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

Their short duct is lined 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 avoid microbial 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 a perception of acne as an inflammatory disorder. In this view androgens, hormone receptors, regulatory neuropeptides, and environmental factors are portrayed being factors able to interfere with the biological 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 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 damage or infection which originate intracellular signals which stimulate 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 work 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

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 may also have a much stronger reaction 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 production is exacerbated and the first load of sebum through the previously empty duct might originate forces of sufficient magnitude that injure the pilosebaceous gland. The body reacts 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 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 forming what is commonly referred to as a black head. The water content of the comedone is eliminated by evaporation and osmosis into the adjacent horny layer (keratin) of the upper epidermis resulting in a hardening of the comedone, starting at the external surface. The comedone may become attached 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.