Articles

The hair follicle and sebaceous glands continually undergo dynamic remodelling in a cyclical manner involving tightly 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 short duct is lined by stratified squamous epithelium. Sebum is formed by the total breakdown of the cells and can lubricate the hair shaft, protect the skin from drying and moisture, and prevent microbial infection.

View on the Cause of Acne is Changing

Ongoing research is changing the old view of acne as caused by Propionibacterium acnes bacteria to a perception of acne as an inflammatory condition. In this view regulatory neuropeptides, hormone receptors, androgens, and environmental factors are portrayed as factors able to interfere with the natural cyclical dynamic breakdown of dead cells into sebum within the sebaceous follicles. Interruption of emission 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 released by cells at the site of damage or infection which give rise to intracellular signals which stimulate cell motion, and cytokines (cell-secreted proteins that modify the expression of growth factors as well as migration of leukocytes to an injured site and fibroblast proliferation), seem to act as promoters for the appearance of acne lesions. Propionibacterium acnes is not originally involved but can mediate later inflammatory episodes 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, innate 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 excessive 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 production is exacerbated and the first load of sebum through the previously empty duct might originate forces of sufficient magnitude that damage the pilosebaceous gland. The body responds with the release 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 conducts to the creation of a dry "plug" (comedone) which obstructs the continued flow of sebum. On exposure to oxygen, the comedone turns dark forming what is usually known as a black head. The aqueous content of the comedone is eliminated by evaporation and osmosis into the adjacent horny layer (keratin) of the surface 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 changed chemically, as well as physically, thus becoming an element which is strange to the body. This state of "foreignness" initiates a further inflammatory response, including immune activities and other responses of several defense systems, specially those associated with granulocytes and macrophages.