The Sequence of Inflammation, Relevant Biomarkers, and the Pathogenesis of Acne Vulgaris: What Does Recent Research Show and What Does it Mean to the Clinician?

August 2013 | Volume 12 | Issue 8 | Supplement | s109 | Copyright © 2013

James Q. Del Rosso DO FAOCDa and Leon H. Kircik MDb

aLas Vegas Skin and Cancer Clinics/West Dermatology, JDRx Dermatology LLC, Henderson, NV;
Touro University College of Osteopathic Medicine, Henderson, NV
bMount Sinai Medical Center, New York, NY; Indiana University School of Medicine, Indianapolis, IN;
Physicians Skin Care, PLLC, Louisville, KY

Abstract

Acne vulgaris (AV) remains one of the most common skin disorders seen in dermatology practices worldwide. Despite an abundance of publications, AV continues to be a formidable therapeutic challenge due to its complex pathogenesis and chronicity. Regarding the sequence of AV lesion formation, the traditional model teaches that the primary lesion is the microcomedone, a subclinical lesion caused by follicular hyperkeratinization. From the microcomedone, visible AV emerges with development of comedonal (“noninflammatory”) and inflammatory lesions. Research published over the past decade has provided information about inflammatory mechanisms that warrant us reconsidering the traditional model of AV pathogenesis. More specifically, there is evidence that specific cascades of inflammation occur early during the initial subclinical formation and visible emergence of AV lesions, later during progression, and finally during resolution including scarring. It has also been shown that subclinical inflammation occurs before or concurrently with microcomedone formation. This article reviews an updated model of acne lesion development and its progression based on a literature review that highlights the role of inflammatory mediators, cellular infiltration patterns, and expression of receptors that signal specific immunologic and inflammatory responses. Clinical relevance related to this updated model is also addressed.

J Drugs Dermatol. 2013;12(suppl 8):s109-s115.

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INTRODUCTION

Acne vulgaris (AV) is the most common skin disorder encountered in dermatology practice in the United States, regardless of race.1 Based on the 2009 National Ambulatory Medical Care Survey, AV accounted for 10.2% and 0.4% of non-Federal office-based visits to dermatologists and non-dermatologists, respectively.2 Estimated to affect up to 50 million people in the United States, AV occurs commonly during adolescence, affecting up to 95% of individuals between 12 and 18 years of age.1,3,4

Many preteens and teenagers with AV experience a protracted course into their postadolescent years that can vary in severity and frequency of exacerbations.4-7 Preteen and postadolescent AV are both common.4,6-11 Although AV can sometimes “burn out” inexplicably after the teenage years, approximately 50% and 12% of women, and 40% and 3% of men, are reported to have AV in their thirties and in their forties, respectively.4 Postadolescent AV is a subset that is rising in prevalence, with a notable increase in dermatology visits for adult women with AV observed over the past decade.8,10,11

The depth and progression of our traditional understanding of AV pathogenesis has been well described and correlated with clinical and laboratory findings, including histologic studies.12-15 The predominant pathogenic factors associated with AV development and/or severity are follicular hyperkeratinization, excess sebum production, proliferation of Propionibacterium acnes, and cutaneous inflammation induced by upregulated proinflammatory mediators.6,7,12-15 Literature review shows that the current understanding of AV pathogenesis evolves as valid and relevant research findings emerge.14-20

The traditional model of acne pathogenesis, better described as acne lesion development and progression, states that follicular hyperkeratinization (microcomedone formation) is the first step in the life cycle of an AV lesion.12-15,20 A fully developed microcomedone and abnormal desquamation produces an intrafollicular keratinous plug behind which sebum accumulates. As follicular enlargement, hyperkeratinization, and excess sebum production progress, a microcomedone may transcend to form an open or closed comedone, which remain visibly noninflammatory.13,20 An individual comedone may then remain at this stage until resolution, or may progress to form an inflammatory lesion (ie, papule, pustule). Although not often stressed in discussions of the traditional model, inflammatory lesions may also arise from visibly normal skin, possibly from a precursor microcomedone that bypasses the visible comedonal stage (Figure 1).17 Subsequent to the microcomedone, a sequence of events may occur that lead to either superficial or deep inflammatory lesions, with P acnes proliferation contributing a variety of pathophysiologic effects. Many of these effects are proinflammatory and initiate or propagate inflammatory cascades in AV, and are explained by the genome of strains of P acnes.14-18,20-23

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