Oral Pathology

TL;DR

Key Facts

Introduction to Oral Pathology

Oral pathology is the branch of dentistry concerned with the nature, identification, and management of diseases affecting the oral and maxillofacial structures. It encompasses diseases of the oral mucosa, salivary glands, jaws and alveolar bone, teeth and supporting periodontium, as well as associated soft tissues of the head and neck. The oral pathologist works at the interface of clinical dentistry and laboratory medicine — receiving biopsy specimens, preparing histological sections, and interpreting microscopic findings to provide a definitive tissue diagnosis that guides patient management.

The importance of oral pathology in dental education and clinical practice cannot be overstated. Many systemic diseases have oral manifestations that may be the presenting sign, and the clinician who can recognise an abnormal lesion — and know when and how to biopsy it — is in a position to dramatically alter patient outcomes. Oral cancer detected at Stage I has a 5-year survival rate exceeding 80%; the same cancer found at Stage IV carries a survival rate below 30%.

The diagnostic process in oral pathology follows a logical sequence: clinical description of the lesion (size, colour, surface texture, borders, consistency, site, duration, symptoms); radiographic assessment where appropriate; and, ultimately, tissue biopsy for histopathological confirmation. Major disease categories include developmental anomalies, inflammatory and reactive lesions, infections, potentially malignant disorders, benign and malignant neoplasms, cysts, and metabolic or systemic bone disease.

Developmental Anomalies of Teeth

Developmental anomalies arise during tooth formation and may affect number, size, shape, or structure. Many are identified on routine radiographic examination and have implications for treatment planning.

Anomalies of Number

Hypodontia (oligodontia when six or more teeth are missing, anodontia when all teeth are absent) is the most common dental developmental anomaly. The most frequently missing permanent teeth are the maxillary lateral incisors, mandibular second premolars, and maxillary second premolars. Hypodontia may be isolated or associated with syndromes including ectodermal dysplasia. Hyperdontia refers to supernumerary teeth. The most common supernumerary is the mesiodens — a small peg-shaped or conical tooth located between the maxillary central incisors — which can cause eruption delay, crowding, or median diastema. Other supernumeraries include paramolars (adjacent to molars) and distomolars (distal to third molars). Supernumeraries are more common in the permanent dentition and may be associated with cleft lip/palate, Gardner syndrome, and cleidocranial dysostosis.

Anomalies of Size

Microdontia (abnormally small teeth) may be generalised or localised. The maxillary lateral incisor is the most commonly affected tooth, often presenting as a peg-shaped lateral. True generalised microdontia is rare and associated with pituitary dwarfism. Macrodontia (abnormally large teeth) may similarly be generalised (associated with pituitary gigantism) or localised (often due to fusion or gemination — see below).

Anomalies of Shape

• Gemination: Attempted division of a single tooth germ results in a large bifid crown with a single root and root canal. The tooth count appears normal (the anomalous tooth is counted as one).
• Fusion: Union of two adjacent tooth germs produces a large tooth with two root canals (usually). The tooth count is one fewer than normal. Fusion can involve a normal tooth and a supernumerary.
• Taurodontism: Enlarged pulp chamber with apical displacement of the pulp floor. Common in Klinefelter syndrome and amelogenesis imperfecta. Clinically relevant for endodontic access.
• Dilaceration: Abrupt bend or curve in the root or crown, usually following trauma to the primary predecessor during development. The affected tooth may fail to erupt.
• Dens invaginatus (dens in dente): An infolding of the enamel organ into the dental papilla. Most common in maxillary lateral incisors. The deep invagination creates a communication with the oral environment, predisposing to early pulp necrosis. Classified by Oehlers Type I–III by depth.
• Dens evaginatus (Leong’s premolar): An accessory cusp-like projection on the occlusal surface. Most common in mandibular premolars, especially in individuals of Asian descent. The tubercle contains pulp tissue; occlusal wear or fracture can cause pulp exposure.

