Acne: Evolving Concepts of Pathogenesis Need to Guide Therapeutic Developments
June 2013 | Volume 12 | Issue 6 | Supplement | s66 | Copyright © 2013
Jonathan S. Weiss MD
No abstract available
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For decades, acne has been and remains one of the most common diseases diagnosed and treated by dermatologists. Despite this prominence in our field, a full understanding of the pathogenesis of acne remains uncertain. We are continually unfolding the complex nature of this prevalent condition, but the more we learn, the more we question our preconceived notions. This supplement reviews 3 presentations at a recent symposium that focused on newer issues in acne pathogenesis and treatment.
Two articles in this supplement discuss the evolving concepts in acne pathogenesis. For years we have pointed to the 4 basic components of acne pathogenesis: hyperkeratinization, excess sebum production, bacterial proliferation, and inflammation. While these factors remain central to our current thinking, their relative importance may not be what we believed as recently as 5 years ago. The notion that hyperkeratinization leading to microcomedone formation is the initiating event in the development of acne appears, at best, to be debatable. In her article, Linda F. Stein Gold MD eloquently points to the presence of inflammation throughout the course of acne lesions, even predating the formation of the microcomedone and lasting through what was previously thought to be the postinflammatory phase of scarring. Her article also points out the intertwining of hormonal influences and dietary factors with the other pathogenic factors.
Another important issue in the current arena of acne therapy is bacterial resistance. Leon H. Kircik MD writes extensively on the importance of this resistance in our current therapeutic choices. Specifically, he points out the key role of benzoyl peroxide (BP) in combating not only the development of resistant Propionibacterium acnes, but also its importance in reducing the use of antibiotics as we fight against community-acquired methicillin-resistant Staphylococcus aureus.
The implications for acne therapy of the studies reviewed in this supplement are enormous. As pointed out in my article, new concepts of pathogenesis require a different focus as we develop new therapeutic entities. Clearly, a focus on better, more pure anti-inflammatory molecules will be essential moving forward, especially those that are not antibiotics. Research on the role of diet may also augment current pharmacologic therapies. Finally, the development of more therapeutic molecules to which P acnes cannot or will not develop resistance will be extremely important. Retinoids and BPs appear to be mainstays of acne therapy, to which we need to add new classes of effective therapeutic molecules.
Jonathan S. Weiss MD
Gwinnett Dermatology, Snellville, GA