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

Their short duct is lined by stratified squamous epithelium. Sebum is formed by the total breakdown of the cells and can lubricate the hair shaft, protect the skin from drying and moisture, and prevent bacterial 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 an approach of acne as an inflammatory disorder. In this view androgens, hormone receptors, regulatory neuropeptides, and environmental factors are portrayed being agents able to interrupt the biological cyclical dynamic breakdown of devitalized cells into sebum within the sebaceous follicles. Interruption of emission 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 produced by cells at the site of injury or infection which originate intracellular signals which promote cell motion, and cytokines (cell-secreted proteins that modify the expression of growth factors as well as migration of white blood cells to an injured site and fibroblast proliferation), seem to act as mediators for the initiation 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, innate immunity in the skin and some can also have a much powerful reaction to external stimuli, and that depends vaguely on hereditary 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 flow of sebum through the previously empty duct can create forces of enough magnitude that injure the pilosebaceous gland. The body responds with the release of inflammatory molecules to promote 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 external orifice of the sebaceous gland duct and/or the hair follicle conducts to the creation of a dry "plug" (comedone) which obstructs the continued flow of sebum. On contact with oxygen, the comedone turns dark forming what is usually referred to 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 resulting in a hardening of the comedone, starting at the upper surface. The comedone can become linked to the keratin and thus "moored" to nearby elements of the skin. The comedone becomes changed chemically, as well as physically, thus becoming a material which is foreign to the body. This state of "foreignness" provokes a further inflammatory reaction, including immune activities and other responses of various defense systems, particularly those associated with granulocytes and macrophages.