Anomalies of Structure

Amelogenesis imperfecta (AI) is a group of hereditary conditions affecting enamel formation, classified into hypoplastic (insufficient enamel quantity), hypomaturation (defective enamel maturation), and hypocalcification (deficient enamel mineralisation) types. Enamel is thin, soft, or discoloured. Dentinogenesis imperfecta (DI) affects dentine, producing opalescent, blue-grey or brown discolouration, bulbous crowns, cervical constriction, and obliteration of pulp chambers and root canals on radiographs. DI Type I is associated with osteogenesis imperfecta; DI Types II and III are isolated dentinal defects (previously called “hereditary opalescent dentine”).

Inflammatory Conditions of the Oral Mucosa

Aphthous Ulcers (Recurrent Aphthous Stomatitis)

Aphthous ulcers are the most common oral mucosal ulcers, affecting approximately 20% of the population. They are characterised by painful, round or oval ulcers with a fibrinous yellow-grey base and an erythematous halo, occurring on non-keratinised mucosa (labial and buccal mucosa, floor of mouth, ventral tongue). Three clinical forms are recognised:

• Minor aphthae (Mikulicz ulcers): Most common type (80%). Diameter <1 cm; heal within 7–14 days without scarring. One to five lesions at a time.
• Major aphthae (Sutton’s disease / periadenitis mucosa necrotica recurrens): Diameter >1 cm; persist for weeks to months; heal with scarring. Extremely painful; may affect soft palate and tonsillar fauces.
• Herpetiform aphthae: Multiple (10–100) small (<3 mm) ulcers that may coalesce; resembles primary herpes clinically but is not caused by herpes simplex virus. More common in women; tends to occur on keratinised mucosa.

Management is symptomatic: topical corticosteroids (triamcinolone acetonide in Orabase, betamethasone mouthwash), topical analgesics (benzydamine), and chlorhexidine mouthwash. Systemic thalidomide or colchicine may be used for severe major aphthae. Precipitating factors include stress, trauma, sodium lauryl sulphate in toothpaste, and haematinic deficiencies (iron, B12, folate).

Viral Infections

Primary herpetic gingivostomatitis (HSV-1) is the most common viral oral infection in children, presenting with fever, malaise, lymphadenopathy, erythematous gingivae, and multiple vesicles that rupture to form painful ulcers on both keratinised and non-keratinised mucosa. It is self-limiting (10–14 days) but may be treated with aciclovir in severe cases. Recurrent herpes labialis (“cold sore”) represents viral reactivation and presents as a cluster of vesicles at the vermilion border, preceded by a prodrome of tingling or burning.

Herpes zoster (shingles) involving the trigeminal nerve produces a unilateral painful vesicular eruption along the distribution of V2 or V3, with intraoral ulceration that does not cross the midline. Post-herpetic neuralgia is a significant complication. Treatment: valaciclovir or famciclovir.

Hand-foot-and-mouth disease (Coxsackievirus A16, Enterovirus 71) affects young children and produces small oval ulcers on the buccal mucosa, tongue, and palate, with concurrent vesicular lesions on the palms and soles. Management is supportive.

Oral Candidiasis

Oral candidiasis is caused by Candida albicans (most common) in the context of predisposing local or systemic factors (xerostomia, immunosuppression, antibiotic use, denture wearing, diabetes). Clinical forms include:

• Pseudomembranous candidiasis (thrush): White curd-like plaques on buccal mucosa, tongue, and palate that wipe off to leave an erythematous base. Associated with infancy, HIV/AIDS, and corticosteroid use.
• Erythematous candidiasis: Red, atrophic patches — includes denture stomatitis (erythema under a maxillary denture) and median rhomboid glossitis (rhomboid red patch on dorsal midline tongue).
• Hyperplastic candidiasis (candidal leukoplakia): White patch on the buccal commissure or tongue that does not wipe off; considered potentially malignant.
• Angular cheilitis: Erythematous fissuring at the oral commissures; often mixed infection with Candida and Staphylococcus aureus.

