Article
Acne affects almost all adolescents and adults at some point in their lives but is highly treatable with topical retinoids and antibacterials. The type and severity of acne guide early intervention, which can prevent disfigurement and its psychosocial sequelæ.
CONTRIBUTOR
ALAN R. SHALITA, MD, Distinguished Teaching Professor and Chairman, Department of Dermatology, SUNY Downstate Medical Center, Brooklyn, NY.
Acne is a chronic inflammatory disease of the pilosebaceous follicles, which are most common on the face, neck, and upper trunk. These pilosebaceous units consist of large sebaceous glands associated with small hair follicles. Sebaceous glands excrete sebum, a complex lipid mixture of triglycerides, squalene, cholesterol, and wax esters. Sebum is transported up the follicular canal to the skin surface, carrying with it desquamated cells from the follicular epithelium.
When the normal flow of sebum onto the skin surface is obstructed by follicular hyperkeratosis, microcomedones are formed. Early stages of acne typically manifest 1 to 2 years before the onset of puberty as a result of androgenic stimulation of the sebaceous glands. The microcomedo, the precursor of all acne lesions, evolves into either a noninflammatory closed comedo (whitehead), an open comedo (blackhead), or an inflammatory pustule, papule, or nodule. Acne arises from the interaction of the following 4 factors:
Teens and preteens with genetically susceptible follicles will develop acne. Acne usually resolves in the third decade as adrenal androgen levels decline, although the condition may persist or develop de novo in adulthood. Postadolescent acne mainly affects women, about one-third of whom have features of hyperandrogenicity.
Therapies for acne are directed at the multiple factors that combine to cause it and are individualized according to the fluctuating severity of the disorder. The principle of treatment is to disrupt the cycle of follicular plugging, increased sebum production, colonization of P acnes, and inflammation. When these processes are targeted early, the microcomedo can be significantly reduced and the inflammatory stages of disease that produce scarring can be prevented. While oral estrogen therapy and oral isotretinoin are the only available treatments that affect sebum production, P acnes proliferation and microcomedones can be well managed with antimicrobials and topical retinoids.