Recurrent aphthous stomatitis (RAS) affects 20 to 30% of adults and a greater percentage of children at some time in their life.
Etiology is unclear, but recurrent aphthous stomatitis (RAS) tends to run in families. The damage is predominately T–cell-mediated. Cytokines, such as IL-2, IL-10, and particularly TN-alpha, play a role.
Predisposing factors include
Allergy does not seem to be involved.
Factors that may, for unknown reasons, be protective include oral contraceptives, pregnancy, and tobacco, including smokeless tobacco and nicotine-containing tablets.
Symptoms and signs usually begin in childhood (80% of patients are < 30 years) and decrease in frequency and severity with aging. Symptoms may involve as few as one ulcer 2 to 4 times a year or almost continuous disease, with new ulcers forming as old ones heal. A prodrome of pain or burning for 1 to 2 days precedes ulcers, but there are no antecedent vesicles or bullae. Severe pain, disproportionate to the size of the lesion, can last from 4 to 7 days.
Aphthous ulcers are well-demarcated, shallow, ovoid, or round and have a necrotic center with a yellow-gray pseudomembrane, a red halo, and slightly raised red margins.
Minor aphthous ulcers account for 85% of cases. They occur on the floor of the mouth, lateral and ventral tongue, buccal mucosa, and pharynx; are < 8 mm (typically 2 to 3 mm); and heal in 10 days without scarring.
Major aphthous ulcers (Sutton disease, periadenitis mucosa necrotica recurrens) constitute 10% of cases. Appearing after puberty, the prodrome is more intense and the ulcers are deeper, larger (> 1 cm), and longer lasting (weeks to months) than minor aphthae. They appear on the lips, soft palate, and throat. Fever, dysphagia, malaise, and scarring may occur.
Herpetiform aphthous ulcers (morphologically resembling but unrelated to herpesvirus) account for 5% of cases. They begin as multiple (up to 100) 1- to 3-mm crops of small, painful clusters of ulcers on an erythematous base. They coalesce to form larger ulcers that last 2 weeks. They tend to occur in women and at a later age of onset than do other forms of recurrent aphthous stomatitis.
Evaluation proceeds as described previously under stomatitis. Diagnosis is based on appearance and on exclusion because there are no definitive histologic features or laboratory tests.
Primary oral herpes simplex may mimic recurrent aphthous stomatitis (RAS) but usually occurs in younger children, always involves the gingiva and may affect any keratinized mucosa (hard palate, attached gingiva, dorsum of tongue), and is associated with systemic symptoms. Viral culture can be done to identify herpes simplex. Recurrent herpetic lesions are usually unilateral.
Similar recurrent episodes, often with multiple ulcers, can occur with Behçet disease, inflammatory bowel disease, celiac disease, HIV infection, periodic fevers with aphthous stomatitis, pharyngitis, and adenitis (PFAPA) syndrome, and nutritional deficiencies; these conditions generally have systemic symptoms and signs. Isolated recurrent oral ulcers can occur with herpes infection, HIV, and, rarely, nutritional deficiency. Viral testing and serum hematologic tests can identify these conditions.
Drug reactions may mimic RAS but are usually temporally related to ingestion. However, reactions to foods or dental products may be difficult to identify; sequential elimination may be necessary.
General treatments for stomatitis may help patients with recurrent aphthous stomatitis (RAS).
Chlorhexidine gluconate mouthwashes and topical corticosteroids, the mainstays of therapy, should be used during the prodrome, if possible. The corticosteroid can be dexamethasone 0.5 mg/5 mL 3 times a day used as a rinse and then expectorated or clobetasol ointment 0.05% or fluocinonide ointment 0.05% in carboxymethylcellulose mucosal protective paste (1:1) applied 3 times a day. Patients using these corticosteroids should be monitored for candidiasis. If topical corticosteroids are ineffective, prednisone (eg, 40 mg orally once a day) may be needed for ≤ 5 days.
Continuous or particularly severe RAS is best treated by a specialist in oral medicine. Treatment may require prolonged use of systemic corticosteroids, azathioprine or other immunosuppressants, pentoxifylline, or thalidomide. Intralesional injections can be done with betamethasone, dexamethasone, or triamcinolone. Supplemental B1, B2, B6, B12, folate, or iron lessens RAS in some patients.