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

Their small duct is lined 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 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 a perception of acne as an inflammatory disorder. In this view hormone receptors, regulatory neuropeptides, androgens, and environmental factors are portrayed being factors able to interrupt the natural cyclical dynamic breakdown of dead cells into sebum inside the sebaceous follicles. Blockage of emission of sebum to the surface of skin leads to obstruction of the ducts (microcomedones) and then enlarged comedones that become inflammatory lesions.

The acne inflammation goes through certain stages. Pro-inflammatory lipids, chemokines (molecules released by cells at the site of injury or infection which give rise to intracellular signals which stimulate cell motion, and cytokines (cell-secreted proteins that modify the expression of growth factors as well as migration of leukocytes to a damaged site and fibroblast proliferation), seem to work as promoters for the initiation 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

Acne usually appears in people whose skin has suffered a variation in its natural immunity. Some people have better levels of constitutive, natural immunity in the skin and some may also have a much powerful reaction to external stimuli, and that depends vaguely on genetic factors related to excess androgen activity in puberty, that cause sterile inflammatory phenomena.

Bacteria does not initiate acne; the real cause is an inflammatory signal to the neural system. During puberty sebum secretion is exacerbated and the first load of sebum through the previously empty duct might originate forces of enough magnitude that damage the pilosebaceous gland. The body reacts with the release 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 conducts to the formation of a dry "plug" (comedone) which obstructs the continued flow of sebum. On contact with oxygen, the comedone turns dark forming what is commonly 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 surface epidermis leading to a hardening of the comedone, starting at the upper surface. The comedone may become attached 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" initiates a further inflammatory reaction, including immune activities and other responses of several defense systems, particularly those related to granulocytes and macrophages.