The hair follicle and sebaceous glands regularly undergo dynamic remodelling in a cyclical way involving tightly coordinated sequences of cell multiplication, differentiation and death of cells. Sebaceous glands are clustered by the side of a hair follicle, into which they discharge their secretion - sebum.

Their small duct is covered by stratified squamous epithelium. Sebum is created by the total breakdown of the cells and can lubricate the hair shaft, protect the skin from drying and moisture, and avoid bacterial infection.

View on the Cause of Acne is Changing

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

The acne inflammation goes through certain stages. Pro-inflammatory lipids, chemokines (substances 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 an injured site and fibroblast proliferation), seem to act as promoters for the appearance of acne lesions. Propionibacterium acnes is not initially related but can mediate later inflammatory events 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 higher levels of constitutive, natural immunity in the skin and some can also have a much powerful reaction to external stimuli, and that depends indirectly on hereditary factors related to excessive androgen activity in puberty, that trigger 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 flow of sebum through the previously empty duct can create forces of enough magnitude that injure the pilosebaceous gland. The body responds with the production of inflammatory molecules to promote cell division and quickly restore the lining of the inner surface of the ducts.

Causes of Acne Lesions

At the same time, the sebum in the external orifice of the sebaceous gland duct and/or the hair follicle leads to the creation of a dry "plug" (comedone) which blocks the continued flow of sebum. On exposure to oxygen, the comedone turns dark originating what is usually known as a black head. The water content of the comedone is reduced by evaporation and osmosis into the adjacent horny layer (keratin) of the surface epidermis leading to a hardening of the comedone, starting at the external surface. The comedone can become linked to the keratin and thus "moored" to adjacent elements of the skin. The comedone becomes modified chemically, as well as physically, thus becoming a material which is foreign to the body. This status of "foreignness" provokes a further inflammatory reaction, including immune reactions and other responses of various defense systems, particularly those associated with granulocytes and macrophages.

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