INTRODUCTION
Acne is the most common of all skin disorders, afflicting 30%
to 85% of adolescents and, in lesser proportions, mature individuals
as well1. In recent years, advances in the understanding
of the pathophysiology of acne and acne inflammation,
retinoid receptor biology, and Propionibacterium acnes (P. acnes)
microbiology has led to the development of new therapeutic
agents and new management regimens. As a result, the disease
can be targeted somewhat more precisely than in the past.
Consequently, many patients can hope to negotiate adolescence
with fewer of the embarrassing stigmata of acne that
impact so adversely on quality of life in this age group.
Moreover, we now have the potential to prevent the lasting
sequelae of the disease – scarring and post-inflammatory
hyperpigmentation – in many of our patients.
A brief summary of the newest understanding of the pathophysiology
of acne is useful for the clinician in order to optimize
patient care. Acne is a chronic inflammatory process that
begins within the pilosebaceous canal and affects areas of the
skin with the highest densities of sebaceous follicles: the face,back and chest2. At pubarche, increased androgen production
triggers the enlargement of the sebaceous glands, which then
produce increased amounts of sebum. Epithelial cell turnover
increases, and hyperproliferation of corneocytes lining the follicular
canal begins to occur. The abnormally desquamated
corneocytes and excessive sebum form a bulging follicular plug,
known as a microcomedo. Normal drainage from the follicle is
blocked, creating an ideal microenvironment for the growth of
P. acnes, an anaerobic bacterium normally present in the follicle.
ADDRESS FOR CORRESPONDENCE:
Jonathan S Weiss MDGwinnett Clinical Research Center2383 Pate StreetSnellville, GA 30078Phone: (770) 972-4845Fax: (770) 972-0358
The mechanisms controlling the abnormal desquamation are
still unclear. However, there is some evidence that changes in
sebum composition or secretion may irritate follicular keratinocytes,
leading to the release of interleukins and the initiation
of comedogenesis3,4.
The microcomedo is the invisible precursor to all acne lesions
including closed and open comedones – non-inflammatory
lesions inside pilosebaceous follicles – as well as later inflammatory
papules and pustules that arise from comedones. In
one study, biopsies of papules revealed a microcomedone in
52%, a whitehead in 22%, and a blackhead in 10%5. About 28%
of biopsy sections of normal-appearing skin in an individual
with acne show histological features of microcomedos6.
Current best practice dictates that acne management focus
strongly on preventing microcomedo formation and resolving
existing ones. Closed comedos (whiteheads) and open comedos
(blackheads) develop from microcomedos and are the first
visible acne lesions. It is now believed that the dark color of
open comedos results from blockage of light transmission
