitis), reactive soft tissue and neural lesions, pigmented lesions, MRONJ and osteoradionecrosis, and cancer-related syndromes. Requires completion of a CODA-accredited Oral and Maxillofacial Pathology residency (minimum 3 years) after a DDS/DMD.

Questions

100 scored questions

Time Limit

Multi-day — Written (CBT), Practical (microscopic slides), and Oral (examiner interview)

Passing Score

Criterion-referenced standard set by ABOMP (modified Angoff method)

Exam Fee

~$2,500-$3,500 total for Written + Practical + Oral (ABOMP 2026 — verify current schedule) (American Board of Oral and Maxillofacial Pathology (ABOMP))

ABOMP Oral Pathology Exam Content Outline

~15%

Odontogenic Tumors

Ameloblastoma (conventional with BRAF V600E — mandibular; SMO — maxillary; unicystic; peripheral; metastasizing), adenomatoid odontogenic tumor (AOT — two-thirds rule: two-thirds in young females, anterior maxilla, around impacted canines; ductal/rosette pattern), calcifying epithelial odontogenic tumor (Pindborg — amyloid with Congo red apple-green birefringence, Liesegang calcifications), odontogenic myxoma, ameloblastic fibroma/fibro-odontoma, compound vs complex odontoma, cementoblastoma, squamous odontogenic tumor, ghost cell lesions (calcifying odontogenic cyst/Gorlin cyst, dentinogenic ghost cell tumor, ghost cell odontogenic carcinoma).

~10%

Developmental Anomalies

Cleft lip and palate, ankyloglossia, fissured/geographic tongue (benign migratory glossitis), lingual thyroid, thyroglossal duct cyst (midline), branchial cleft cyst (lateral neck), dermoid/epidermoid cyst, hemifacial microsomia, Treacher Collins (TCOF1), Pierre Robin sequence (micrognathia-glossoptosis-cleft palate), ectodermal dysplasia, amelogenesis imperfecta (hypoplastic/hypomaturation/hypocalcified), dentinogenesis imperfecta (DSPP; type I associated with osteogenesis imperfecta — blue sclerae), dens invaginatus/evaginatus, taurodontism, regional odontodysplasia (ghost teeth), white sponge nevus (KRT4/KRT13).

~10%

Odontogenic Cysts

Radicular (periapical) cyst — most common odontogenic cyst, follows pulpal necrosis; dentigerous cyst — pericoronal around crown of impacted tooth (3rd molar, canine); odontogenic keratocyst (OKC) — parakeratinized lining with palisaded hyperchromatic basal layer and corrugated luminal surface, PTCH1 mutation; multiple OKCs = nevoid basal cell carcinoma (Gorlin) syndrome (BCCs, palmar pits, bifid ribs, medulloblastoma); orthokeratinized odontogenic cyst; lateral periodontal cyst and botryoid variant; glandular odontogenic cyst (mimics MEC); gingival cyst of adult/newborn (Bohn nodules, Epstein pearls); eruption cyst; buccal bifurcation cyst; calcifying odontogenic cyst (Gorlin — ghost cells).

~10%

Bone Lesions (Fibro-osseous, Giant Cell, Dysplasias)

Fibrous dysplasia (GNAS, monostotic vs polyostotic, Chinese-character woven-bone trabeculae, radiographic ground-glass, McCune-Albright triad — FD + café-au-lait + endocrinopathy), ossifying fibroma (COF; juvenile trabecular and psammomatoid variants), cemento-osseous dysplasia (periapical/focal/florid — do NOT biopsy), central giant cell granuloma vs peripheral giant cell granuloma vs brown tumor of hyperparathyroidism (check calcium/phosphate/PTH), aneurysmal bone cyst (USP6 rearrangement), simple (traumatic) bone cyst, cherubism (SH3BP2), Paget disease (elevated ALP, mosaic reversal lines), osteoma (Gardner — APC), osteosarcoma of jaw, Langerhans cell histiocytosis (CD1a+, S100+, Birbeck granules on EM, BRAF V600E).

