Conflict of interest None.
Acne sans P. acnes
Article first published online: 28 MAR 2012
© 2012 The Authors. Journal of the European Academy of Dermatology and Venereology © 2012 European Academy of Dermatology and Venereology
Journal of the European Academy of Dermatology and Venereology
Volume 27, Issue 1, pages 1–10, January 2013
How to Cite
Shaheen, B. and Gonzalez, M. (2013), Acne sans P. acnes. Journal of the European Academy of Dermatology and Venereology, 27: 1–10. doi: 10.1111/j.1468-3083.2012.04516.x
- Issue published online: 18 DEC 2012
- Article first published online: 28 MAR 2012
- Received: 9 May 2011; Accepted: 20 February 2012
Acne vulgaris is a common disease that carries an enormous financial and psychosocial impact. Androgens, excessive sebum production, ductal hypercornification, changes in the microbial flora, as well as inflammation and immunological host reactions are considered the major contributors to acne pathogenesis. Despite extensive research on acne pathogenesis, the exact sequence of events and their possible mechanisms leading to the development of a microcomedone and its transformation into an inflamed lesion has remained unclear.
There is a significant amount of in vitro evidence suggesting a possible pathogenetic role for Propionibacterium acnes in comedogenesis as well as inflammation in inflammatory acne. However, the microbiological data from non-inflamed as well as inflamed acne lesions, cultured individually, do not entirely support the hypothesis that these micro-organisms are actually responsible for their initiation. There appears to be comedones and inflamed lesions in which there is no clear evidence of Propionibacterium acnes involvement. Considering this microbiological data, alongside the in vitro evidence, we have tried to delineate the possible sequence of events and their mechanisms, leading to the development of a microcomedone and its transformation into an inflamed lesion. Based on the available literature we have analysed the evidence of both non-inflamed as well as inflamed acne lesions occurring in the absence of Propionibacterium acnes from the pilosebaceous follicles. We propose that the development of an inflamed acne lesion depends on an imbalance between the pro-inflammatory and anti-inflammatory pathways rather than the incitement of inflammation by Propionibacterium acnes.