ABSTRACT
Acne vulgaris is a multifactorial disease of the skin in areas rich in sebaceous follicles. It is characterized by seborrhea, hypercornification of the infundibulum (the neck of the sebaceous gland), and the presence of comedones and inflammatory lesions such as papules and pustules. The inflammatory pathway is mediated by antigenic and inflammatory products of Propionibacterium acnes (1). Although acne is mostly associated with puberty, persistent or late onset acne may be similar in physiology to pubertal acne, with hyperandrogenicity and increased sebogenesis, being the key factors (2). The hyperproliferation of the infundibulum keratinocytes, characterized by the expression of the hyperproliferative marker proteins, Ki67 and K6/16, and the resulting immature stratum corneum does not desquamate efficiently, leading to clumps of squames that attach to the hair follicle causing a blockage to sebum flow. Hypercornification of the infrainfundibulum is an early feature of the microcomedones, preceding the clinically observable inflammatory process (3).
