Oral Mucosal Melanosis
L. Feller, Razia A. G. Khammissa, Johan Lemmer
Abstract
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L. Feller, Razia A. G. Khammissa, Johan Lemmer
Abstract
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In the mouth, melanin is produced by melanocytes residing in the basal cell layer of the oral epithelium. Melanin influences the colour of the oral mucosa and provides protection against reactive oxygen species and bacterial-derived enzymes and toxins and acts as a physical barrier to both microorganisms invading the oral epithelium and to other microenvironmental stressors. The functional activity of epithelial melanocytes is regulated by biological agents in the microenvironment, including proopiomelanocortin-derived peptides, and by reciprocal interactions between melanocytes on the one hand and neighbouring keratinocytes and signals from the underlying lamina propria on the other hand. Oral mucosal melanin hyperpigmentation is common and may be physiological or pathological, and in either case the pattern of distribution and the intensity of the melanosis are variable. Physiological melanin hyperpigmentation is the result of increased melanin biosynthesis by melanocytes in the basal cell layer of the oral epithelium, but pathological melanin pigmentation may be the result of increased number of normal melanocytes or atypical melanocytes, of increased melanogenic activity of normal or atypical melanocytes, or of both. Oral mucosal melanin hyperpigmentation may be secondary to disease, medications, or smoking, and physiological oral melanin hyperpigmentation may be clinically and histopathologically similar so that the differentiation between pathological and physiological oral melanosis can at times be difficult.
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In the mouth, melanin is produced by melanocytes residing in the basal cell layer of the oral epithelium. Melanin influences the colour of the oral mucosa and provides protection against reactive oxygen species and bacterial-derived enzymes and toxins and acts as a physical barrier to both microorganisms invading the oral epithelium and to other microenvironmental stressors. The functional activity of epithelial melanocytes is regulated by biological agents in the microenvironment, including proopiomelanocortin-derived peptides, and by reciprocal interactions between melanocytes on the one hand and neighbouring keratinocytes and signals from the underlying lamina propria on the other hand. Oral mucosal melanin hyperpigmentation is common and may be physiological or pathological, and in either case the pattern of distribution and the intensity of the melanosis are variable. Physiological melanin hyperpigmentation is the result of increased melanin biosynthesis by melanocytes in the basal cell layer of the oral epithelium, but pathological melanin pigmentation may be the result of increased number of normal melanocytes or atypical melanocytes, of increased melanogenic activity of normal or atypical melanocytes, or of both. Oral mucosal melanin hyperpigmentation may be secondary to disease, medications, or smoking, and physiological oral melanin hyperpigmentation may be clinically and histopathologically similar so that the differentiation between pathological and physiological oral melanosis can at times be difficult.
Key concepts: Melanin, Melanocyte, Hyperpigmentation, Melanosis, Oral mucosa, Lamina propria, Pathology, Biology