Pathogenesis of follicular distention, rupture, and inflammation in acne vulgaris
Pathogenesis of follicular distention, rupture, and inflammation in acne vulgaris
Acne is a disease of the follicular canal of a sebaceous follicle. A compact stratum corneum and a thickened granular layer in the infrainfundibulum are the beginning of the formation of a comedo. Microcomedones (A) and closed (B) and open (C) comedones form. Excessive sebum secretion occurs, and the bacterium Cutibacterium (formerly Propionibacterium) acnes proliferates. The organism produces chemotactic factors, leading to neutrophil migration into the intact comedo. Neutrophilic enzymes are released and the comedo ruptures, inducing a cycle of chemotaxis and intense neutrophilic inflammation (D and E).