RECURRENT APHTHOUS STOMATITIS: ETIOLOGY, SERUM AUTOANTIBODIES, ANEMIA, HEMATINIC DEFICIENCIES, AND MANAGEMENT

Recurrent aphthous stomatitis (RAS) is one of the most common chronic inflammatory disorders of the oral mucosa and is characterized by repeated episodes of painful, shallow ulceration on non-keratinized mucosal surfaces. Although its exact cause remains unresolved, current evidence supports a multifactorial pathogenesis involving genetic susceptibility, T-cell-mediated immune dysregulation, local trauma, psychological stress, systemic disease, and nutritional deficiency. Increasing attention has been directed toward serum autoantibodies and hematologic abnormalities in patients with RAS. Studies have shown elevated frequencies of antigastric parietal cell and antithyroid autoantibodies in subsets of patients, suggesting that autoimmune mechanisms or autoimmune comorbidity may contribute to disease expression in selected cases. In parallel, anemia and hematinic deficiencies, particularly iron, vitamin B12, and folate deficiency, are repeatedly associated with RAS and may impair epithelial integrity, oxygen delivery, and mucosal repair. Management is therefore not limited to symptomatic ulcer control; it also requires identification and correction of predisposing systemic abnormalities. First-line treatment remains topical corticosteroid therapy, while severe or refractory disease may require systemic corticosteroids, immunomodulatory therapy, and specialist referral. This article reviews the current understanding of RAS etiology, the clinical significance of serum autoantibodies, the role of anemia and hematinic deficiency, and contemporary management strategies.