MJDF Oral Medicine and Pathology 2 — Questions and Answers

Question 1: A patient presents with a white patch on the lateral border of the tongue that cannot be wiped off. Which diagnosis should be considered first and investigated?

Pseudomembranous candidiasis
Leukoplakia — a potentially malignant disorder requiring biopsy to exclude dysplasia (Correct answer)
Traumatic white line (linea alba)
Geographic tongue (erythema migrans)

Correct answer: Leukoplakia — a potentially malignant disorder requiring biopsy to exclude dysplasia

A white patch that cannot be wiped off is a leukoplakia by definition. As a potentially malignant disorder with variable rates of malignant transformation, it requires biopsy and histological examination to assess for dysplasia.

Leukoplakia is defined clinically as a white patch or plaque that cannot be wiped off and cannot be characterised as any other defined lesion. It is a diagnosis of exclusion. The lateral border of the tongue is a high-risk site for oral squamous cell carcinoma (OSCC) and its precursors. Key points about leukoplakia: it is a potentially malignant disorder (PMD) — the annual malignant transformation rate is 0.13-1% in homogeneous leukoplakia and higher (up to 18% over 10 years) in non-homogeneous (speckled, nodular, verrucous) leukoplakia; the floor of mouth and lateral/ventral tongue have the highest rates of malignant transformation; smoking and tobacco use are major risk factors, though non-smoking leukoplakias (idiopathic) may carry higher transformation risk; alcohol is a co-carcinogen. Management: biopsy is mandatory for any leukoplakia except those in obvious locations with clear aetiology (e.g., a white line exactly at the occlusal plane fitting classic linea alba). The biopsy should include the most suspicious area (red components, nodular areas, indurated or ulcerated areas). Histology should be reported for epithelial dysplasia (mild, moderate, severe) or OSCC. Differential diagnosis of white patches: pseudomembranous candidiasis (wipes off to reveal erythematous base); erythematous/atrophic candidiasis; oral lichen planus (Wickham's striae, bilateral, can be confirmed histologically); white sponge naevus (hereditary, widespread, family history); chemical burn (history of aspirin/medication held in mouth); frictional keratosis (resolves when cause removed). MJDF candidates must distinguish potentially malignant disorders from benign conditions and know the appropriate investigation and referral pathways.

Question 2: Which of the following is the MOST common type of oral cancer?

Adenocarcinoma of the minor salivary glands
Squamous cell carcinoma (SCC) (Correct answer)
Malignant melanoma of the oral mucosa
Lymphoma of the oral soft tissues

Correct answer: Squamous cell carcinoma (SCC)

Squamous cell carcinoma accounts for over 90% of oral malignancies. It arises from the stratified squamous epithelium lining the oral cavity and is strongly associated with tobacco and alcohol use.

Oral squamous cell carcinoma (OSCC) is by far the most common malignancy of the oral cavity, accounting for approximately 90-95% of all oral cancers. It arises from the transformation of stratified squamous epithelium through a process of progressive genetic mutations, often preceded by potentially malignant disorders. Epidemiology: incidence is increasing in the UK, particularly in younger patients and in those with HPV-related oropharyngeal SCC (though this is technically the oropharynx, not oral cavity proper). Overall 5-year survival for oral SCC is approximately 50-60%, largely because the majority of cases are diagnosed at a late stage. Early diagnosis dramatically improves prognosis. Risk factors: tobacco use (smoking and smokeless tobacco — all forms, dose-dependent); alcohol consumption (synergistic with tobacco — multiplicative risk); areca nut/betel quid chewing (major risk factor in South Asian populations); HPV (particularly HPV-16, more important for oropharyngeal than oral cavity SCC); immunosuppression; poor oral hygiene; chronic trauma (though traumatic keratosis rarely transforms without other risk factors). High-risk sites: lateral and ventral tongue, floor of mouth, soft palate/retromolar trigone — these areas are sometimes called the 'coffin' or 'graveyard' areas as they are associated with the highest transformation rates from leukoplakia and the most frequent sites of early SCC. Clinical features of OSCC: ulceration (often with raised, rolled, indurated margins), non-healing ulcer, white patch, red patch (erythroplakia — highest risk), exophytic growth, induration, pain (may be absent in early stages), cervical lymphadenopathy (late feature — indicates regional spread). Early referral using the urgent suspected cancer (2-week wait) pathway is crucial when OSCC is suspected.

Question 3: A patient presents with multiple painful oral ulcers, each measuring 3-5mm, affecting the labial and buccal mucosa but not the attached gingiva. The ulcers heal without scarring within 7-10 days but recur regularly. What is the most likely diagnosis?