~10%

Salivary Gland Pathology

Mucocele (minor salivary, extravasation) and ranula (sublingual), sialolithiasis (Wharton duct — submandibular), necrotizing sialometaplasia (palate; mimics SCC — preserved lobular architecture), Sjögren syndrome (anti-Ro/SSA, anti-La/SSB; lymphoepithelial sialadenitis; MALT lymphoma risk), IgG4-related sialadenitis, pleomorphic adenoma (PLAG1, HMGA2 rearrangements; most common benign salivary tumor), Warthin tumor (older male smokers, bilateral), basal cell adenoma, canalicular adenoma (upper lip), mucoepidermoid carcinoma (MAML2 — CRTC1/CRTC3-MAML2 fusion; most common malignant), adenoid cystic carcinoma (MYB-NFIB; cribriform, perineural spread, indolent-but-relentless), acinic cell carcinoma (NR4A3), polymorphous adenocarcinoma (PRKD1; palate), secretory carcinoma (ETV6-NTRK3; targetable with larotrectinib/entrectinib), salivary duct carcinoma (androgen receptor, HER2).

~8%

Squamous Cell Carcinoma

Oral SCC — tobacco, alcohol, betel quid (buccal SCC in South Asia); classical sites: lateral tongue, floor of mouth, lower lip; oropharyngeal SCC and HPV-16 association — p16 IHC surrogate (AJCC 8 has a distinct staging system for HPV+ OPSCC; basaloid nonkeratinizing morphology; better prognosis), verrucous carcinoma (Ackerman tumor — well-differentiated, broad pushing margins, locally aggressive, does NOT metastasize), carcinoma cuniculatum, basaloid SCC, spindle (sarcomatoid) SCC, adenosquamous carcinoma, NUT carcinoma (NUTM1 rearrangement), TNM staging with depth of invasion.

~8%

Viral Infections

HSV-1 primary herpetic gingivostomatitis vs recurrent herpes labialis (cytology — Tzanck smear with multinucleated giant cells, steel-gray nuclei, Cowdry A intranuclear inclusions), VZV (herpes zoster — unilateral trigeminal distribution, Ramsay Hunt with VII involvement), EBV (oral hairy leukoplakia — lateral tongue corrugations in HIV/immunocompromised), CMV, Coxsackie A (hand-foot-mouth — A16; herpangina — soft palate vesicles), measles (Koplik spots), HPV — verruca vulgaris, squamous papilloma, condyloma acuminatum (HPV 6, 11), focal epithelial hyperplasia/Heck disease (HPV 13, 32; Native American/Inuit), HHV-8 (Kaposi sarcoma — HIV-associated, palate KS; LANA-1 IHC).

~8%

Ulcerative & Immune-Mediated

Recurrent aphthous stomatitis (minor <1 cm, major/Sutton >1 cm heals with scar, herpetiform multiple tiny), Behçet (HLA-B51, oral and genital ulcers, uveitis, pathergy), TUGSE — traumatic ulcerative granuloma with stromal eosinophilia (CD30+ atypical T-cell infiltrate), oral lichen planus (reticular Wickham striae, erosive, plaque; band-like T-cell infiltrate, liquefactive basal degeneration, Civatte/colloid bodies; low-rate malignant transformation), lichenoid drug/contact reactions, pemphigus vulgaris (IgG to desmoglein 3 > 1, suprabasilar acantholysis with tombstone appearance, Tzanck cells, DIF — intercellular fishnet/chicken-wire IgG and C3; Nikolsky sign positive), mucous membrane (cicatricial) pemphigoid (IgG to BP180/BP230/laminin-332, subepithelial split, DIF — linear basement membrane IgG and C3), bullous pemphigoid, erythema multiforme/SJS/TEN (drug, HSV, Mycoplasma), orofacial granulomatosis, Melkersson-Rosenthal (facial palsy + fissured tongue + lip swelling), Crohn disease cobblestone mucosa, granulomatosis with polyangiitis (strawberry gingivitis, c-ANCA/PR3).

~6%

Premalignant Lesions

Leukoplakia — clinical diagnosis of exclusion; biopsy for dysplasia grading (mild/moderate/severe/carcinoma in situ; WHO two-tier low/high grade); erythroplakia — highest rate of dysplasia/carcinoma at biopsy; proliferative verrucous leukoplakia (PVL) — multifocal, progressive, high malignant transformation rate, predilection for elderly women, verrucous-to-SCC progression; actinic cheilitis/cheilosis (solar damage, lower lip vermillion, sharp demarcation blurred); oral submucous fibrosis (betel/areca nut, trismus, blanched fibrotic mucosa, high SCC risk); oral lichen planus (potentially malignant disorder); oral lichenoid lesion; discoid lupus; dyskeratosis congenita.

