Recurrent Aphthous Stomatitis
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Direct answer
Round or ovoid, shallow ulcers with a yellow-grey fibrinous floor, an erythematous halo and a painful course that recurs over years — confined to non-keratinised mobile mucosa — defines recurrent aphthous stomatitis, among the commonest oral conditions in Indian clinics. minor aphthae heal in one to two weeks without scarring; major aphthae (Sutton's disease) exceed a centimetre and scar; herpetiform aphthae occur as crops of pinpoint ulcers. Aetiology is multifactorial — haematinic deficiency, stress, trauma, food sensitivity, smoking cessation and genetics — and management runs from trigger elimination and topical corticosteroids to systemic agents, always after excluding Behçet disease.
What you must remember
- The three forms: minor — up to about a centimetre, few at a time, heal in 7 to 14 days without scarring; major (periadenitis mucosa necrotica recurrens, Sutton's disease) — over a centimetre, deep, weeks to months to heal, with scarring; herpetiform — many 1 to 2 millimetre ulcers in crops, heal without scarring.
- Site rule: strictly non-keratinised mucosa — lip, cheek, floor of mouth, ventral tongue, soft palate; ulcers on keratinised gingiva, hard palate or tongue dorsum are not aphthous until proven otherwise.
- Herpetiform aphthae versus herpes simplex: herpetic lesions begin as vesicles on keratinised mucosa with prodrome; aphthae have no vesicle stage and spare attached gingiva — a pair examiners ask by name.
- Aetiological screen: iron, folate and vitamin B12 deficiency, coeliac disease, stress, sodium lauryl sulphate pastes, and the paradox that smoking cessation can worsen aphthae while nicotine appears protective.
- The systemic escalations: Behçet disease — recurrent oral aphthae, genital ulceration and ocular inflammation, classically Silk Route with HLA-B51 — plus PFAPA, cyclic neutropenia and HIV-associated major aphthae; genital, ocular or articular features escalate the workup.
- Treatment ladder: trigger elimination; topical corticosteroids such as triamcinolone acetonide 0.1 per cent paste at onset; chlorhexidine; tetracycline rinses for herpetiform disease; systemic agents — colchicine, thalidomide with its teratogenicity acknowledged — for refractory major aphthae. The natural history is eventual quiescence, and most patients need only reassurance, trigger review and topical therapy.
A five-year ulcer diary, worked through
A 26-year-old postgraduate student reports ulcers "every exam season" for five years, currently three painful ulcers of five days' duration. Step one, confirm the phenotype: 5 to 7 millimetre ovoid ulcers, yellow floor, red halo, mobile mucosa only, healing within ten days and never scarring — minor aphthae, with flares linked to exam stress. Step two, run the screen: full blood count, ferritin, folate and vitamin B12; coeliac serology if gastrointestinal history coexists; deficiencies corrected — sometimes curing the ulcers outright. Step three, treat episodes: topical triamcinolone paste from the first tingle, a chlorhexidine rinse to prevent secondary infection, and soft diet during flares. Step four, reduce triggers: adjust orthodontic wires, trial a sodium-lauryl-sulphate-free paste, and counsel sleep and stress. Step five, define the escalation point — ulcers over a centimetre, lasting beyond a month, scarring, or accompanied by genital, ocular, joint or bowel symptoms — prompting Behçet referral and systemic therapy. Step six, review at three months with an ulcer diary.
Where examiners set the trap
The first trap is the site rule inverted: a confident answer that aphthae "occur anywhere in the mouth" loses the mark, because sparing of keratinised mucosa separates them from traumatic, herpetic and immunobullous disease. The second is herpetiform aphthae over-diagnosed as herpes simplex: the correction — no vesicle stage, no prodrome, non-keratinised mucosa, negative viral studies — is a standing viva question. The third is the Behçet escalation: oral plus genital ulcers and eye pain expects the triad, the HLA-B51 association and the word referral, since ocular inflammation threatens sight. The fourth is treatment realism: thalidomide reached for too early ignores the ladder and teratogenicity; omitting the haematinic screen misses the deficiency that cures without immunosuppression. The Indian note: vegetarian diets make B12 and iron deficiency common background in young patients, so the screen is a genuine yield here.
Frequently asked questions
How are the three forms of recurrent aphthous stomatitis distinguished?
Minor aphthae are under a centimetre and heal in 7 to 14 days without scarring, major aphthae exceed a centimetre and scar, and herpetiform aphthae are crops of tiny ulcers.
Why do aphthae spare the keratinised mucosa?
They arise on non-keratinised, mobile mucosa — lip, cheek, floor of mouth, ventral tongue and soft palate — a site rule that separates them clinically from herpetic and traumatic lesions favouring attached gingiva and hard palate.
Which deficiencies and conditions should be screened in recurrent aphthae?
Iron, folate and vitamin B12 deficiency, coeliac disease, and — when ulcers are major, scarring or accompanied by systemic features — Behçet disease, cyclic neutropenia, PFAPA and HIV.
What constitutes the Behçet disease triad?
Recurrent oral aphthae, genital ulceration and ocular inflammation such as uveitis, classically associated with HLA-B51 and Silk Route populations.
What is first-line treatment for minor aphthae?
Trigger identification and correction, topical corticosteroid such as triamcinolone acetonide 0.1 per cent paste applied early in each episode, chlorhexidine rinses and analgesia, reserving systemic agents for refractory major disease.