Herpetic gingivostomatitis
Minor recurrent aphthous stomatitis (minor RAS) (Correct answer)
Erythema multiforme
Behcet's disease

Correct answer: Minor recurrent aphthous stomatitis (minor RAS)

Minor RAS (aphthous ulcers, canker sores) classically presents as recurring small round/oval ulcers on non-keratinised movable mucosa, healing without scarring in 7-10 days. They are the most common oral mucosal ulcerative condition.

Recurrent aphthous stomatitis (RAS) is the most common cause of recurrent oral ulceration, affecting approximately 20% of the population. It presents as round or oval ulcers with a central yellowish-grey pseudomembrane surrounded by an erythematous halo, occurring on non-keratinised movable mucosa (labial, buccal, ventral tongue, floor of mouth, soft palate). The three clinical subtypes: Minor RAS (80% of cases) — ulcers <1cm diameter (typically 3-5mm), heal within 7-14 days without scarring, affect non-keratinised movable mucosa only; Major RAS (Sutton's disease) — ulcers >1cm diameter, last weeks to months, heal with scarring, may occur anywhere including dorsal tongue and attached gingiva; Herpetiform RAS — multiple very small ulcers (1-3mm) that coalesce, affect any mucosal surface, can be confused with herpetic infection (but no virus is present — the name is descriptive only). Pathogenesis is incompletely understood — immune-mediated mechanism, possibly triggered by local trauma, stress, hormonal changes, sodium lauryl sulphate in toothpaste, food triggers (benzoic acid, cinnamon, cow's milk). No definitive cure exists; treatment is symptomatic: topical analgesics (benzydamine), topical corticosteroids (triamcinolone acetonide, betamethasone), antiseptic mouthwashes (chlorhexidine). Differential diagnosis: herpetic gingivostomatitis (primary HSV — causes fever, vesicles on keratinised and non-keratinised mucosa, lymphadenopathy, not recurrent in the same pattern); erythema multiforme (target lesions on skin, haemorrhagic lip crusting, affects mucosa extensively, associated with HSV or drug trigger); Behcet's disease (if accompanied by genital ulcers and/or uveitis — a systemic vasculitis). Investigation is indicated if ulcers are atypical, severe, or failing to heal — blood tests for haematinic deficiencies (iron, B12, folate — deficiency exacerbates RAS), coeliac screening, HIV if indicated.

Question 4: Which salivary gland is MOST commonly affected by pleomorphic adenoma?

Sublingual gland
Submandibular gland
Parotid gland (Correct answer)
Minor salivary glands of the hard palate

Correct answer: Parotid gland

Pleomorphic adenoma (benign mixed tumour) most commonly arises in the parotid gland, which accounts for approximately 80% of salivary gland tumours, with the majority being benign and pleomorphic adenoma being the most common benign type.

Pleomorphic adenoma is the most common benign salivary gland tumour overall, accounting for approximately 60-70% of all salivary gland neoplasms. It is a mixed tumour containing epithelial and mesenchymal components (hence 'pleomorphic' — many forms), which explains its varied histological appearance. Distribution: 80% in the parotid gland (most commonly the superficial lobe, presenting as a slow-growing, painless, firm mass anterior and inferior to the ear); 10% in the submandibular gland; 10% in minor salivary glands (hard palate is most common intraoral site) and sublingual gland (rare). Clinical features: slow-growing, painless, well-encapsulated mass; mobile (not fixed to surrounding structures — fixation suggests malignancy); no facial nerve involvement (involvement would suggest malignant transformation or a malignant tumour); has been present for years in many cases. Important characteristics: pleomorphic adenoma has a pseudocapsule (not a true capsule) — finger-like projections of tumour extend through the capsule, explaining the high recurrence rate if simple enucleation is attempted; therefore, superficial parotidectomy (with clear margins) rather than simple excision is the treatment of choice for parotid pleomorphic adenoma. Malignant transformation: occurs in approximately 5% of cases (carcinoma ex pleomorphic adenoma), usually after many years. Recurrent pleomorphic adenoma has a higher rate of malignant transformation. Differential diagnosis of parotid swelling includes: Warthin's tumour (second most common benign parotid tumour, bilateral in 10%), parotid carcinoma (mucoepidermoid, adenoid cystic), parotitis (inflammation), Sjögren's syndrome, sarcoidosis, lymphoma.

