Lesions of the oral mucosa are frequently caused by infection with yeasts belonging to the genus Candida. The prevalence of oral candidosis ranges from 34 to 51% in geriatric inpatients. Factors that predispose patients to develop oral candidosis include old age itself, denture wearing, poor dental hygience, diabetes mellitus, xerostomia, and treatment with antibiotics and corticosteroids. Altered immunological states render an individual extremely susceptible to colonization and the development of oropharyngeal candidosis. A possible mechanism may be a deficiency in cell-mediated immunity. Also, immune function is known to decline with age and nutritional deficiency. However, little attention has been paid to the nutritional factors which may be involved in the pathogenesis of oral candidosis. A few studies have investigated factors, such as iron, folic acid, vitamins, and carbohydrate-rich diets, and have suggested a possible role of these factors by means of alteration of the oral mucosal integrity.
There are a number of virulence attributes of Candida that contribute to the pathogenesis of oral candidosis, including adhesion to host surfaces, morphological transformation and extracellular enzyme production. During the early stages of superficial mucosal infection C. albicans forms filamentous hyphae which demonstrate thigmotropism, in addition to releasing various hydrolytic enzymes. Interestingly, C. glabrata is found more commonly in the oral cavity of elderly people. Since this yeast does not form filaments adhesion and colonization must be facilitated by alternative mechanisms. Ultrastructural studies have shown confirmed that multiple cellular interactions such as internalisation, thigmotropism and extracellular phospholipase production contribute to oral candidosis.
