Novel Pathogenic Factors in Acne Vulgaris: Sebaceous Lobular Hyperkeratosis and Comedonal Mucinosis

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For decades, no new structural events have been proposed in acne, except for my proposal that a sebum calculus (sebolith) is the cause of follicular erosion and rupture leading to inflammatory acne. I now submit that the hyperkeratosis that matters in acne is that of the sebaceous lobule itself, wherein a meshwork of keratinous membranes from sebocytes can be incrusted by lipidic crystals, leading to the sebolith by aggregation. The sebaceous lobular hyperkeratosis depends on a failure of holocrinity: the sebocytes fail to undergo disintegrating apoptosis. Instead, ghostly voluminous sebocytes remain attached to one another as a keratinous honeycomblike mass (seboberg), prone to crystal nidation or to inherent damage to the folliculosebaceous wall on its own. Because mucin in comedones is a very frequent phenomenon, I further propose that the matrix on which sebum crystals coalesce is often formed by acid mucopolysaccharides of apocrine or even sebaceous origin. Mucin is known in other systems of calculous formation (cholelithiasis) to play an important role in the crystallization of cholesterol. It is feasible, therefore, that an equivalent interaction of lipids and mucin plays a role in the formation of a follicular sebolith. In sum, understanding the pathogenesis of acne is not a dead-end pursuit, if a more solid and precise structural scaffolding is added to the vague concepts that have dominated the thought about the disease for so many years.

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