dermatologic disorders
Acne Vulgaris
Pathophysiology of Acne Vulgaris
Acne occurs through the interplay of 4 major factors: Excess sebum production Follicular plugging with sebum and keratinocytes Colonization of follicles byCutibacterium acnes(formerlyPropionibacterium acnes), a normal human anaerobe Release of multiple inflammatory mediators Acne can be classified as Noninflammatory: Characterized by comedones Inflammatory: Characterized by papules, pustules, nodules, and cysts Comedonesare sebaceous plugs impacted within follicles. They are termed open or closed depending on whether the follicle is dilated or closed at the skin surface. Plugs are easily extruded from open comedones but are more difficult to remove from closed comedones. Closed comedones are the precursor lesions to inflammatory acne. Papules and pustulesoccur whenC. acnescolonizes the closed comedones, breaking down sebum into free fatty acids that irritate the follicular epithelium and eliciting an inflammatory response by neutrophils and then lymphocytes, which further disrupts the epithelium. The inflamed follicle ruptures into the dermis (sometimes precipitated by physical manipulation or harsh scrubbing), where the comedone contents elicit a further local inflammatory reaction, producing papules. If the inflammation is intense, grossly purulent pustules occur. Nodules and cystsare other manifestations of inflammatory acne. Nodules are deeper lesions that may involve > 1 follicle, and cysts are large fluctuant nodules. 