PA23.1-2 | Oral & Oesophageal Cancers — Summary & Reflection

REFLECT

Consider the 38-year-old gutka-chewer from the opening scenario:
1. What three findings in his history and examination already pointed toward malignancy — and what is the pathological basis of each?
2. How does field cancerisation change your plan if his oral biopsy confirms SCC?
3. Barrett oesophagus is described as a 'protective' metaplasia (more acid-tolerant). Yet it is also pre-malignant. How do you reconcile these two ideas?
4. If this patient had instead presented in a rural health centre without endoscopy access, what clinical signs would you look for to estimate stage before referring?

KEY TAKEAWAYS

Oral Cancer (PA23.1):
• Over 90 % are squamous cell carcinoma; India has the world's highest incidence driven by tobacco (smokeless forms — gutka, khaini), areca nut, and alcohol
• Premalignant lesions in order of malignant potential: erythroplakia (~90 %) > leukoplakia with dysplasia (up to 30 %) > OSMF (7–13 %) — OSMF is areca nut-specific and causes trismus
• Histology hallmarks: keratin pearls, intercellular bridges, nuclear pleomorphism; Broder's grading I–III
• Field cancerisation explains multiple synchronous primaries across the aerodigestive tract
• Spread: local → submandibular/deep cervical nodes → haematogenous (late)

Carcinoma Oesophagus (PA23.2):
• Two types: SCC (upper/middle, tobacco/alcohol, India-dominant) vs adenocarcinoma (lower third, Barrett background, GERD-driven, rising in West)
• Barrett oesophagus: GERD → intestinal metaplasia (goblet cells) → low-grade dysplasia → high-grade dysplasia → adenocarcinoma
• Progressive dysphagia (solids → liquids) is the cardinal symptom; late presentation due to absent serosa
• Prognosis: poor overall (~15–20 % 5-year survival); stage is the dominant determinant
• Gross patterns: fungating, ulcerative, infiltrative/annular
• Intramural lymphatic spread mandates wide resection margins