Aphthous stomatitis (canker sores): A consequence of high oral submucosal viscosity (the role of extracellular matrix and the possible role of lectins)

Abstract

Recurrent aphthous stomatitis (RAS) or canker sores occur in 20–60% of all persons. The lesion occurs because of increased viscosity of oral submucosal extracellular matrix (ECM). The lesions begin in the second decade and peak in the third decade. Sex hormones are an important influence on fibroblasts, especially in the early phase of exposure. Sex hormones are known to concentrate, to a degree, in the bucal mucosa in animals. Lesions of RAS localize clinically and experimentally at sites of trauma. In the skin, edema is known to trigger early cellular inflammation. Increased viscosity of ECM heightens the response. The histopathology of the ulcerated lesions is similar to that which occurs under sites of acute inflammation in the skin. Systemic corticosteroids completely supress the lesions. Caustics, such as silver nitrate and phenol, stop the growth and pain of lesions. Irritants are known to break ECM viscosity. The oral mucosa exerts some control on underlying ECM. Substances such as lectins influencing the mucosa could influence ECM. Soluble substances in food or organisms could also penetrate to influence ECM. A number of different foods have been incriminated as trigger agents in individual cases. This includes gluten in patients with gluten sensitive enteropathy. Gluten is know to alter the mucosa of the small intestine in persons with celiac disease.