Acne vulgaris begins with the formation of microcomedones, subclinical lesions characterized by hyperproliferation of the follicular epithelium. These lesions can evolve more into inflammatory lesions or non-inflammatory comedones, of which there are two types, open and closed.

Clinically invisible, microcomedones are lesions present in regions of apparently healthy skin in a patient with acne. Histological examination of the microcomedones reveals dilated pilosebaceous ducts containing an excess of keratinocytes and modified sebum, with a prominent granular layer on the ductal epithelium.

Under normal circumstances, keratinocytes are loosely arranged in normal pilosebaceous follicles. The sebum flow transports them to the surface of the skin after peeling, maintaining a balance between new and flaked keratinocytes. However, in comedones, this balance is disturbed, leading to accumulation of keratinocytes in the pilosebaceous duct.

The hyperproliferation of basal keratinocytes plays a central role in this accumulation. As more keratinous material accumulates, the follicular wall continues to stretch and thin. At the same time, sebaceous glands atrophy and are replaced by epithelial cells. The open comedo contains keratinous material arranged in concentric sheets, while the closed comedo contains less compact keratinous material and a narrow follicular orifice.

The mechanism of follicular hyperkeratinization is not yet fully clear and may involve changes in lipid composition, androgen response, cytokines, and the presence of P. acnes.

To reverse this process, COMEDOPEEL provides biochemical action that helps regulate cell keratinization, improves desquamation, regulates lipid balance of the dermis, and prevents bacterial proliferation.