Overseas Registration Exam (ORE) Oral Surgery, Oral Medicine and Pathology Syllabus

Compare a recurrent aphthous stomatitis minor ulcer with a major aphthous ulcer.

Minor aphthae: <10 mm, shallow, round/oval, non-keratinised mucosa, heal in 7–14 days without scarring. Major aphthae: >10 mm, deeper, last weeks to months, may scar, often affect keratinised mucosa too. Both spare keratinised gingiva/hard palate typically and recur.

List systemic/haematinic causes that should be excluded in a patient with recurrent oral ulceration.

Deficiency of iron, folate or vitamin $\ce{B12}$; coeliac disease; Crohn's disease/ulcerative colitis; Behçet's disease; HIV; haematological disorders; and drug causes (e.g. nicorandil, NSAIDs, methotrexate). Investigate persistent or atypical ulceration with FBC and haematinics.

What is the single most important red flag for any oral ulcer and the rule about persistence?

A solitary ulcer (often with rolled/indurated raised margins, bleeding, fixation to deep tissues) that fails to heal within 3 weeks must be regarded as oral squamous cell carcinoma until proven otherwise and referred urgently (2-week-wait) for biopsy.

What is leukoplakia and how does it differ from a frictional/keratotic white patch?

Leukoplakia is a clinical diagnosis of exclusion: a white plaque of questionable malignant risk that cannot be rubbed off and cannot be attributed to any other defined lesion. A frictional keratosis has an identifiable cause (cheek-biting, sharp tooth) and resolves when the cause is removed; leukoplakia is a potentially malignant disorder.

Distinguish leukoplakia from erythroplakia in terms of malignant potential.

Erythroplakia is a red velvety patch that cannot be attributed to another condition; it has a much HIGHER risk of containing dysplasia or carcinoma than leukoplakia and almost always warrants biopsy. Speckled (erythro)leukoplakia is also high risk. Erythroplakia is the most likely premalignant lesion to be or become malignant.

What are the clinical types of oral lichen planus and which feature confirms the diagnosis?

Types: reticular (Wickham's striae – most common, often asymptomatic), papular, plaque-like, atrophic, erosive/ulcerative, and bullous. Reticular white lacy striae (Wickham's striae), often bilateral and symmetrical on the buccal mucosa, are characteristic; biopsy shows band-like subepithelial lymphocytic infiltrate and basal cell liquefaction.

What is the difference between pemphigus vulgaris and mucous membrane (cicatricial) pemphigoid in terms of antibody target and Nikolsky sign?

Pemphigus vulgaris: IgG against desmoglein (desmosomes), intra-epithelial split, fragile bullae, positive Nikolsky sign, potentially life-threatening, acantholytic Tzanck cells. Mucous membrane pemphigoid: antibodies against the basement membrane (hemidesmosomes), sub-epithelial split, tense blisters, may cause ocular scarring (symblepharon). Both are vesiculobullous autoimmune disorders.

What direct immunofluorescence pattern is seen in pemphigus vulgaris versus pemphigoid?

Pemphigus vulgaris: intercellular ('fishnet'/chicken-wire) IgG and C3 deposition between keratinocytes. Pemphigoid: linear IgG and/or C3 deposition along the basement membrane zone. DIF on perilesional tissue is the key confirmatory investigation.

Compare the typical clinical features and aetiology of pleomorphic adenoma versus Warthin tumour of the salivary glands.

Pleomorphic adenoma: most common salivary tumour, usually parotid, slow-growing painless mobile mass, mixed epithelial/myoepithelial with chondromyxoid stroma, risk of malignant transformation if untreated. Warthin tumour (adenolymphoma): second most common benign parotid tumour, can be bilateral, associated with smoking, contains lymphoid tissue.

What is a mucocele versus a ranula, and how do they arise?

Mucocele: a mucus extravasation (trauma-induced) or retention cyst, most commonly on the lower lip, presenting as a bluish fluctuant swelling. Ranula: a mucocele of the floor of mouth arising from the sublingual gland; a 'plunging' ranula herniates through mylohyoid into the neck.

List the major causes of xerostomia (dry mouth).

