Increased bacterial activity and resulting inflammation

Even where there is no evidence of active acne, P. acnes exists on the skin surface; indeed, there does not seem to be any correlation between the levels of P. acnes on the skin surface and severity of acne. However, some aspect of the hair follicle itself and the microenvironment found there causes P. acnes to proliferate and colonise the hair follicle leading to inflammation. The intensity of the inflammation varies depending on the individual which may, in part, be due to the individual’s sensitivity to the inflammatory mediators associated with P. acnes. Although the mechanisms are not fully understood, it is thought that the action of the proliferating bacteria causes release of inflammatory cytokines, primarily CD4⁺ T-lymphocytes. Initially, papules and pustules are seen. Pustules form the typical yellow spot of acne. Because of the inflammatory response, lots of white blood cells are attracted to the area where there are increased levels of bacteria. Pus is formed largely from the dead white blood cells.

As these inflammatory mediators move out into the surrounding dermis, the lesions are more likely to be nodular and/or cystic and there is an increased likelihood of permanent scarring. Nodules are solid and larger than pustules extending deeper into the layers of skin. They are caused when large comedones rupture releasing their inflammatory contents into the surrounding skin. Because they extend deeper into the skin affecting the dermis as well as epidermis, they do lead to scarring. Cysts occur less frequently than nodules but when they do they are even more destructive, leading to greater levels of scarring. They are not as solid as a nodule and will often occur where there are two or three nodules close together (Figure 10.4).