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Here are thorough answers to both parts of SAQ 1:
SAQ 1a — Four Common Pre-malignant Conditions of the Oral Cavity [2 marks]
1. Leukoplakia
A white hyperkeratotic lesion of the oral mucosa that may or may not show dysplasia on histology. It is the most common pre-malignant oral mucosal lesion. Associated with smoking, chewing tobacco, betel nut use, and chronic sun exposure (lip). Malignant transformation risk ranges from 0.13–17.5%, and is higher in heterogeneous, speckled, or nodular forms.
2. Erythroplakia
A fiery red, granular, sharply demarcated lesion that cannot be classified as any other definable lesion. It carries a much higher malignant transformation rate of up to 50%, making it more dangerous than leukoplakia despite being less common.
3. Oral Submucous Fibrosis (OSF)
A multifactorial chronic inflammatory disorder caused primarily by habitual use of areca (betel) nut. Results in failure of collagen remodeling, leading to progressive pallor, scar bands, trismus, and restricted tongue mobility. Malignant transformation rate: 7–30%.
4. Oral Lichen Planus
A mucocutaneous autoimmune disorder mediated by T-cell lymphocytic reaction against epithelial antigens. Associated with hepatitis C, Sjögren syndrome, and primary biliary cirrhosis. The erosive/atrophic variants carry the highest malignant potential.
(Other recognised conditions include proliferative verrucous leukoplakia and actinic cheilitis.)
SAQ 1b — Risk Factors Associated with Oral Cancer [3 marks]
1. Tobacco (smoked and smokeless)
The single most important preventable risk factor. Tobacco smoke increases oral SCC risk 1.9-fold in males and 3-fold in females. Risk is dose-dependent (years smoked × cigarettes per day). Smokeless tobacco carries a 4-fold increased risk due to carcinogens N-nitrosornicotine and 4-methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK).
2. Alcohol
Alcohol alone confers a 1.7-fold risk at 1–2 drinks/day, rising to >3-fold in heavy drinkers. Crucially, alcohol acts synergistically with tobacco — individuals who both smoke (2 packs/day) and drink heavily (4 units/day) are 35 times more likely to develop oral cancer than non-users of either.
3. Betel Nut (Areca Nut) / Betel Quid
Chewed by ~10% of the world population, particularly in South and Southeast Asia. Causes oral submucous fibrosis and directly carcinogenic. Malignant transformation rate >5% with habitual use.
4. HPV (Human Papillomavirus)
HPV (especially HPV-16) is a major risk factor, particularly for oropharyngeal squamous cell carcinoma. Oral HPV is sexually transmitted. While classically linked to the oropharynx, it contributes to oral cavity SCC, especially in younger patients without traditional risk factors.
5. Sun Exposure
Relevant for lower lip cancers (actinic cheilitis). Chronic UV exposure leads to keratotic changes and eventual SCC of the lip vermilion.
6. Poor Oral Hygiene / Dentition
Chronic mechanical irritation from sharp/broken teeth, ill-fitting dentures, and poor oral hygiene are co-factors in oral carcinogenesis.
7. Immunosuppression
Impairs immune surveillance, allowing malignant transformation to proceed unchecked (e.g., in HIV/AIDS, transplant recipients).
Sources: K.J. Lee's Essential Otolaryngology; Cummings Otolaryngology Head and Neck Surgery; Harrison's Principles of Internal Medicine 22E; Goldman-Cecil Medicine
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