Acne vulgaris is a disorder of sebaceous follicles that usually begins at the time of the sharp increase in androgen production that occurs in adolescence. This disease is most prevalent among teenagers, but it does occur in patients in their twenties and thirties. Three major areas of pathophysiology have been identified in acne: hyperkeratinization and obstruction of sebaceous follicles, resulting from abnormal desquamation of follicular epithelium; an androgen-stimulated increase in the production of sebum; and proliferation of Propionibacterium acnes, which generates inflammation. Disruption of the preclinical precursor lesion known as the microcomedo produces inflammation, which leads to the pustules and papules of clinical disease and may eventually result in scarring. Rational therapy for acne should be directed at the three factors involved in the pathophysiology of the disease. Tretinoin (all-trans-retinoic acid) acts to normalize desquamation of follicular epithelium, promote drainage of comedones, and inhibit formation of new ones. Salicylic acid is also comedolytic, but to a much lesser degree. Benzoyl peroxide and topical or systemic antibiotics work by decreasing the follicular population of P. acnes, thus reducing inflammation. Direct injection of corticosteroids may be used to reduce large inflammatory lesions. Physical removal of comedones is also useful. Severe nodulocystic acne and other cases that fail to respond to these measures may be treated systemically with isotretinoin (13-cis-retinoic acid).