~5%

Fungal Infections

Candidiasis — pseudomembranous (thrush, white scrapable); erythematous/atrophic (denture stomatitis; median rhomboid glossitis); hyperplastic (non-scrapable, biopsy required); angular cheilitis; chronic mucocutaneous candidiasis; PAS/GMS show budding yeast and pseudohyphae; histoplasmosis (Histoplasma capsulatum — Ohio/Mississippi river valleys; small intracellular yeast in macrophages; HIV-associated oral ulcers), blastomycosis (broad-based budding yeast, double-contoured wall), coccidioidomycosis (spherules with endospores, Southwest US), cryptococcosis (mucicarmine-positive capsule, India ink preparation), paracoccidioidomycosis (mariner's-wheel budding), mucormycosis/zygomycosis (diabetic ketoacidosis, neutropenia; broad nonseptate ribbon-like hyphae with right-angle branching; rhinocerebral with palatal necrosis), aspergillosis (septate hyphae at acute 45° angles).

~5%

Bacterial & Periodontal

Dental caries (Streptococcus mutans biofilm acid demineralization), pulpitis and periapical abscess/granuloma/cyst, 2017 AAP/EFP Classification of Periodontal and Peri-implant Diseases (Stages I-IV based on severity and complexity; Grades A/B/C based on rate of progression; replaces older aggressive/chronic terminology), necrotizing periodontal diseases — NUG/NUP (Fusobacterium nucleatum, Prevotella intermedia, Treponema; punched-out interdental papillae; HIV/malnutrition), noma/cancrum oris, actinomycosis (Actinomyces israelii — yellow sulfur granules, filamentous gram+ bacteria), syphilis (primary chancre, secondary mucous patches and condyloma lata, tertiary gumma, congenital — Hutchinson incisors, mulberry molars; Treponema pallidum on silver stain/IHC), gonococcal pharyngitis, tuberculosis (caseating granuloma, AFB), leprosy, scarlet fever (strawberry tongue), cat-scratch.

~5%

Reactive & Soft Tissue

Irritation fibroma, giant cell fibroma, pyogenic granuloma (pregnancy tumor, lobular capillary hemangioma), peripheral ossifying fibroma, peripheral giant cell granuloma (do NOT confuse with CGCG or brown tumor), traumatic neuroma, mucocele/ranula, lipoma (signet-ring adipocytes), schwannoma (S100+, SOX10+, encapsulated, Antoni A palisades with Verocay bodies vs Antoni B loose), neurofibroma (plexiform is pathognomonic for NF1 — NF1 gene), granular cell tumor (S100+, pseudoepitheliomatous hyperplasia overlying — do not mistake as SCC; dorsal tongue), congenital epulis of the newborn (alveolar ridge of female newborn; S100 NEGATIVE — distinguishes from granular cell tumor), hemangioma (infantile — GLUT1+; congenital — GLUT1−), lymphangioma, leiomyoma, rhabdomyoma, solitary fibrous tumor (STAT6).

~3%

Pigmented Lesions

Physiologic (racial) pigmentation, amalgam tattoo (most common cause of focal oral pigmentation), smoker's melanosis, oral melanotic macule, melanoacanthoma, oral nevus (intramucosal most common intraorally; palate common), Peutz-Jeghers syndrome (STK11/LKB1 — mucocutaneous lentigines around lips plus hamartomatous GI polyps; increased GI cancer risk), Laugier-Hunziker (acquired mucocutaneous pigmentation, no systemic association), Addison disease (ACTH-driven mucocutaneous bronzing), McCune-Albright café-au-lait, oral mucosal melanoma (palate/maxillary gingiva — aggressive, poor prognosis).

~4%

Miscellaneous / Syndromic

TMJ disorders and internal derangement, synovial chondromatosis, osteonecrosis of the jaw — MRONJ (medication-related; bisphosphonates, denosumab, antiangiogenics) and osteoradionecrosis (prior head-and-neck radiotherapy), Gorlin/nevoid basal cell carcinoma syndrome (PTCH1 — multiple OKCs, BCCs, bifid ribs, palmar/plantar pits, medulloblastoma, calcified falx cerebri), Gardner (APC — osteomas of jaw, supernumerary and impacted teeth, desmoids, colorectal cancer — variant of FAP), Cowden (PTEN — mucocutaneous tricholemmomas/papillomas, breast/thyroid/endometrial cancer), MEN2B (RET — mucosal neuromas, marfanoid habitus, medullary thyroid carcinoma, pheochromocytoma), Ehlers-Danlos, osteogenesis imperfecta (COL1A1/COL1A2 — blue sclerae, dentinogenesis imperfecta type I, bone fragility).

