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How Acne Appears
The hair follicle and sebaceous glands continually undergoes dynamic remodeling in a cyclical way involving tightly coordinated sequences of cellular division, differentiation and death of cells. Sebaceous glands are gathered by the side of a hair follicle, into which they pour the secretion - sebum. Their short duct is made of stratified squamous epithelium. Sebum is formed by the total breakdown of the cells and may lubricate the hair shaft, defend the skin from drying and moisture, and prevent bacterial invasion. Ongoing research is modifying the classical view of breakouts as initiated by Propionibacterium acnes bacteria to a perspective of breakouts as an inflammatory episode with androgens, hormonal receptors, signalling neuropeptides, and environmental influences being agents able to alter the natural cyclical dynamic breakdown of devitalized cells into sebum within the sebaceous follicles. Interruption of discharge of sebum to the surface of skin causes occlusion of the ducts (microcomedones) and then enlarged comedones that become inflammatory lesions. Pro-inflammatory lipids, chemokines (molecules released by cells at the site of injury or infection which originate intracellular signals which promote cellular motion, and cytokines (cell-produced 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 act as mediators for the appearance of acne lesions. Propionibacterium acnes is not directly involved but may mediate later inflammatory events leading to worsening of the lesions. Variation in the innate defences of the skin predisposes to acne. Some people have higher levels of constitutive, innate, immunity in the skin and some may also possess a much stronger reaction 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 nervous system without involvement of bacteria in its initiation. During adolescence sebum production is exacerbated and the first flow of sebum through the previously empty duct might create shear forces of enough magnitude that injure the pilosebaseous gland. The body reacts with the release of inflammatory molecules to stimulate cell division and quickly restore the lining of the inner wall of the ducts. At the same time sebum at the external orifice of the sebaceous gland duct and/or the hair follicle leads to formation of a dry "plug" (comedone) which obstructs the flow of sebum. On exposure to oxygen, the comedone turns dark forming what is commonly referred to as a black head. The water content of the comedone is reduced by evaporation and diffusion into the adjacent horny layer (keratin) of the surface epidermis producing a hardening of the comedone, beginning at the external layer. The comedone may become attached to the keratin and thus "moored" to adjacent elements of the skin. The comedone is changed chemically, as well as morphologically, thus becoming a material which is foreign to the body. Article Directory: http://www.articledashboard.com We now bring to you a biological skin care product that is an effective solution for a wide variety of skin problems, including acne, stretch marks, scars, and others. |
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