Update on the Pathogenesis and Management of Acne Vulgaris
Acne vulgaris is an easily recognizable dermatologic disease. It is also very common. Acne is seen in nearly 100% of individuals at some time during their lives. Small, noninflamed acne lesions may not be more than a slight nuisance but, in individuals with more severe inflammatory nodular acne, pain, social embarrassment, and both physical and psychological scarring can be life altering. Fortunately, our understanding of the pathogenesis of acne has progressed and our therapeutic armamentarium has greatly expanded in the last twenty-five years.
The four key pathogenetic factors of acne have been recognized for decades. These include follicular epithelial hyperproliferation and resultant follicular plugging, excess sebum, inflammation, and the presence and activity of Propionibacterium acnes (Table I). The earliest microscopic lesion observed in acne vulgaris is the microcomedo. This lesion is characterized by follicular plugging. Inflammation and the bacteria, P acnes, are not observed. The stimulus for microcomedo formation is still unknown. Leading hypotheses implicate androgen hormones, alterations in follicular linoleic acid levels, and the inflammatory cytokine interleukin-1a (IL- 1a). The microcomedo is the precursor of other acne lesions. With time, the microcomedo fills with P acnes, whose cell wall and biological byproducts are chemoattractant and proinflammatory. As a result, inflammatory cells surround the follicle, diffuse through the follicular wall, and produce enzymes that disrupt the follicular wall. The degree of inflammation seen in acne vulgaris may be dependent upon individual immune responsiveness to P acnes.
Recently, the toll-like receptor 2 (TLR-2) has been implicated in the pathogenesis of acne. TLR-2 is a pattern recognition receptor that is activated by P acnes. When bound, TLR-2 activates a transcription factor that upregulates production and the release of proinflammatory cytokines like interleukin-12 and interleukin-8 from monocytes. TLR-2 is expressed on infiltrating inflammatory cells around the pilosebaceous follicle in those with acne. Its expression increases as the acne lesion ages and becomes more inflamed.
The role of androgen hormones in the pathogenesis of acne has also been carefully evaluated. Overall, circulating androgen hormone levels are normal in individuals with acne who do not have other signs or symptoms of hyperandrogenism. The enzyme 5a-reductase type 1 has been studied in those with and without acne. 5a-reductase type 1 is present in the sebaceous gland and converts testosterone to the more potent androgen receptor ligand, dihydrotestosterone (DHT). It has been hypothesized that those with acne might have more active 5areductase type 1. However, no statistically significant difference in enzyme activity has been observed to date between those with and without acne, but subject numbers have been very low.
Source: An update on the pathogenesis and management of acne vulgaris
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