Articles

The hair follicle and sebaceous glands regularly undergo dynamic remodelling in a cyclical way involving highly coordinated sequences 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 short 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 prevent microbial 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 an approach of acne as an inflammatory condition. In this view regulatory neuropeptides, androgens, hormone receptors, and environmental factors are portrayed being factors able to interrupt the natural cyclical dynamic breakdown of devitalized cells into sebum inside the sebaceous follicles. Interruption 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 (substances produced by cells at the site of damage or infection which originate intracellular signals which promote cell motion, and cytokines (cell-produced 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 promoters 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

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 can 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 flow of sebum through the previously empty duct might create forces of enough magnitude that injure the pilosebaceous gland. The body reacts with the production of inflammatory molecules to stimulate 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 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 contact with oxygen, the comedone turns dark originating what is usually 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 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 a material which is foreign to the body. This status of "foreignness" initiates a further inflammatory response, including immune reactions and other responses of several defense systems, specially those associated with granulocytes and macrophages.