Diagnosis: clinical appearance, PAS staining of smear, or culture. Treatment: topical nystatin or miconazole; systemic fluconazole for resistant or disseminated cases.

Geographic Tongue (Benign Migratory Glossitis)

Geographic tongue presents as erythematous patches of depapillation with a white serpiginous border on the dorsal and lateral tongue. The lesions migrate over time and are typically asymptomatic, though some patients report sensitivity to spicy or acidic foods. It is associated with fissured tongue and, less consistently, with psoriasis. No treatment is required; reassurance is appropriate.

Benign Oral Mucosal Lesions

Benign mucosal lesions are extremely common in dental practice. Correct identification avoids unnecessary biopsy while ensuring genuinely suspicious lesions are not dismissed. The following comparison table summarises the key features.

Potentially Malignant Disorders (PMDs)

Potentially malignant disorders (formerly “premalignant lesions”) are clinical presentations that carry a risk of malignant transformation to oral squamous cell carcinoma. They require biopsy for definitive diagnosis and ongoing surveillance.

Leukoplakia

Leukoplakia is defined as a white patch of the oral mucosa that cannot be rubbed off and cannot be attributed to any other definable disease — it is a clinical term, not a histopathological diagnosis. It affects approximately 1–3% of the general population and has an overall malignant transformation rate of approximately 5–17% over 10 years.

Two main clinical forms are recognised:

• Homogeneous leukoplakia: Uniformly white, flat or slightly raised, smooth or fissured surface. Lower risk of dysplasia. May regress with tobacco cessation.
• Non-homogeneous leukoplakia: Includes speckled (erythroleukoplakia — red and white mixed), nodular (white nodules on red base), and verrucous (irregular, corrugated, white surface) subtypes. Higher risk of harbouring dysplasia or carcinoma. Proliferative verrucous leukoplakia (PVL) is a particularly aggressive multifocal variant with high malignant transformation rate (~70%).

Erythroplakia

Erythroplakia is a red patch of the oral mucosa that cannot be attributed to any other definable cause. It is far less common than leukoplakia but carries a dramatically higher malignant transformation rate of approximately 40–50% — making it the highest-risk potentially malignant disorder. On histology, the majority already show severe dysplasia or carcinoma in situ at the time of biopsy. Sites of predilection include the soft palate, floor of mouth, and ventral tongue.

Erythroleukoplakia (Speckled Leukoplakia)

Erythroleukoplakia (mixed red and white lesion) carries a risk intermediate between pure leukoplakia and pure erythroplakia, but closer to the higher end. The red component reflects areas of epithelial atrophy and represents the highest-risk zones within the lesion — these areas should be targeted for biopsy.

Oral Submucous Fibrosis (OSMF)

Oral submucous fibrosis is a chronic, progressive, potentially malignant condition characterised by submucosal fibrosis leading to trismus and mucosal rigidity. It is strongly associated with areca nut (betel quid) chewing, predominantly affecting individuals from South and Southeast Asia. Features include burning sensation, blanching and hardening of the buccal mucosa, progressive reduction in mouth opening, and fibrous bands in the buccal mucosa, retromolar region, and soft palate. Malignant transformation occurs in approximately 7–13% of cases.

Actinic Cheilitis

Actinic cheilitis results from chronic ultraviolet (UV) radiation exposure and affects the lower lip predominantly. It presents as a dry, scaly, atrophic lower lip with blurring of the vermilion border, areas of erythema, and focal leukoplakia. It is the oral PMD most closely associated with outdoor/agricultural workers and fair-skinned individuals. Malignant transformation to OSCC of the lip occurs in approximately 10–20% of cases.

