Assessment of etiologic agents in acne pathogenesis.

Acne is a chronic inflammatory disease of the pilosebaceous units. Traditional etiologic factors include increased sebum production, ductal hyperkeratosis, abnormality of the microbial flora within the pilosebaceous unit, and mediators of inflammation. Recent developments do not refute these familial elements, but rather refine particular aspects. Interleukin-1a influences hypercornification of the infundibulum as well as the inflammatory response by inducing the production of vascular endothelial growth factor in dermal papilla cells and follicular keratinocytes of the pilosebaceous unit. New retinoids have been developed based on controlling cellular proliferation and differentiation in the pilosebaceous unit by their action on nuclear receptors of cells. Dermal inflammation is not due to presence of bacteria, but from biologically active mediators produced by Propionibacterium acnes. The environment within the pilosebaceous unit is probably more important than the absolute number of P. acnes organisms. Indeed, the major role of the sebaceous gland appears to be supplying P. acnes needed nutrients. Moreover, the microbiologic principle of biofilms appears to be applicable to P. acnes in acne.