Decoding Acne: Genetic Markers, Molecules, and Propionibacterium Acnes openaccess articles

June 2013 | Volume 12 | Issue 6 | Supplement | s61 | Copyright © 2013

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Abstract

The understanding of acne vulgaris (AV) has evolved with a greater recognition of the sequence of inflammation, especially prelesional inflammation. Propionibacterium acnes is not the primary inducer of acne pathogenesis, but it promotes multiple mechanisms of inflammation that correlate mostly with inflammatory lesions. An important facet of the new paradigm is that a specific follicular pattern of innate inflammation occurs before and during follicular hyperkeratinization. Moreover, this inflammation persists during the resolution of the macular phase after inflammatory lesions flatten toward the end of their life cycle. The current understanding of AV pathogenesis presents novel therapeutic options for patients because the use of benzoyl peroxide and a topical retinoid suppresses several components of acne pathogenesis, including reduced follicular hyperkeratinization, decreased innate inflammation, and dermal matrix degradation.

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