Management Principles for PMDs

• All PMDs require biopsy for histopathological staging of dysplasia (mild, moderate, severe/carcinoma in situ)
• Risk stratification guides management: high-grade dysplasia warrants surgical excision; low-grade dysplasia may be monitored with regular review
• Tobacco and alcohol cessation counselling is essential and may lead to lesion regression
• HPV status (particularly HPV-16) should be considered in oropharyngeal lesions
• Even after removal, patients require long-term follow-up due to field cancerisation

Oral Squamous Cell Carcinoma (OSCC)

Oral squamous cell carcinoma accounts for approximately 90% of all oral malignancies. It is one of the ten most common cancers worldwide, with approximately 300,000 new cases per year globally. Early detection is the single most important prognostic factor.

Risk Factors

• Tobacco: Smoking (all forms) and smokeless tobacco are the most significant risk factors. Risk is dose-dependent and synergistic with alcohol.
• Alcohol: Independent risk factor; combined tobacco and alcohol use multiplies risk by up to 15-fold.
• HPV-16 and HPV-18: The primary aetiological agent in oropharyngeal SCC (base of tongue, tonsillar region). HPV-associated OSCC has a better prognosis than tobacco-associated disease.
• Betel nut (areca nut): Predominant risk factor in South and Southeast Asia.
• UV radiation: Risk factor specifically for carcinoma of the lip (especially lower lip, actinic cheilitis precursor).
• Immunosuppression: Organ transplant recipients, HIV/AIDS.
• Iron deficiency: Plummer-Vinson (Paterson-Kelly) syndrome — iron-deficiency anaemia, dysphagia, post-cricoid web, and increased risk of upper aerodigestive tract SCC.

Common Sites

The lateral and ventral tongue and floor of mouth are the two highest-risk sites for intraoral OSCC — together accounting for the majority of cases. Other common sites include the soft palate and oropharynx (HPV-associated), retromolar trigone, gingiva, and buccal mucosa. The dorsal tongue and hard palate are relatively uncommon sites.

Clinical Features

Early OSCC may be asymptomatic — a painless ulcer, white or red patch, or exophytic growth. Advanced features include:

• Indurated (hardened) ulcer with raised, rolled, everted edges and a necrotic base
• Fixation to underlying structures (bone, tongue musculature)
• Cervical lymphadenopathy — firm, non-tender, fixed nodes indicate metastatic spread
• Trismus (involvement of masticatory muscles or pterygomandibular space)
• Paraesthesia or anaesthesia (inferior alveolar nerve involvement)
• Unexplained tooth mobility or loosening without periodontal cause

TNM Staging

The TNM (Tumour-Node-Metastasis) system is used for staging OSCC:

• T1: Tumour ≤2 cm; depth of invasion (DOI) ≤5 mm
• T2: Tumour ≤4 cm; or DOI >5 mm but ≤10 mm
• T3: Tumour >4 cm; or DOI >10 mm
• T4: Moderately or very advanced local disease (bone invasion, skin invasion, floor of mouth, carotid encasement)
• N0–N3: Regional lymph node involvement (N0 = none; N3 = massive nodal disease)
• M0/M1: Absence or presence of distant metastases

Treatment is multimodal: surgery (wide local excision ± neck dissection) is the primary modality; radiotherapy (with or without concurrent chemotherapy) is used for advanced disease or as primary treatment where surgery would compromise function. The 5-year survival rate is approximately 85% for Stage I, 65% for Stage II, 40% for Stage III, and 25% for Stage IV disease.

Periapical Pathology

Periapical pathology develops as a consequence of pulp necrosis — typically from caries, trauma, or iatrogenic injury — and represents the spread of infection or inflammatory products into the periapical tissues. The following comparison table distinguishes the major periapical lesions.

Jaw Cysts

Jaw cysts are pathological cavities lined by epithelium and containing fluid or semi-fluid material. They are classified into odontogenic (derived from tooth-forming epithelium) and non-odontogenic (derived from other epithelial remnants) types. The following table provides a comparative overview of the most clinically significant jaw cysts.