~3%

Diagnostic Techniques & Lab

Specimen handling and grossing, routine H&E, histochemistry (PAS and GMS for fungi; mucicarmine for cryptococcus and mucin; Congo red with apple-green birefringence for amyloid — CEOT, plasmacytoma; Masson trichrome; Fontana-Masson for melanin), immunohistochemistry (p16 for HPV+ OPSCC, p63/p40 basal/squamous, CK5/6, CK7/CK20, S100 and SOX10 for melanocytic/neural, CD20/CD3/CD30/CD1a for lymphoid/Langerhans, LANA-1 for HHV-8/KS, androgen receptor and HER2 for salivary duct carcinoma), direct immunofluorescence (pemphigus intercellular fishnet IgG/C3 vs pemphigoid linear BMZ IgG/C3), indirect immunofluorescence (circulating anti-desmoglein or anti-BP autoantibodies), molecular testing (BRAF V600E for ameloblastoma and LCH; MAML2 FISH for MEC; MYB-NFIB for AdCC; ETV6-NTRK3 for secretory carcinoma; PLAG1/HMGA2 for pleomorphic adenoma; EWSR1 for Ewing/round-cell tumors), cytopathology (oral brush cytology, FNA of salivary and neck masses), frozen section, digital pathology and AI-assisted diagnosis.

How to Pass the ABOMP Oral Pathology Exam

What You Need to Know

Passing score: Criterion-referenced standard set by ABOMP (modified Angoff method)
Exam length: 100 questions
Time limit: Multi-day — Written (CBT), Practical (microscopic slides), and Oral (examiner interview)
Exam fee: ~$2,500-$3,500 total for Written + Practical + Oral (ABOMP 2026 — verify current schedule)

Keys to Passing

Complete 500+ practice questions
Score 80%+ consistently before scheduling
Focus on highest-weighted sections
Use our AI tutor for tough concepts

ABOMP Oral Pathology Study Tips from Top Performers

1Odontogenic keratocyst (OKC) — parakeratinized, thin epithelium (6-8 cell layers), palisaded hyperchromatic basal layer, corrugated luminal surface, no rete ridges. High recurrence after enucleation due to daughter cysts and thin friable lining. PTCH1 mutations; multiple OKCs in a young patient should trigger workup for nevoid basal cell carcinoma (Gorlin) syndrome — BCCs, palmar/plantar pits, bifid ribs, calcified falx cerebri, medulloblastoma.

2Salivary gland molecular fingerprints — memorize these fusions cold: pleomorphic adenoma PLAG1/HMGA2; mucoepidermoid carcinoma CRTC1/CRTC3-MAML2 (do FISH if in doubt); adenoid cystic carcinoma MYB-NFIB (also MYBL1); acinic cell carcinoma NR4A3; polymorphous adenocarcinoma PRKD1 (palate); secretory (mammary analogue) carcinoma ETV6-NTRK3 (targetable with larotrectinib/entrectinib); salivary duct carcinoma androgen receptor and frequently HER2.

3HPV+ oropharyngeal SCC — p16 IHC (strong diffuse nuclear and cytoplasmic in >70% of cells) is the clinical surrogate for transcriptionally active HPV-16. Basaloid nonkeratinizing morphology, lymphoepithelial pattern, crypt tonsil/base-of-tongue origin. AJCC 8 uses a completely SEPARATE staging system for p16+ OPSCC vs p16-negative; prognosis is notably better. Oral cavity SCC does NOT use the HPV+ staging framework.

4Pemphigus vulgaris vs mucous membrane pemphigoid — this is a classic DIF question. Pemphigus vulgaris: IgG vs desmoglein 3 (mucosa dominant) and desmoglein 1; suprabasilar acantholysis with tombstone row of basal keratinocytes; DIF shows intercellular fishnet (chicken-wire) IgG and C3 throughout the spinous layer; Nikolsky sign positive. Mucous membrane pemphigoid: IgG vs hemidesmosomal antigens (BP180, BP230, laminin-332); subepithelial split; DIF shows LINEAR deposition of IgG and C3 along the basement membrane zone.

