An update on the pathogenesis and management of acne vulgaris.

A cne 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 (IL1a). 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.