Odontogenic Tumours

Odontogenic tumours arise from the epithelial, mesenchymal, or mixed components of the tooth-forming apparatus. They range from hamartomas (odontomas) to locally aggressive neoplasms (ameloblastoma). The following table compares the most frequently tested odontogenic tumours.

Salivary Gland Pathology

Obstructive and Inflammatory Conditions

Sialolithiasis (salivary calculi) is most common in the submandibular gland and Wharton’s duct (approximately 80% of cases), owing to the viscous secretion, upward flow against gravity, and tortuous duct anatomy. Patients present with pain and swelling at mealtimes (obstructive sialadenitis). Calculi are often radiopaque on plain radiographs. Treatment: duct dilation and manual expression, sialoendoscopy, or excision of the stone (±gland if recurrent).

Acute suppurative sialadenitis (most commonly parotid) is caused by ascending bacterial infection (Staphylococcus aureus most common) in the setting of dehydration, xerostomia, or duct obstruction. It presents with tender, swollen gland, trismus, and purulent discharge from Stensen’s duct. Treatment: antibiotics, hydration, salivary stimulation.

Chronic sclerosing sialadenitis (Kuttner tumour) most commonly affects the submandibular gland and produces a firm, indurated mass that may be mistaken for a neoplasm clinically. It is associated with IgG4-related disease.

Sjogren’s Syndrome

Sjogren’s syndrome is a systemic autoimmune condition characterised by lymphocytic infiltration of exocrine glands — primarily salivary and lacrimal glands — resulting in xerostomia (dry mouth) and xerophthalmia (dry eyes, keratoconjunctivitis sicca).

• Primary Sjogren’s syndrome: Occurs in isolation without another connective tissue disease
• Secondary Sjogren’s syndrome: Associated with another autoimmune disease — most commonly rheumatoid arthritis, but also SLE and systemic sclerosis
• Autoantibodies: Anti-SSA (anti-Ro) and anti-SSB (anti-La) are the hallmark serological markers
• Oral manifestations: Severe xerostomia, lobular parotid enlargement (bilateral), increased caries, candidiasis, difficulty chewing and swallowing
• Lymphoma risk: Patients with primary Sjogren’s syndrome have a 44-fold increased risk of developing non-Hodgkin’s lymphoma (particularly MALT lymphoma of the parotid)
• Diagnosis: Minor salivary gland biopsy (labial gland biopsy from the lower lip) showing focal lymphocytic sialadenitis (focus score ≥1); Schirmer’s test for tear flow; sialometry; serological tests

Salivary Gland Neoplasms

Pleomorphic adenoma is the most common salivary gland tumour overall and the most common benign salivary gland tumour. It accounts for approximately 60–70% of all parotid tumours. It presents as a slow-growing, painless, firm, mobile mass most commonly in the parotid gland (superficial lobe). Histologically, it contains both epithelial (ductal/myoepithelial) and mesenchymal (chondromyxoid stroma) elements — hence “mixed tumour.” Treatment is superficial parotidectomy with preservation of the facial nerve. If incompletely excised, recurrence is likely (seeding from ruptured pseudopod). Long-standing pleomorphic adenomas may undergo malignant transformation to carcinoma ex pleomorphic adenoma (approximately 5–10% risk over time).

Mucoepidermoid carcinoma is the most common malignant salivary gland tumour. It arises most commonly in the parotid gland but is also the most common malignant salivary tumour of minor salivary glands and the most common salivary gland malignancy in children. It is graded low, intermediate, or high according to histological features (cystic component, mucous cells, nuclear pleomorphism). Low-grade tumours have an excellent prognosis; high-grade behaves aggressively. Treatment: surgical resection; radiotherapy for high-grade or advanced disease.