Drugs (anticholinergics, antidepressants, antihistamines, diuretics, antipsychotics), Sjögren's syndrome, radiotherapy to head and neck, dehydration, diabetes (mellitus/insipidus), anxiety, sarcoidosis, HIV, and salivary gland disease/aplasia. Drug-induced is the most common cause.

What is Sjögren's syndrome and what distinguishes primary from secondary forms?

A chronic autoimmune exocrinopathy causing dry mouth (xerostomia) and dry eyes (keratoconjunctivitis sicca) from lymphocytic destruction of salivary/lacrimal glands. Primary: sicca alone; Secondary: sicca plus a connective tissue disease (e.g. rheumatoid arthritis, SLE). Associated antibodies: anti-Ro (SS-A) and anti-La (SS-B); raised lymphoma risk.

Describe the typical features and diagnostic criteria of trigeminal neuralgia.

Sudden, severe, unilateral, electric-shock/lancinating pain in one or more divisions of the trigeminal nerve, lasting seconds, triggered by light touch/washing/eating/wind, with refractory periods between attacks and no neurological deficit. First-line medical treatment is carbamazepine; MRI is indicated to exclude space-occupying lesions/MS, especially in younger patients.

What features differentiate burning mouth syndrome from secondary causes of oral burning?

Burning mouth syndrome (primary) = burning sensation with clinically normal mucosa and no identifiable medical/dental cause, often worse through the day, relieved by eating. Secondary causes (must be excluded): candidiasis, haematinic/vitamin deficiency, diabetes, xerostomia, parafunction, denture problems, and anxiety/depression.

Compare a radicular (periapical) cyst with a dentigerous cyst regarding origin and radiographic relationship.

Radicular cyst: most common odontogenic cyst, inflammatory, arises from epithelial cell rests of Malassez at the apex of a NON-VITAL tooth, well-defined apical radiolucency. Dentigerous cyst: developmental, surrounds the crown of an UNERUPTED tooth attached at the cemento-enamel junction (most often lower third molar/canine).

What is an odontogenic keratocyst (OKC), its key histological feature, and its clinical significance?

A developmental odontogenic cyst (now sometimes keratocystic odontogenic tumour) with a thin, parakeratinised stratified squamous epithelium, palisaded basal layer and corrugated luminal surface. It has a high recurrence rate, grows along bone (antero-posteriorly), and multiple OKCs suggest Gorlin–Goltz (naevoid basal cell carcinoma) syndrome.

Describe the ameloblastoma: classification, behaviour and radiographic appearance.

A benign but locally aggressive odontogenic epithelial tumour, most often in the posterior mandible. Radiographically a multilocular 'soap-bubble' or 'honeycomb' radiolucency, may cause expansion and root resorption. Despite benign histology it is locally invasive with high recurrence, so requires resection with a margin.

What are the major risk factors for oral squamous cell carcinoma?

Tobacco (smoked and smokeless/paan), areca/betel nut, alcohol (synergistic with tobacco), high-risk HPV (especially oropharyngeal), sunlight (lip), chronic immunosuppression, iron deficiency (Plummer–Vinson), and pre-existing potentially malignant disorders. Age over 40 and male sex are also factors.

Describe the TNM staging concept used for oral cancer and what each letter denotes.

TNM: T = primary tumour size/local extent (T1 $\leq 2$ cm, T2 $>2$–4 cm, T3 $>4$ cm, T4 invading adjacent structures); N = regional lymph node involvement (number, size, laterality); M = distant metastasis (M0 none, M1 present). Higher stage means poorer prognosis and guides treatment (surgery, radiotherapy, chemotherapy).

What clinical features should make you suspect oral squamous cell carcinoma and prompt urgent referral?

A non-healing ulcer >3 weeks, an indurated/rolled raised margin, a red (erythroplakia), white or speckled patch, an exophytic or fungating mass, fixation to deeper tissues, unexplained tooth mobility, numbness (paraesthesia), persistent neck lymphadenopathy, or dysphagia. Refer on a 2-week-wait suspected cancer pathway.

What is fibrous dysplasia of the jaws and its characteristic radiographic appearance?

A developmental bone disorder where normal bone is replaced by fibro-osseous tissue (GNAS gene mutation), causing painless bony expansion, usually in the maxilla, in young patients. Classic radiograph: a diffuse 'ground-glass' radiopacity with poorly defined margins blending into normal bone. Monostotic or polyostotic (McCune–Albright).

