Acne vulgaris is one of the most common cutaneous disorders and occurs in approximately 85% of individuals between the ages of 12 and 24 years. The degree of involvement is quite variable. Many individuals have mild to moderate disease of a transient nature; however, others develop severe disease that can lead to significant scarring and emotional distress.
PATHOGENESIS AND EPIDEMIOLOGY
Acne is a multifactorial disease, involving increased sebum production, abnormal epithelial cell desquamation, microbial proliferation, and inflammation. The increased sebum production is largely driven by the increase in adrenal and gonadal androgens, such as dihydrotestosterone (DHT) and testosterone, that occurs in adolescence. The most common areas of acne involvement are those with the highest sebaceous gland concentration and activity, namely the face, chest, and back.
Hyperkeratinization of the follicular infundibulum occurs early in acne wherein the pore is obstructed, accumulating sebum, desquamated epithelial cells, vellus hairs, and bacteria. The formation of closed comedones (whiteheads) and open comedones (blackheads) is initiated by abnormal cornification of the follicular orifice. The epidermal cells lining the orifice form adherent cornified sheets of cells, which occlude the follicular opening and lead to cystic dilatation of the follicle.
Inflammation occurs early as well. Inflammatory lesions (ie, papules, pustules, or nodules) develop when the intradermal wall of the comedone ruptures, releasing comedonal contents into the dermis and provoking an intense, suppurative, and later foreign-body, granulomatous-type inflammatory reaction. In nodular acne, the inflammatory reaction is extreme, resulting in deep nodules, sinus tracts, and cysts.
Colonization of the follicles by Propionibacterium acnes, an anaerobic diphtheroid, contributes to the inflammatory nature of acne. P acnes secretes several proinflammatory agents, including lipases and proteases, interleukin (IL)-1a, IL-1b, and IL-17, and has been shown to upregulate the innate immune system via Toll-like receptor 2 (TLR-2). Increased delayed hypersensitivity to P acnes has been shown in patients with severe forms of acne.
Systemic factors, such as corticosteroid therapy, and local factors, such as pore-plugging (comedogenic) cosmetics and hair products, may be contributory in some patients. There is little evidence to date that poor skin hygiene is a causal factor. However, the possible link between diet and acne is an area of continued interest. Recent studies suggest potential associations between acne and high-glycemic load diets, particularly in patients with abnormal metabolic parameters. The role of milk in acne is currently being explored as well.
The onset of clinical disease usually occurs in early adolescence, but mild disease may develop as early as 7 to 8 years of age, tending to occur somewhat earlier in girls than in boys. Classification of acne is described in Table 360-1.
Table 360-1CLASSIFICATION OF ACNE