Adenoid cystic carcinoma is the second most common malignant salivary gland tumour. It has a characteristically infiltrative growth pattern with perineural invasion — producing pain and facial nerve palsy — and late distant metastases (especially to the lung). Three histological patterns: cribriform (“Swiss cheese”), tubular, and solid (worst prognosis). Despite a deceptively slow clinical course, long-term prognosis is poor due to late recurrences and metastases.

Bone Pathology of the Jaws

Fibrous Dysplasia

Fibrous dysplasia is a non-neoplastic developmental condition in which normal bone is replaced by fibrous connective tissue containing disorganised woven bone trabeculae. It results from activating mutations in the GNAS1 gene encoding the Gs-alpha protein. Two main forms exist:

• Monostotic: Single bone involved; most common form. In the craniofacial skeleton, it produces painless expansion of the jaw (maxilla more than mandible), facial asymmetry, and obliteration of the maxillary antrum (“leonine” changes).
• Polyostotic: Multiple bones involved; more severe. When associated with cafe-au-lait skin pigmentation and endocrine abnormalities (precocious puberty in girls), it is termed McCune-Albright syndrome.

Radiographic appearance: “ground-glass” homogeneous radiopacity with ill-defined borders that blend with adjacent normal bone (no cortication). Treatment: conservative; surgical contouring for cosmetic purposes after skeletal maturity, as the lesion tends to stabilise then.

Paget’s Disease of Bone (Osteitis Deformans)

Paget’s disease affects older patients (usually >50 years), involving disordered osteoclastic and osteoblastic activity that results in structurally weak, enlarged bone. Elevated serum alkaline phosphatase. Cranial and facial involvement produces skull enlargement and characteristic facial changes (“leontiasis ossea” or “lion facies”). Oral features include:

• Progressive jaw enlargement — patients may report that dentures no longer fit
• Hypercementosis — excessive cementum deposition on roots, making extraction extremely difficult
• “Cotton-wool” radiographic appearance — mixed radiolucent and radiopaque patches

Malignant transformation to osteosarcoma is a rare but recognised complication (<1%).

Cherubism

Cherubism is a rare autosomal dominant condition characterised by bilateral symmetrical swelling of the posterior mandible (and sometimes maxilla) beginning in early childhood, due to replacement of bone by fibrous tissue containing multinucleated giant cells. Children have a characteristic “cherubic” appearance with full cheeks and upward-tilted eyes. Lesions typically regress after puberty. SH3BP2 gene mutation. Histology resembles central giant cell granuloma but the clinical/genetic context distinguishes them.

Central Giant Cell Granuloma (CGCG)

CGCG is a non-neoplastic lesion of the jaws characterised by a fibrous stroma containing numerous multinucleated osteoclast-like giant cells and areas of haemorrhage. It occurs most commonly in young females in the anterior mandible. Two clinical forms: non-aggressive (most common — well-defined, asymptomatic, no root resorption) and aggressive (rapid growth, cortical perforation, root resorption, high recurrence after curettage). Differentiate from giant cell tumour of long bones (CGCG does not metastasise), hyperparathyroidism (check parathyroid hormone levels — “brown tumour” is histologically identical to CGCG), and Noonan syndrome/neurofibromatosis. Treatment: curettage; peripheral CGCG (on gingiva) has low recurrence.

Osteoradionecrosis (ORN)

Osteoradionecrosis is bone death resulting from radiation damage to the vasculature, characterised by hypoxic-hypovascular-hypocellular tissue. It most commonly affects the mandible (due to its end-arterial blood supply) following radiotherapy for head and neck cancer. Exposed necrotic bone >3 months in a previously irradiated field is the clinical definition. Risk factors: radiation dose >60 Gy, post-irradiation dental extractions, poor oral hygiene. Prevention: complete dental rehabilitation before radiotherapy (extractions with >2 weeks healing time). Treatment: conservative (antiseptic rinses, antibiotics, sequestrectomy) to radical resection; hyperbaric oxygen therapy is controversial.

