Articles

The hair follicle and sebaceous glands regularly undergo dynamic remodelling in a cyclical manner 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 discharge their secretion - sebum.

Their small duct is lined by stratified squamous epithelium. Sebum is formed by the total breakdown of the cells and may lubricate the hair shaft, shield the skin from drying and moisture, and avoid bacterial 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 an approach of acne as an inflammatory disorder. In this view androgens, hormone receptors, regulatory neuropeptides, and environmental factors are portrayed as agents able to interfere with the biological cyclical dynamic breakdown of dead cells into sebum within the sebaceous follicles. Interruption of emission of sebum to the surface of skin leads to occlusion 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 leukocytes to an injured site and fibroblast proliferation), seem to work as mediators for the appearance of acne lesions. Propionibacterium acnes is not originally involved but may 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 better levels of constitutive, natural immunity in the skin and some may also have a much powerful response to external stimuli, and that depends vaguely on hereditary factors related to excessive 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 production is exacerbated and the first flow of sebum through the previously empty duct can create 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 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 contact with oxygen, the comedone turns dark originating what is commonly 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 surface epidermis leading to a hardening of the comedone, starting at the upper 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 a material which is foreign to the body. This state of "foreignness" initiates a further inflammatory response, including immune reactions and other responses of several defense systems, specially those related to granulocytes and macrophages.