Also known as: aphthous ulcers, canker sores, recurrent aphthous stomatitis, RAS, aphthous stomatitis
Overview
A common, idiopathic, recurrent ulcerative disorder of non-keratinized oral mucosa, characterized by painful, round or oval ulcers with a yellowish fibrinous base, erythematous halo, and well-defined margins. Three classic clinical forms: minor, major, and herpetiform.
Epidemiology
Affects 10-25% of the population at some point. Most common cause of recurrent oral ulceration. Onset typically in childhood or adolescence, with decreased frequency after age 40. Female predominance. Tobacco use is paradoxically associated with reduced incidence (hyperkeratosis is protective).
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Question 1EENTMedium
A 22-year-old woman presents with a 3-day history of two painful mouth sores. She reports similar lesions every few weeks since adolescence, often around her menstrual period or during exam stress, that resolve on their own within 1-2 weeks. She has no fever, rash, genital lesions, or gastrointestinal symptoms. On exam, vital signs are normal and there are two shallow 4-mm ulcers with a yellow-gray fibrinous base and surrounding erythematous halo on the buccal mucosa and ventral tongue; the hard palate and gingiva are spared. The remainder of the exam is unremarkable. Which of the following is the most appropriate initial treatment?
ATopical triamcinolone 0.1% dental paste
BOral acyclovir 400 mg five times daily
CTopical nystatin 100,000-unit oral rinse
DOral prednisone 1 mg/kg with a daily taper
EOral colchicine 0.6 mg twice daily
Reveal answer & full explanation
Correct answer: A — Topical triamcinolone 0.1% dental paste
ATopical triamcinolone 0.1% dental paste✓
BOral acyclovir 400 mg five times daily
CTopical nystatin 100,000-unit oral rinse
DOral prednisone 1 mg/kg with a daily taper
EOral colchicine 0.6 mg twice daily
Why Topical triamcinolone 0.1% dental paste is correct
This is classic minor recurrent aphthous stomatitis: recurrent, self-limited, well-defined ulcers with a yellow fibrinous base and erythematous halo on NON-keratinized mucosa (buccal mucosa, ventral tongue), sparing the hard palate and gingiva.
For typical, mild-to-moderate disease, guideline-supported first-line therapy is a topical corticosteroid applied directly to the ulcer, which targets the underlying T-cell-mediated mucosal inflammation, shortens healing time, and reduces pain. Triamcinolone 0.1% in a dental paste (Orabase), or fluocinonide or clobetasol gel, is a standard agent.
Topical anesthetics (viscous lidocaine, "magic mouthwash") and chlorhexidine rinses are reasonable adjuncts, and trigger avoidance is advised.
Why the others are wrong
Oral acyclovir 400 mg five times daily — antiviral for herpes simplex; recurrent HSV begins as clustered vesicles on the lip vermilion or, intraorally, only on KERATINIZED mucosa (hard palate, attached gingiva), and primary HSV causes fever with diffuse gingivostomatitis involving any oral mucosa. Aphthae are not infectious, so antivirals are ineffective.
Oral prednisone 1 mg/kg with a daily taper — systemic corticosteroids are reserved for severe, disabling, or major/refractory outbreaks; using them for two small minor aphthae overtreats and exposes the patient to unnecessary systemic steroid risk.
Topical nystatin 100,000-unit oral rinse — an antifungal for oral candidiasis, which presents as removable white plaques on an erythematous base, not discrete punched-out ulcers; it has no role in aphthous stomatitis.
Oral colchicine 0.6 mg twice daily — colchicine is used as systemic prophylaxis for Behcet disease and for severe, frequently recurrent complex aphthosis, which the recurrent course might suggest, but in simple recurrent aphthous stomatitis systemic agents are reserved for severe disease or ulcers that fail topical therapy; two small minor aphthae without genital ulcers, rash, or GI symptoms call for a topical corticosteroid first.
Question 2EENTMedium
A 17-year-old girl presents with a 3-year history of recurrent, painful oral ulcers that erupt every few weeks. The lesions are shallow, less than 1 cm, with a yellow-gray fibrinous base and an erythematous halo, located on the buccal mucosa and lateral tongue. They heal without scarring in about 10 days. She has no genital ulcers, eye symptoms, GI complaints, or systemic illness. A diagnosis of recurrent aphthous stomatitis is made. Which of the following is the strongest risk factor for her condition?
ALatent HSV-1 infection
BRegular tobacco smoking
CSodium lauryl sulfate use
DPositive family history
EFrequent citrus intake
Reveal answer & full explanation
Correct answer: D — Positive family history
ALatent HSV-1 infection
BRegular tobacco smoking
CSodium lauryl sulfate use
DPositive family history✓
EFrequent citrus intake
Why Positive family history is correct
A positive family history is the single strongest predictor of recurrent aphthous stomatitis, present in roughly 30-40% of patients and linked to HLA-associated genetic susceptibility.
Children with an affected parent develop ulcers earlier and more often, reflecting an inherited T-cell-mediated mucosal immune predisposition rather than an environmental exposure.
Why the others are wrong
Regular tobacco smoking is paradoxically protective because mucosal hyperkeratosis guards the epithelium; outbreaks may instead flare after smoking cessation, so it lowers rather than raises risk.
Sodium lauryl sulfate use is a controversial and at most weak trigger; some patients improve on SLS-free toothpaste, but it is not an established major risk factor.
Frequent citrus intake can provoke pain and occasionally precipitate lesions in sensitive people, but food sensitivities are minor, inconsistent triggers far weaker than heredity.
Latent HSV-1 infection — recurrent oral ulcers suggest a viral cause, but recurrent intraoral herpes produces clustered vesicles that ulcerate on keratinized mucosa such as the hard palate and attached gingiva, whereas aphthae form on nonkeratinized mucosa such as the buccal mucosa and are not caused by HSV.
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Not infectious. Considered a T-cell-mediated mucosal immune response, with focal cytotoxicity to epithelium triggered by various antigens or local trauma. There is increased TNF-alpha and other pro-inflammatory cytokine activity. Genetic susceptibility (HLA associations) and micronutrient deficiencies modulate frequency and severity.
Clinical presentation
Symptoms
Burning or pricking sensation 1-2 days before ulcer appears (prodrome)
Painful, sharply defined ulcer of non-keratinized mucosa (buccal mucosa, lateral/ventral tongue, floor of mouth, soft palate, labial mucosa)
Pain disproportionate to lesion size; worse with food, especially acidic or spicy
Episodes recur every few weeks to months; lesions heal in 7-14 days (minor) or up to 6 weeks (major)
Signs / physical exam
Minor (80%): single or few ulcers, less than 1 cm, shallow, yellow-gray fibrinous base, erythematous halo; heal without scarring
Major (10-15%, Sutton disease): 1-3 cm, deeper, lasts 2-6 weeks, often heals with scarring
Herpetiform (5-10%): clusters of small (1-3 mm) ulcers that coalesce; despite name, NOT viral
Lesions on NON-keratinized mucosa (key distinguishing feature from recurrent intraoral HSV, which is confined to keratinized mucosa)
No systemic signs in isolated RAS
Classic findings
Recurrent, painful, round, well-defined ulcer with yellow base and red halo on non-keratinized oral mucosa, sparing the hard palate and gingiva.
Differential diagnosis
Herpes simplex stomatitis — Primary HSV-1 in children — fever, gingivostomatitis, diffuse vesicles on any oral mucosa (keratinized and non-keratinized) with swollen gingiva; recurrent HSV on lip vermilion or, intraorally, only on keratinized mucosa (hard palate, attached gingiva); Tzanck or PCR
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