The hair follicle and sebaceous glands continually undergo dynamic remodelling in a cyclical way involving highly coordinated patterns of cell proliferation, 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 formed by the total breakdown of the cells and can lubricate the hair shaft, shield the skin from drying and moisture, and avoid microbial infection.

View on the Cause of Acne is Changing

Modern 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 regulatory neuropeptides, androgens, hormone receptors, and environmental factors are portrayed being agents able to interfere with the natural cyclical dynamic breakdown of dead cells into sebum within the sebaceous follicles. Blockage of discharge 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 (substances produced 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 affect the expression of growth factors as well as migration of leukocytes to an injured site and fibroblast proliferation), seem to work as promoters for the initiation of acne lesions. Propionibacterium acnes is not originally involved 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 genetic factors related to excess androgen activity in puberty, that trigger 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 can originate forces of sufficient magnitude that injure the pilosebaceous gland. The body reacts with the release of inflammatory molecules to stimulate 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 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 commonly known as a black head. The water content of the comedone is eliminated by evaporation and diffusion into the adjacent horny layer (keratin) of the upper epidermis leading to 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 modified chemically, as well as physically, thus becoming an element which is foreign to the body. This state of "foreignness" initiates a further inflammatory response, including immune activities and other responses of various defense systems, particularly those associated with granulocytes and macrophages.