The hair follicle and sebaceous glands regularly undergo dynamic remodelling in a cyclical manner involving highly coordinated patterns of cell proliferation, differentiation and death of cells. Sebaceous glands are gathered near a hair follicle, into which they discharge their secretion - sebum.

Their small duct is covered by stratified squamous epithelium. Sebum is formed by the total breakdown of the cells and may lubricate the hair shaft, protect the skin from drying and moisture, and prevent microbial infection.

View on the Cause of Acne is Changing

Ongoing research is changing the classical view of acne as caused by Propionibacterium acnes bacteria to a perception of acne as an inflammatory condition. In this view androgens, regulatory neuropeptides, hormone receptors, and environmental factors are portrayed as factors able to interrupt the biological cyclical dynamic breakdown of devitalized cells into sebum inside the sebaceous follicles. Blockage of emission of sebum to the surface of skin leads to occlusion of the ducts (microcomedones) and then bigger comedones that become inflammatory lesions.

The acne inflammation goes through certain stages. Pro-inflammatory lipids, chemokines (molecules released by cells at the site of damage or infection which originate intracellular signals which stimulate cell motion, and cytokines (cell-secreted proteins that affect the expression of growth factors as well as migration of white blood cells to a damaged site and fibroblast proliferation), seem to work as mediators for the appearance of acne lesions. Propionibacterium acnes is not initially related but may mediate later inflammatory episodes leading to worsening of the lesions.

Immune System Affects Acne

Variation in the innate immunity of the skin predisposes to acne breakouts. Some people have better levels of constitutive, innate immunity in the skin and some may also have a much powerful reaction to external stimuli, and that depends indirectly on genetic factors related to excess androgen activity in puberty, that cause sterile inflammatory phenomena.

Acne is initiated by an inflammatory signal to the neural system without involvement of bacteria in its initiation. During puberty sebum production is exacerbated and the first load of sebum through the previously empty duct can originate forces of enough magnitude that injure the pilosebaceous gland. The body responds with the production of inflammatory molecules to stimulate cell division and quickly recover the lining of the inner surface of the ducts.

Causes of Acne Lesions

At the same time, the sebum in the distal orifice of the sebaceous gland duct and/or the hair follicle conducts to the formation of a dry "plug" (comedone) which obstructs the continued flow of sebum. On exposure to oxygen, the comedone turns dark originating what is usually known as a black head. The aqueous content of the comedone is reduced by evaporation and diffusion into the adjacent horny layer (keratin) of the upper epidermis resulting in a hardening of the comedone, starting at the external surface. The comedone may become attached to the keratin and thus "moored" to adjacent elements of the skin. The comedone becomes changed chemically, as well as physically, thus becoming an element which is strange to the body. This state of "foreignness" initiates a further inflammatory response, including immune reactions and other responses of various defense systems, particularly those associated with granulocytes and macrophages.