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

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

View on the Cause of Acne is Changing

Ongoing research is changing the old view of acne as caused by Propionibacterium acnes bacteria to an approach of acne as an inflammatory condition. In this view androgens, hormone receptors, regulatory neuropeptides, and environmental factors are portrayed as agents able to interfere with the natural cyclical dynamic breakdown of devitalized cells into sebum inside the sebaceous follicles. Blockage of discharge of sebum to the surface of skin leads to obstruction of the ducts (microcomedones) and then bigger comedones that become inflammatory lesions.

The acne inflammation goes through certain stages. Pro-inflammatory lipids, chemokines (substances released by cells at the site of injury or infection which give rise to intracellular signals which stimulate cell motion, and cytokines (cell-produced 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 act as promoters for the initiation of acne lesions. Propionibacterium acnes is not initially related but may 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 better levels of constitutive, natural immunity in the skin and some may also have a much powerful response 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 production is exacerbated and the first flow of sebum through the previously empty duct can 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 distal orifice of the sebaceous gland duct and/or the hair follicle leads to the creation of a dry "plug" (comedone) which obstructs the continued flow of sebum. On exposure to oxygen, the comedone turns dark forming what is commonly referred to 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 leading to 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 modified chemically, as well as physically, thus becoming an element which is strange to the body. This status of "foreignness" initiates a further inflammatory response, including immune reactions and other responses of various defense systems, specially those associated with granulocytes and macrophages.