Oral cavity infections, inflammatory disorders, ulcers and benign/malignant lesions

Overview

The mouth is a common site for infections, inflammatory disease and cancer. It also shows signs of systemic illness such as iron deficiency, HIV, Crohn disease and Behçet disease.

For PGET you need a simple approach: is it an ulcer, a white patch, a red patch, a swelling or pigmentation? Then ask whether it is local, part of a systemic disease, or premalignant/malignant.

Pakistan and the rest of South Asia have some of the highest rates of oral cancer in the world, mainly because of areca nut and tobacco chewing.

Approach to a mouth ulcer

Recurrent aphthous ulceration

• The most common cause of mouth ulcers; affects up to a quarter of people.
• Painful, round or oval ulcers with a grey-white base and a red halo.
• Starts in childhood, more common in women and non-smokers, and becomes less frequent with age.
• No systemic illness.

Treatment: avoid trauma and acidic foods; topical steroid (for example 1% triamcinolone); chlorhexidine or tetracycline mouthwash. Severe cases may need systemic steroids, colchicine, dapsone or thalidomide.

Causes of mouth ulcers

Red flags in an oral ulcer

• Lasts more than 3 weeks despite removing any cause.
• Painless, hard (indurated) base, raised and rolled edges.
• Bleeds easily; associated neck lymph node.
• Smoker, drinker, areca nut user.

Any such ulcer needs a biopsy.

Oral infections

Viral

• Primary herpes simplex (HSV-1) gingivostomatitis: usually in children; fever, many vesicles that burst into painful ulcers on gums, tongue and lips. Treated with aciclovir and fluids. The virus stays latent and recurs as cold sores on the lip.
• Herpangina: Coxsackie A virus; vesicles then ulcers on the soft palate, fauces and uvula; short illness with fever.
• Hand, foot and mouth disease: Coxsackie A16 (and enterovirus 71); mouth ulcers plus vesicles on palms and soles; mainly children; settles within a week.
• Oral hairy leukoplakia: white, ridged plaques on the sides of the tongue in HIV; caused by Epstein–Barr virus; cannot be scraped off.

Bacterial and gum infections

Fungal

Oral candidiasis (thrush) appears as white plaques that can be wiped off, leaving a red base. It follows antibiotics, inhaled steroids, diabetes, dentures and immunosuppression. It is covered fully in the chapter on oral and oesophageal candidiasis.

Inflammatory and other benign conditions

• Glossitis: red, smooth, sore tongue. Causes: iron, B12, folate, riboflavin and niacin deficiency, and Candida.
• Angular stomatitis (cheilitis): cracks at the corners of the mouth; iron or B vitamin deficiency, Candida, dentures.
• Geographic tongue: red patches with raised pale borders that change shape; harmless; reassure.
• Oral lichen planus: lacy white streaks (Wickham striae) on the buccal mucosa; may erode; small malignant risk.
• Gingival hyperplasia (gum overgrowth): drugs (phenytoin, ciclosporin, nifedipine and other calcium-channel blockers), pregnancy, scurvy, and infiltration in acute myeloid leukaemia.
• Desquamative gingivitis: smooth red gums from lichen planus or mucous membrane pemphigoid; confirm by biopsy.
• Dry mouth (xerostomia): Sjögren syndrome, anticholinergic drugs, tricyclics, lithium, radiotherapy, dehydration.

Pigmented lesions

Premalignant lesions

Leukoplakia is a clinical term: a white patch that will not wipe away and cannot be classed as any other disease. It is linked to smoking and alcohol. About 2% of people have one. Every persistent white patch needs a biopsy to look for dysplasia.

Oral submucous fibrosis

• Almost entirely seen in South Asians; strongly linked to areca nut (paan, supari, gutka, pan masala).
• Fibrous bands form under the mucosa, so the cheeks feel stiff and blanched.
• Progressive trismus (reduced mouth opening), burning with spicy food, restricted tongue movement.
• Premalignant. Stopping the habit can halt it; intralesional steroids and surgery give only limited benefit.

Tobacco smoking on its own does not cause submucous fibrosis; the key agent is areca nut.

Oral cancer

Risk factors

• Tobacco (smoked or chewed, including naswar), alcohol (the two act together).
• Areca nut / betel quid (paan), the main reason for the high rate in South Asia.
• Poor nutrition, poor dental hygiene.
• HPV-16: important for oropharyngeal (tonsil, tongue base) cancer, much less for the mouth itself.
• Premalignant lesions listed above.

Pathology and sites

• Squamous cell carcinoma is by far the commonest type.
• Usual sites: lateral border of the tongue, floor of the mouth, buccal mucosa (common in areca chewers), and the retromolar area.
• Spread is mainly to cervical lymph nodes.
• Smokers and drinkers are at risk of a second primary cancer elsewhere in the upper aerodigestive tract (field change).

Clinical features

• Early lesions are often painless.
• Later: a hard ulcer with rolled edges, a lump, bleeding, pain referred to the ear, loose teeth, difficulty speaking or swallowing, and a neck lump.

Investigations and management

• Biopsy of the lesion for histology.
• Staging with CT or MRI of the head and neck, and chest imaging.
• Surgery (wide excision, often with neck dissection) and/or radiotherapy; chemoradiotherapy for advanced disease.
• Stop tobacco, alcohol and areca nut.

Quick revision

• Commonest mouth ulcer: aphthous; minor under 10 mm, heals in about 2 weeks without a scar.
• Ulcer over 3 weeks, painless, indurated, rolled edge: biopsy for SCC.
• Oral + genital ulcers + uveitis: Behçet.
• Wipes off = Candida; does not wipe off = leukoplakia.
• Erythroplakia: highest malignant risk.
• Areca nut: submucous fibrosis (trismus) and oral cancer.
• Oral SCC sites: lateral tongue, floor of mouth, buccal mucosa.
• ANUG: metronidazole; gum overgrowth: phenytoin, ciclosporin, nifedipine, AML.
• Hairy leukoplakia: EBV in HIV, sides of the tongue.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine; Bailey & Love's Short Practice of Surgery).

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