Inflammatory Comedogenic Acne
Despite extensive research over the past century, the pathogenesis of acne vulgaris remains unclear. In particular, the sequences of events that are involved in comedogenesis have yet to be clarified. Comedogenesis is one of the four main etiological factors of acne; the others are increased production and secretion of sebum, colonization of the follicular ducts with Propionibacterium acnes (P. acnes), and the inflammatory response. These four factors should not be viewed as different phases, but rather as closely interrelated mechanisms that ultimately lead to the clinical disease of acne vulgaris.
That comedones are essential lesions in acne was first suggested in 1960. It is widely accepted that their pathogenesis is multifactorial, attributable to follicular hyperkeratinization, increased sebum production, increased androgenic activity, impaired quality of sebum lipids, dysregulation of cutaneous steroidogenesis, neuropeptide production, inflammation and follicular hypercolonization by P. acnes bacteria.
One of the most widely used mechanisms to stop the hyperkeratinization process consists of the physical or chemical elimination of the excess proliferation of keratinocytes in the deregulated stratum and thus prevent the obstruction of the pilosebaceous duct.
