The main hormonal driver of oily sebum production in the skin is dihydrotestosterone. Another androgenic hormone responsible for increased sebaceous gland activity is DHEA-S. Higher amounts of DHEA-S are secreted during adrenarche (a stage of puberty), and this leads to an increase in sebum production. In a sebum-rich skin environment, the naturally occurring and largely commensal skin bacterium P. acnes readily grows and can cause inflammation within and around the follicle due to activation of the innate immune system. P. acnes triggers skin inflammation in acne by increasing the production of several pro-inflammatory chemical signals (such as IL-1α, IL-8, TNF-α, and LTB4); IL-1α is known to be essential to comedo formation.
Acne appears when a pore in our skin clogs. This clog begins with dead skin cells. Normally, dead skin cells rise to surface of the pore, and the body sheds the cells. When the body starts to make lots of sebum (see-bum), oil that keeps our skin from drying out, the dead skin cells can stick together inside the pore. Instead of rising to the surface, the cells become trapped inside the pore.