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Acne - A Skin Inflammatory Disorder

Expert Author: Angelique Jodein | Submitted: 2008-03-27 | Word Count: 490 words | Views: 105 view(s) [View Summary]
Angelique Jodein
Acne is an inflammatory ailment of the pilosebaceous follicles.

The hair follicle and sebaceous glands permanently suffers dynamic remodeling in a cyclical way involving finely coordinated sequences of cellular division, differentiation and death of cells. Sebaceous glands are clustered by the side of a hair follicle, into which they discharge the secretion - sebum.

Their short canal is lined by stratified squamous epithelium. Sebum is made by the total breakdown of the cells and can lubricate the hair shaft, protect the skin from drying and moisture, and prevent microbial invasion.

Ongoing research is changing the classical view of breakouts as initiated by Propionibacterium acnes bacteria to a perception of breakouts as an inflammatory episode with androgens, hormonal receptors, signalling neuropeptides, and environmental influences being agents able to interrupt the natural cyclical dynamic breakdown of devitalized cells into sebum within the sebaceous follicles. Alteration of discharge of sebum to the surface of skin leads to occlusion of the canals (microcomedones) and then enlarged comedones that become inflammatory lesions.

Pro-inflammatory lipids, chemokines (elements released by cells at the site of injury or infection which originate intracellular signals which promote cellular motion, and cytokines (cell-secreted proteins that influence 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 initiation of acne lesions. Propionibacterium acnes is not directly involved but can mediate later inflammatory events leading to worsening of the lesions.

Variation in the natural defences of the skin predisposes to acne. Some people have higher levels of constitutive, natural, immunity in the skin and some can also possess a much stronger response to external stimuli, and such depends indirectly on inherited factors related to excess androgen activity in puberty, that start sterile inflammatory phenomena.

What Starts Acne during Puberty?

Acne is started by an inflammatory signal to the neural system without participation of bacteria in its origins. During adolescence sebum production is exacerbated and the first flow of sebum through the previously empty duct can create shear forces of sufficient magnitude that damage the pilosebaseous gland. The body responds with the release of inflammatory molecules to stimulate cell division and quickly restore the lining of the inner wall of the conducts. At the same time sebum at the external orifice of the sebaceous gland duct and/or the hair follicle produces the appearance of a dry "plug" (comedone) which obstructs the flow of sebum. On exposure to oxygen, the comedone gets dark creating what is commonly known as a black head.

The water content of the comedone is reduced by evaporation and diffusion into the nearby horny layer (keratin) of the surface epidermis resulting in a hardening of the comedone, beginning at the external layer. The comedone can 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.

We now bring to you a natural skin care product that is an effective cure for a wide variety of dermal problems, including stretch marks, scars, acne, and others.

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