5Ameloblastoma BRAF V600E — conventional solid/multicystic ameloblastoma arising in the mandibular posterior region is BRAF V600E-driven in ~60-70% of cases, analogous to cutaneous melanoma and papillary thyroid carcinoma. Maxillary ameloblastomas skew toward SMO (Smoothened) mutations. This has therapeutic implications: dabrafenib + trametinib can shrink unresectable/recurrent BRAF-mutant disease. MRONJ (medication-related ONJ) and osteoradionecrosis stages and management (AAOMS staging) are also high-yield.

Frequently Asked Questions

What is the ABOMP Certification examination?

The American Board of Oral and Maxillofacial Pathology (ABOMP) Certification is the specialty board examination that confers Diplomate status in Oral and Maxillofacial Pathology. It is a multi-component examination comprising a Written (multiple-choice) section, a Practical microscopic slide identification session, and an Oral examiner interview covering odontogenic tumors and cysts, developmental anomalies, bone lesions, salivary gland pathology, oral squamous cell carcinoma, viral/fungal/bacterial infections, immune-mediated disease, premalignant lesions, soft tissue and pigmented lesions, and related diagnostic techniques.

Who is eligible to sit for the ABOMP exam?

Candidates must hold a DDS, DMD, or equivalent dental degree and must have completed a CODA-accredited Oral and Maxillofacial Pathology residency of at least 3 years. The program director must attest to satisfactory clinical performance and ethical conduct. Candidates must hold a valid unrestricted dental license at the time of examination and adhere to the ABOMP Code of Ethics.

What is the format of the ABOMP exam?

ABOMP certification is earned by passing three components: (1) a Written section of single-best-answer multiple-choice questions covering the full breadth of oral and maxillofacial pathology; (2) a Practical section requiring microscopic slide identification and diagnosis under time pressure; and (3) an Oral examination in which candidates are interviewed by ABOMP examiners on case-based scenarios. Each component must be passed independently to achieve Diplomate status.

How much does the 2026 ABOMP exam cost?

The combined ABOMP Written, Practical, and Oral examination fees are approximately $2,500-$3,500 — always verify the current schedule on the ABOMP website. Retake fees apply per failed component and require re-registration within the eligibility window. Continuing Certification (MOC) fees apply after becoming a Diplomate.

When is the 2026 exam administered?

ABOMP typically offers the examination annually, often in conjunction with the American Academy of Oral and Maxillofacial Pathology (AAOMP) meeting cycle. Applications open months in advance with firm deadlines. Exact 2026 dates and locations should be confirmed on the ABOMP website.

How is the exam scored?

ABOMP uses criterion-referenced scoring with pass/fail standards set by subject-matter experts through the modified Angoff method. A candidate's result depends on performance relative to the fixed cut-score rather than the performance of other candidates. Written, Practical, and Oral components are scored independently and each must be passed to earn Diplomate status.

What are the highest-yield topics?

Highest-yield topics include odontogenic tumors (ameloblastoma BRAF V600E, AOT, Pindborg tumor), odontogenic cysts (OKC with PTCH1 and Gorlin syndrome), fibro-osseous lesions (fibrous dysplasia GNAS, ossifying fibroma, COD), salivary gland molecular signatures (PLAG1 in pleomorphic adenoma, MAML2 in MEC, MYB-NFIB in AdCC, ETV6-NTRK3 in secretory carcinoma), HPV+ oropharyngeal SCC with p16 IHC and AJCC 8 staging, proliferative verrucous leukoplakia, submucous fibrosis, pemphigus vulgaris (desmoglein 3, Nikolsky sign, fishnet DIF) vs mucous membrane pemphigoid (linear BMZ DIF), MRONJ, and Gorlin/Gardner/Peutz-Jeghers syndromes. The 2017 AAP/EFP periodontal classification is mandatory.

How should I study for this exam?

Use a structured 12-24 month plan aligned to the ABOMP content outline: begin with odontogenic cysts and tumors and developmental anomalies, then bone lesions and salivary gland pathology, then oral SCC and premalignancy and infections, and finally immune-mediated disease and syndromes. Integrate primary texts (Neville — Oral and Maxillofacial Pathology; Regezi — Oral Pathology; WHO Classification of Head and Neck Tumours), AAOMP review series, and the ABOMP content outline. High-volume MCQ practice plus repeated timed microscopic slide sessions are essential — the Practical is often the decisive component. Complete 2-3 full mock exams covering all three components.