Describe Paget's disease of bone and its dental/jaw implications.

A disorder of disordered bone remodelling (excess osteoclastic then osteoblastic activity) in older patients, causing enlarged, deformed bone. In the jaws (more often maxilla) it causes expansion, spacing of teeth, hypercementosis, and a 'cotton-wool' radiographic appearance. Raised serum alkaline phosphatase with normal calcium/phosphate; bone is hypervascular and prone to osteomyelitis.

What distinguishes a cemento-osseous dysplasia/periapical condition from a periapical granuloma on radiograph and vitality testing?

Periapical (cemento-osseous) dysplasia occurs on VITAL teeth (positive vitality test), commonly lower incisors, and matures from radiolucent to mixed to radiopaque over time, requiring no treatment. A periapical granuloma is associated with a NON-VITAL tooth and remains radiolucent, needing endodontics or extraction.

What are the recognised oral potentially malignant disorders (OPMDs) requiring surveillance?

Leukoplakia, erythroplakia, proliferative verrucous leukoplakia, oral submucous fibrosis, oral lichen planus (especially erosive), actinic cheilitis, oral lupus erythematosus, dyskeratosis congenita, and chronic hyperplastic candidosis. They carry an increased risk of malignant transformation and warrant biopsy and review.

What is oral submucous fibrosis, its main cause, and why does it matter?

A chronic progressive fibrosis of the oral mucosa caused chiefly by areca (betel) nut chewing, producing mucosal blanching, palpable fibrous bands, burning, and progressive trismus (limited mouth opening). It is a potentially malignant disorder with significant risk of malignant transformation and is largely irreversible.

How are dental fractures of the crown/root classified by tissue involvement (Ellis-type/WHO concept)?

Enamel infraction (crack, no loss); enamel-only fracture; enamel-dentine fracture (uncomplicated); enamel-dentine-pulp fracture (complicated, pulp exposed); crown-root fracture (with/without pulp involvement); root fracture; alveolar fracture. Management depends on pulp exposure, maturity (open/closed apex) and time elapsed.

State the immediate first-aid advice and storage media for an avulsed permanent tooth.

Hold by the crown, do NOT scrub the root (preserve PDL cells), rinse gently in milk/saline if dirty, and replant immediately into the socket then bite on gauze. If not possible, store in cold milk, saliva (buccal sulcus/under tongue), or HBSS/saline — NOT water — and seek dental care urgently. Extra-oral dry time >60 min has poor prognosis.

After replantation of an avulsed permanent tooth with a closed apex, outline the splinting and endodontic protocol.

Reposition, verify with radiograph, apply a flexible (physiological) splint for about 2 weeks, give systemic antibiotics, check tetanus status, and advise chlorhexidine and soft diet. For a closed apex, initiate root canal treatment within 7–10 days (before splint removal) because the pulp will not revascularise; open-apex teeth may be monitored for revascularisation.

What clinical signs suggest a fractured mandible and what is the most common fracture site?

Signs: pain, swelling, malocclusion/step deformity, mobility of fragments, sublingual haematoma (pathognomonic of body fracture), numbness of the lower lip (IAN involvement), trismus, and an obvious step in the occlusion. The condylar neck and the angle (often through an impacted third molar) are common sites; fractures are frequently bilateral ('ring bone' principle).

Describe the Le Fort classification of mid-face fractures.

Le Fort I: horizontal fracture above the teeth apices separating the maxillary alveolus/palate (floating palate). Le Fort II: pyramidal fracture through the nasal bones, orbital floors and maxilla (floating maxilla/nose). Le Fort III: craniofacial disjunction separating the mid-face from the skull base through the zygomatic arches, orbits and nasofrontal region (floating face).

What are the priorities in the initial assessment of a patient with maxillofacial soft-tissue injuries and facial trauma?

Follow ATLS: secure the Airway (with C-spine control — facial trauma threatens the airway via bleeding, debris, displaced fragments), Breathing, Circulation (control haemorrhage), Disability, Exposure. Then assess for associated head/C-spine injury, examine wounds for foreign bodies, facial nerve and parotid duct involvement, check tetanus status, debride, irrigate, and close in layers minimising tissue loss.