Medication-Related Osteonecrosis of the Jaw (MRONJ)

MRONJ (formerly BRONJ — bisphosphonate-related osteonecrosis of the jaw) is defined as exposed or necrotic bone in the maxillofacial region that has persisted for more than 8 weeks in a patient taking or previously exposed to an antiresorptive or antiangiogenic agent, without a history of radiotherapy. Causative medications include:

• Bisphosphonates (alendronate, zoledronic acid): inhibit osteoclastic bone resorption; incorporated into bone permanently; dental extractions are the most common precipitating event
• Denosumab (RANK-L inhibitor): similar mechanism; risk resolves after cessation as it does not incorporate into bone
• Antiangiogenic agents (bevacizumab, sunitinib)

Risk is markedly higher with intravenous bisphosphonates (used for multiple myeloma and bone metastases) than oral bisphosphonates (used for osteoporosis). Management: drug holiday (controversial), conservative debridement, antiseptic mouthwash, antibiotics; surgical resection for refractory cases. Prevention: comprehensive dental treatment before starting antiresorptive therapy is strongly recommended.

Summary Table & Exam Tips

High-Yield Comparisons for INBDE

Related Topics

Oral pathology integrates closely with the following disciplines and foundational sciences.

References & Sources

The following foundational texts and peer-reviewed sources inform this article.

1. Neville BW, Damm DD, Allen CM, Chi AC, 2015. Oral and Maxillofacial Pathology. 4th ed. Elsevier.
2. Regezi JA, Sciubba JJ, Jordan RCK, 2016. Oral Pathology: Clinical Pathologic Correlations. 7th ed. Elsevier.
3. Warnakulasuriya S, 2018. Global epidemiology of oral and oropharyngeal cancer. Oral Oncology, 45(4-5):309–316.
4. van der Waal I, 2010. Potentially malignant disorders of the oral and oropharyngeal mucosa; terminology, classification and present concepts of management. Oral Oncology, 46(6):396–398.
5. Ruggieri M, Pavone V, Polizzi A et al., 2010. Cherubism: best clinical practice. Orphanet Journal of Rare Diseases, 5:38.
6. Speight PM, Carlos R, 2006. Maxillofacial fibro-osseous lesions. Current Diagnostic Pathology, 12(1):1–10.
7. Ruggiero SL, Dodson TB, Aghaloo T et al., 2022. American Association of Oral and Maxillofacial Surgeons’ position paper on medication-related osteonecrosis of the jaws — 2022 update. Journal of Oral and Maxillofacial Surgery, 80(5):920–943.
8. Shiboski CH, Shiboski SC, Seror R et al., 2017. 2016 American College of Rheumatology/European League Against Rheumatism classification criteria for primary Sjogren’s syndrome. Annals of the Rheumatic Diseases, 76(1):9–16.

Summary

Oral pathology is a broad and clinically essential discipline that underpins much of dental practice. From recognising the subtle white patch that may herald oral cancer, to correctly classifying a jaw cyst that dictates surgical approach, the oral pathologist’s expertise — anchored in histopathology — provides the definitive answers that guide patient care. For the dental student and INBDE candidate, mastery of oral pathology means understanding not just individual lesions but the underlying biological processes: why an OKC recurs (daughter cysts, thin friable lining, active epithelial turnover), why erythroplakia is higher risk than leukoplakia (atrophic epithelium with disrupted barrier function), and why ameloblastoma demands wide resection (pseudopodial infiltration of cancellous bone beyond the visible lesion boundary).

About the Author

Dr. Andries Smith

Founder, Dental Panda

Dr. Andries Smith founded Dental Panda in 2020. As an immigrant to the United States, he had to take the INBDE exam, even though he was practicing dentistry for over 10 years. This revealed an opportunity. Andries noticed that INBDE prep course companies were putting profit over students. With his expertise and experience in dentistry, he created free dental wiki resources for students and the general public to have access to.