Mechanism of PDT in Acne

The data from several published studies indicate that the mechanism of PDT in treating acne lesions is through the targeting of sebaceous gland activity, as is the case for many effective acne treatments. Hormonal activation of the pilosebaceous unit results in hyper – cornification, sebum production, and proliferation of P acnes. Among the hormones impli­cated in acne pathogenesis are dihydrotestosterone, dehydroepiandrosterone sulfate and insulin-like growth factor 1, with serum levels correlating with acne lesion counts [35]. Sebocytes have been shown to express androgen receptors, which explains their response to these hormones [36,37]. Exogenous ALA is converted to PpIX which accumulates preferen­tially in acne lesions, and endogenous porphyrins produced by P. acnes also accumulate contributing to the photosensitization of acne lesions, making them amenable to destruction through PDT [7,8,38]. PDT results in decreased sebaceous gland size and vacuolization of sebocytes [8] . This may be the result of direct thermal injury to the sebaceous glands, destruction of P. acnes, or manipulation of keratinocyte proliferation in the infundibulum [8]. The level of efficacy of PDT in achieving complete clearance may rely on various factors, including the photosensitizer and light source used, the degree of hormonal stimulation, and the size and level of sebaceous activity at baseline.