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

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

View on the Cause of Acne is Changing

Modern research is modifying the old view of acne as caused by Propionibacterium acnes bacteria to an approach of acne as an inflammatory condition. In this view hormone receptors, androgens, regulatory neuropeptides, and environmental factors are portrayed being factors able to interrupt the biological cyclical dynamic breakdown of devitalized cells into sebum inside the sebaceous follicles. Interruption of emission 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 (molecules produced by cells at the site of injury or infection which give rise to intracellular signals which promote cell motion, and cytokines (cell-secreted 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 appearance of acne lesions. Propionibacterium acnes is not originally related but may 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, innate immunity in the skin and some may also have a much stronger response to external stimuli, and that depends vaguely on genetic 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 flow of sebum through the previously empty duct might originate forces of sufficient magnitude that damage the pilosebaceous gland. The body reacts with the production 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 external 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 originating 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 surface epidermis leading to a hardening of the comedone, starting at the external surface. The comedone may 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 reactions and other responses of various defense systems, particularly those associated with granulocytes and macrophages.