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Acne: An Inflammatory Disorder

Expert Author: Angelique Jodein | Submitted: 2008-05-05 | Word Count: 535 words | Views: 113 view(s)
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Angelique Jodein
The hair follicle and sebaceous glands regularly undergo dynamic remodelling in a cyclical manner involving tightly coordinated patterns of cell proliferation, differentiation and death of cells. Sebaceous glands are clustered near a hair follicle, into which they pour 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 microbial infection.

View on the Cause of Acne is Changing

Ongoing research is modifying the old view of acne as caused by Propionibacterium acnes bacteria to a perception of acne as an inflammatory disorder. In this view regulatory neuropeptides, androgens, hormone receptors, and environmental factors are portrayed as agents able to interfere with the biological cyclical dynamic breakdown of devitalized cells into sebum inside the sebaceous follicles. Blockage 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 (molecules released by cells at the site of damage 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 work as mediators for the initiation 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

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 powerful reaction to external stimuli, and that depends indirectly on genetic factors related to excess androgen activity in puberty, that cause 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 blocks the continued flow of sebum. On contact with oxygen, the comedone turns dark forming what is commonly referred to as a black head. The aqueous 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 changed chemically, as well as physically, thus becoming an element which is foreign to the body. This state of "foreignness" initiates a further inflammatory reaction, including immune activities and other responses of several defense systems, particularly those related to granulocytes and macrophages.

About the Author

You can now clear acne and erase the related spots with topical application of a natural cream for pimple marks. When treating the acne inflammation, this natural acne product works with your body without bieffects.

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