Acne is the most common dermatological disease that afflicts human beings. For anyone who has suffered moderate to severe skin problems, the physical and emotional effects of acne vulgaris can be devastating, especially during the teenage years.
For decades, the main causes of acne were thought to be related to increased production of sebum (seborrhea) in the sebaceous glands due to changes in hormone production, along with keratinization of the skin and colonization by P. acnes (Propionibacterium acnes). Moreover, androgens (usually steroid hormones) or a genetic predisposition were considered primary triggers for the papules, pustules and nodules that occur mainly on the forehead, nose, chin, chest and back.
However, research* indicates that these known factors surprisingly appear to play a secondary or indirect role in the development of acne, along with poor nutrition, stress, and smoking. Instead, modern analysis has produced evidence that inflammatory processes precede the excess growth of cells in the epidermis (hyperproliferation) and the formation of microcomedones (first latent acne lesions).
Researchers found that a higher secretion of interleukin-1É‘ (an endogenous pro-inflammatory signaling molecule) took place even before hyperproliferation of skin cells and conversion into hard tissue (cornification) was observed.
It is true that healthy sebaceous glands produce cytokines as part of their natural cyclical process. However, when pre-clinical inflammation is overstimulated or a fault in the negative feedback regulation** occurs, clinically relevant inflammation may arise.
This leads to the conclusion that acne vulgaris is primarily an inflammatory disease.