Question 5: Erythroplakia in the oral cavity is significant because it:

Is always benign and requires only monitoring
Has the highest risk of all oral mucosal lesions for malignant transformation or existing carcinoma (Correct answer)
Is always associated with candidal infection and resolves with antifungal treatment
Is a normal variant of the oral mucosa seen in smokers

Correct answer: Has the highest risk of all oral mucosal lesions for malignant transformation or existing carcinoma

Erythroplakia (a red patch that cannot be attributed to another cause) carries the highest risk of all oral mucosal lesions — approximately 90% show severe dysplasia, carcinoma in situ, or invasive squamous cell carcinoma on biopsy.

Erythroplakia is defined as a 'bright red velvety plaque that cannot be characterised clinically or pathologically as any other recognisable condition.' It is the most dangerous of all oral potentially malignant disorders in terms of likelihood of existing or future malignancy. Key statistics: approximately 90% of erythroplakias show severe epithelial dysplasia, carcinoma in situ, or invasive SCC on biopsy. This makes erythroplakia considerably more concerning than leukoplakia (where the rate of severe dysplasia/carcinoma is much lower). Mixed red and white lesions (speckled leukoplakia / erythroleukoplakia) also carry high risk. Why erythroplakia is so dangerous: the redness reflects a loss of the keratinised superficial layers, decreased epithelial thickness, increased vascularity of the underlying stroma, and increased mitotic activity in the basal layers — all features associated with dysplastic or malignant change. The lesion does not produce enough keratin to appear white, unlike leukoplakia. Management: any oral erythroplakia requires urgent referral to a specialist oral medicine or oral surgery clinic and biopsy. The 2-week urgent suspected cancer pathway is appropriate. Biopsy should be of the most representative area. Comparison: leukoplakia has variable rates of severe dysplasia/carcinoma (0.1-17% in literature, influenced by site, appearance, and patient factors); erythroplakia has approximately 90% rate. Both are PMDs requiring biopsy and long-term follow-up. This distinction is clinically and examination-relevant: while leukoplakia is far more common, erythroplakia is more likely to represent malignancy. Any unexplained red oral mucosal change that persists for >2-3 weeks should be investigated.

Question 6: Oral candidiasis most commonly presents as pseudomembranous candidiasis ('thrush'). Which patient group is at HIGHEST risk for developing this condition?

Healthy adults with good oral hygiene
Immunocompromised patients, denture wearers, patients on broad-spectrum antibiotics, or inhaled corticosteroid users (Correct answer)
Teenagers with orthodontic appliances
Patients with well-controlled type 2 diabetes on diet control alone

Correct answer: Immunocompromised patients, denture wearers, patients on broad-spectrum antibiotics, or inhaled corticosteroid users

Oral candidiasis predominantly affects those with compromised host defences — HIV/immunosuppression, denture wearers (especially with poor hygiene), patients on antibiotics (disrupting normal flora), and steroid inhaler users.

Oral candidiasis (oropharyngeal candidiasis) is caused by overgrowth of Candida species (predominantly Candida albicans, a commensal fungus normally present in the oral flora in 50-80% of the population). Disease occurs when host defences are reduced or the local oral environment changes to favour Candida proliferation. Risk factors — local: denture wearing (dentures create a warm, anaerobic microenvironment under the denture base, particularly for upper complete dentures — denture-related stomatitis/atrophic candidiasis under the upper denture is extremely common); dry mouth/xerostomia (saliva has antifungal properties — reduced salivary flow from Sjögren's syndrome, post-radiotherapy, or medications favours candidal overgrowth); inhaled corticosteroids (topical immunosuppression in the oropharynx — patients must be advised to rinse after using inhalers); poor oral hygiene; smoking. Risk factors — systemic: HIV infection/AIDS (oral candidiasis was a defining AIDS-related illness); other immunosuppression (chemotherapy, high-dose systemic corticosteroids, transplant immunosuppression); broad-spectrum antibiotics (suppress normal bacterial flora, removing competition for Candida); uncontrolled diabetes mellitus; haematological malignancy; extremes of age (infants, elderly); nutritional deficiency. Forms of oral candidiasis: pseudomembranous (white plaques that wipe off, leaving erythematous base — typical 'thrush'); erythematous/atrophic (red form — under dentures, or dorsal tongue depapillation in antibiotic users); hyperplastic candidiasis (white plaque that does not wipe off — on commissures/anterior buccal mucosa — must be biopsied to exclude dysplasia); angular cheilitis (corners of mouth, often mixed Candida/Staphylococcal infection). Treatment: nystatin (polyene antifungal — topical, not absorbed — pastilles or suspension) or miconazole gel for most cases; systemic fluconazole for severe/immunocompromised cases; always address the underlying predisposing factor.

MJDF Oral Medicine and Pathology 2

A patient presents with a white patch on the lateral border of the tongue that cannot be wiped off.
Which diagnosis should be considered first and investigated?