Do We Really Need Topical Antibiotics in Our New Treatment Paradigm of Acne Vulgaris? A Novel Question to Consider Based on an Updated Model of Pathogenesis

August 2013 | Volume 12 | Issue 8 | Supplement | s107 | Copyright © 2013

Leon H. Kircik MD


No abstract available

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The understanding of the nature of inflammation in acne vulgaris (AV) has evolved with a greater understanding of the sequences of inflammation, especially prelesional inflammation, over the life cycle of an acne lesion. Propionibacterium acnes, although not the primary inducer of acne pathogenesis, promotes multiple mechanisms of inflammation that correlate mostly with inflammatory lesions. An importrant caveat in the updated model of acne pathogenesis is that although the microcomedone remains as an early precursor lesion, a specific folliculocentric pattern of innate inflammation occurs before or along with follicular hyperkeratinization.1,2 In addition, inflammation persists during the resolving macular phase after inflammatory lesions flatten toward the end of their life cycle, even with treatment. The clinical translation based upon this updated model is that anti-inflammatory effects, comedolytic activity, and reduction in P acnes are all important components in acne treatment to help suppress initial lesion formation, and to decrease the intensity and duration of inflammation in visible acne lesions.3,4

From a therapeutic standpoint, the use of benzoyl peroxide (BP) and a topical retinoid suppresses several components of acne pathogenesis, including reduction in P acnes and comedolysis by BP, and reduction in follicular hyperkeratinization, decrease in innate inflammation, and inhibition of dermal matrix degradation by the topical retinoid.2-4 This supplement also depicts how specific biomarkers of inflammation are upregulated in AV, with discussion of how therapies such as topical adapalene and BP may provide augmented therapeutic activity as compared with the indidual agents alone. Although some topical antibiotics also reduce P acnes and may exhibit some anti-inflammatory properties, they can induce antibiotic-resistant P acnes strains, an unwanted sequelae that does not happen with BP.2 Hence, the question arises: Do we really need topical antibiotics in our new treatment paradigm for acne vulgaris?

I want to thank my friend and colleague, Dr. Jim Del Rosso, who carefully studied the currently available basic science and clinical data, conceptualized the overall pathophysiologic process of AV, and presented it to Galderma at their request as a consultant, and to colleagues in 2012. These efforts served as the fundamental framework both for this supplement and for my article entitled "The Role of Benzoyl Peroxide in the New Treatment Paradigm for Acne", published in a June 2013 supplement (Stein Gold L, Weiss J, Kircik L. Decoding Acne: Genetic Markers, Molecules, and Propioniacterium Acnes. J Drugs and Dermatol 2013;12(Supplement): S61-S78.)

Leon H. Kircik MD

Mount Sinai Medical Center, New York, NY
Indiana University School of Medicine, Indianapolis, IN
Physicians Skin Care, PLLC, Louisville, KY


Dr. Kircik has received compensation from the Journal of Drugs in Dermatology for his editorial support.


  1. Webster GF. The pathophysiology of acne. Cutis. 2005;76(suppl 2):s4-s7.
  2. Burkhart CN, Gottwald L. Assessment of etiologic agents in acne pathogenesis. Skinmed. 2003;2(4):222-228.
  3. Kang S. The mechanism of action of topical retinoids. Cutis. 2005;75(suppl 2):s10-s13.
  4. Tenaud I, Khammari A, Dreno B. In vitro modulation of TLR-2, CD1d and IL-10 by adapalene on normal human skin and acne inflammatory lesions. Exp Dermatol. 2007;16(6):500-506.

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