• Food and environmental allergens: association of RAS with increased serum antibodies to food antigens and atopy strongly suggests that allergic reaction is involved. IgE-bearing lymphocytes are increased in aphthous lesions; mast cells are increased in tissue from prodromal stages of recurrent ulcers. Mast cell degranulation is important in producing lesion. Elimination diet gives good results. Allergen does not have to be food; frequent allergens inducing RAS are benzoic acid, cinnamaldehyde, nickel, parabens, dichromate, sorbic acid; allergen elimination usually brings complete resolution or significant improvement. • Gluten sensitivity: gluten sensitivity is the primary cause of RAS in many cases. Incidence of RAS is increased in patients with celiac disease. Jejunal biopsy of patients with RAS reveals villous atrophy typical of celiac disease plus signs of immunologic reactions to food antigens. Gluten may act directly on oral mucosa or produce functional changes in small intestine distinct from those of celiac disease. Gluten-sensitive enteropathy induces nutritional deficiencies. Withdrawing gluten causes complete remission of RAS in patients with celiac disease and some improvement in other patients. Even without villous atrophy, gluten sensitivity can produce RAS. Measure alpha-gliadin antibodies in any patient presenting with RAS. • Stress: precipitating factor in RAS, suggesting breakdown in host protective factors. • Nutrient deficiency: oral cavity often is the first place where nutritional deficiency is visible—high turnover of mucosal epithelium. Thiamin (B1) deficiency is the most significant. Low levels of transketolase (B1-dependent enzyme) found in RAS compared with controls. Nutrient deficiencies are much more common in those with RAS: 14.2% deficient in Fe, folate, B12, or combination of these nutrients; 28.2% deficient in B1, B2, or B6; when deficiencies are corrected, majority are completely remitted. Zinc (50 mg elemental) daily for 1 month has reduced aphthae and prevented reappearance for 3 months. Low nutrient status may explain why patients with RAS have increased oxidant/antioxidant status: decreased catalase and glutathione peroxidase activities and antioxidant potential levels in the erythrocytes and decreased antioxidant potential and increased malondialdehyde in plasma. Enzymatic and nonenzymatic antioxidant defense systems are impaired in patients with RAS. • Quercetin: inhibits mast cell degranulation, basophil histamine release, and formation of other mediators of inflammation. Antiallergy drug disodium cromoglycate has similar structure and function and is effective in treating RAS. Quercetin increased number of ulcer-free days with mild symptomatic relief. Other flavonoids (acacetin, apigenin, chrysin, and phloretin, but not catechin, flavone, morin, rutin, or taxifolin) have antiallergy effects similar to the drug. • Deglycyrrhizinated licorice (DGL): may be effective in promoting healing of RAS lesions. Solution of DGL used as mouthwash (200 mg powdered DGL dissolved in 200 mL warm water q.i.d.)—75% of patients had 50%-75% improvement within 1 day, followed by complete healing of ulcers by third day; DGL tablets may be more convenient and effective. Let them melt in the mouth directly adjacent to the lesions.
Aphthous Stomatitis (Aphthous Ulcer/Canker Sore/Ulcerative Stomatitis)
THERAPEUTIC CONSIDERATIONS
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