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
