Decoding Acne: Genetic Markers, Molecules, and Propionibacterium Acnes
June 2013 | Volume 12 | Issue 6 | Supplement | s61 | Copyright © 2013
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.
This is a CME supplement; visit the JDD Medical Education Library to participate in this activity and earn 1 AMA PRA Category 1 Credit.
Purchase Original Article
Purchase a single fully formatted PDF of the original manuscript as it was published in the JDD.
Download the original manuscript as it was published in the JDD.
Contact a member of the JDD Sales Team to request a quote or purchase bulk reprints, e-prints or international translation requests.
To get access to JDD's full-text articles and archives, upgrade here.
Save an unformatted copy of this article for on-screen viewing.
Print the full-text of article as it appears on the JDD site.→ proceed | ↑ close