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

Their small duct is lined 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 prevent bacterial 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, hormone receptors, androgens, and environmental factors are portrayed as factors able to interfere with the biological cyclical dynamic breakdown of devitalized cells into sebum within the sebaceous follicles. Blockage of discharge 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 produced by cells at the site of damage or infection which originate 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 mediators for the initiation of acne lesions. Propionibacterium acnes is not originally 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 better levels of constitutive, innate immunity in the skin and some can also have a much stronger response to external stimuli, and that depends vaguely 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 secretion is exacerbated and the first load of sebum through the previously empty duct might create 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 leads to the creation of a dry "plug" (comedone) which blocks 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 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 status of "foreignness" provokes a further inflammatory response, including immune activities and other responses of several defense systems, particularly those related to granulocytes and macrophages.