Acne
Acne, the most common of all skin diseases, is a polygenic, multifactorial disease that, depending on how strictly it is defined, afflicts between 50% and 100% of adolescents in the United States. It ranges in severity from a few scattered white-heads and blackheads to disfiguring, painful, deep-seated, pus-filled and bleeding nodulocystic lesions. About 15% of surveyed patients with acne seek medical care. The primary care physician is in a unique position to identify and treat a high proportion of acne sufferers. Properly managing acne requires a thorough understanding of the development of acne in all its phases, so that therapy appropriate to the circumstances can be selected from the available modalities. Early effective treatment minimizes the physical scarring of the disease and prevents or reduces equally important psychic trauma.
The pathogenesis of acne involves the interaction of enzymatic, immunologic, and chemotactic effects of normal cutaneous microflora; hormonal influences; abnormal keratinization of the sebaceous follicular duct wall; increased sebum production; follicular fragility; and host responsiveness.
Acne is a disease of the sebaceous follicles. Each person has approximately 5,000 sebaceous follicles, scattered predominantly on the face and central upper back and chest. The initial event in the pathogenesis of acne is conversion of the loose, easily shed, horny layer of the epithelium lining the follicular duct wall to a self-adhering mass that gradually obstructs the follicular duct. This has been called “retention hyperkeratosis.” It takes 1 to 2 months for the accumulated mass of keratin, sebum, and bacteria to reach visible size as a closed comedo, or white-head. White-heads may expand the duct (“pore”) opening to communicate freely with the outside. The compact, melanin-rich tip then takes on the appearance of a blackhead.
Chemotactic agents produced by bacteria within the duct attract leukocytes, and, in ensuing events, duct walls may rupture to release follicular contents into the surrounding dermis. This provokes a profound inflammatory response, leading to the development of papules, pustules, nodules, and suppurative nodules that are commonly, but mistakenly, termed cysts. These inflammatory lesions may cause permanent scarring.
Propionibacterium acnes, a normal inhabitant of the follicular canal in humans, may participate in the initiation and aggravation of inflammatory lesions by elaborating enzymes, such as lipases, that act on sebum to release potentially irritating free fatty acids. Its hyaluronidase may increase the permeability of the follicular duct wall, and its protease can damage it, which increases the leakage of materials into the surrounding dermis. In addition, P. acnes produces chemotactic substances that contribute to the initiation and evolution of inflammatory lesions.
Acne can most conveniently be divided into two categories, obstructive and inflammatory. The former, resulting from the impaction of horny material, bacteria, and sebum in the dilated follicular duct wall, is characterized by closed comedones (white-heads) and open comedones (black-heads). Leakage of intrafollicular contents from comedones produces an inflammatory response. Depending on the level of leakage into the dermis and the amount of material released, lesions vary from small, erythematous papules and superficial pustules to deeper pustules and larger, persistent, and occasionally suppurative nodules. Genetically determined immunologic factors may contribute to an exaggerated inflammatory response and more severe cystic forms of acne.