Abstract
Acne vulgaris is a disease of the pilosebaceous unit that may manifest as either noninflammatory or inflammatory skin lesions. The microcomedone theory suggests that the first step in the pathogenesis of acne vulgaris is the noninflammatory comedone. The comedone is a collection of keratin and sebum that is trapped within the pilosebaceous unit due to hyperproliferation of keratinocytes in the follicular lining. The biofilm produced byP. acnesbacteria promotes the formation of a comedone by acting as a biological glue that prevents expulsion of the hyperkeratotic plug. In addition to its adhesive properties, the biofilm has virulence factors contributing to the pathogenicity ofP. acnesin acne vulgaris. With further investigation and a better understanding of theP. acnesbiofilm, new therapeutic options for acne vulgaris can be made available. By targeting theP. acnesbiofilm, treatment can be made more effective and precise, without the concern of side effects seen in currently available acne medications.
Highlights
Acne vulgaris is a disease of the pilosebaceous unit
The microcomedone theory suggests that the initial phase of acne formation is comedogenesis, which involves androgens, hyperproliferation of keratinocytes in the follicular lining, and buildup of keratin and sebum within the pilosebaceous unit [1, 4]
Other theories explaining the evolution of comedones suggest that keratinocyte proliferation is a response to variations in sebum composition, such as lower levels of linoleic acid [10], or that hyperkeratinization may be a response to the secretion of proinflammatory cytokines such as IL-1 that is induced by the presence of P. acnes on the skin [11]
Summary
The etiology of acne has been studied extensively, and the pathogenesis is considered to be multifactorial, involving increased sebum production secondary to androgens, follicular hyperkeratinization, and colonization of the skin with Propionibacterium acnes [1]. The microcomedone theory suggests that the initial phase of acne formation is comedogenesis, which involves androgens, hyperproliferation of keratinocytes in the follicular lining, and buildup of keratin and sebum within the pilosebaceous unit [1, 4]. The interaction of these factors and synchronized processes lead to the plugging of sebum and debris within the pilosebaceous unit This presents as a non-inflamed lesion or comedone. The treatment of acne vulgaris can be made more effective and precise, without the concern of side effects seen in currently available acne medications
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