Acne is commonly found on the back . Although not as common as our faces, acne on back is often more debilitating as it can be very difficult to treat. Acne on back has degrees of severity depending upon the number of lesions and the presence of inflammation. It can be mild, moderate, or severe. The degree of skin sensitivity also has a role in the treatment of acne. Different skin types require different treatments and may react differently to the wide variety of treatments.
Acne is the result of excess oil build up and clogged pores of our skin and in case of facial acne, is treated by a strict daily skin regimen. Treatment includes a cleanser, treated gel or lotion, and possibly a moisturizer. Often dermatologist prescribe a glycolic acid treatment. The same is true for acne on back. However, since the back skin is tougher than on the face, therefore stronger acne control products and methods of treatement is required.
The back is also in continous contact with clothing that often irritate and aggravate acne. Clothing irritates acne and synthetic fibers (such as polyester) or tight clothing in general rub against the skin and aggravate acne breakouts as well as promote sweating. (Sweat causes excess oil build-up and blocked pores which result in more breakouts.)
Determining other mechanical cauuses of acne on back is important. For example, heavy backpacks worn across the upper shoulders and covering part of the back might be contributing to acne in these areas. Switching to a pack with convenient carry handles may clear up acne on back lesions.
Acne on back and the appearance industry
Thursday, July 17, 2008
Acne On Back Treatment
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Sunday, July 6, 2008
What are Acne causes?
The three main processes contributing to acne are: increased sebum secretion; pilosebaceous duct obstruction; and inflammation.
Under the influence of local hormone metabolism, androgens stimulate an increase in the size of the sebaceous glands and, hence, more sebum is produced. These large glands themselves produce more active androgen metabolites through the activity of type 1, 5α-reductase; one effect of these metabolites is to further enlarge the sebaceous glands. Sebum acts in partnership with bacteria to produce keratinization and hence blockage of the pilosebaceous duct and comedo formation.
The principal organism responsible is Propionibacterium acnes, which increases in number during flare-ups and is important in the change from non-inflammatory to inflammatory acne. This bacterium produces many inflammatory substances, such as lipases, proteases, hyaluronidases, and chemotactic factors that play a role in producing lesions. Therapy that lowers the Propionibacterium acnes count plays a pivotal role in management, but resistance of the bacterium to some antibiotics, especially erythromycin, is an emerging problem in acne therapy.
Acne may also be drug-induced, particularly secondary to anabolic and corticosteroids, iodides, lithium, phenytoin, streptomycin, and isoniazid. Sebum consists of triglycerides, wax esters, squalene, and sterol esters. The fatty acids in sebum are inflammatory and are formed by the lysolytic enzymes of bacteria, even in healthy skin, from unsaturated 14- to 16- or 18-carbon components of the triglycerides. It is possible that acne in people living in the tropics is due to a secondary response in the rate of turnover of the follicular lining, perhaps induced by occlusion under a belt or braces in such hot environments. The acne of Cushing's disease may also be due to an increased rate of such turnover. Chlorinated hydrocarbons also cause acne. Chloracne is an important symptom of poisoning.
The exact way in which the inflammation is produced is uncertain; as the follicle contains fatty acids and bacterial proteases which activate the classical alternative pathway of complement and attract neutrophils, this may be one mechanism.
Sebaceous gland activity is regulated by hormones and, in particular, by androgens from the testes and adrenals, which stimulate, and estrogens, which seem to suppress activity. In the adult male the glands are normally maximally stimulated, leading to more severe in boys than in girls. The skin itself is a major site for androgenic conversion similar to that observed in the prostate gland and in the male genitalia. Dihydrotestosterone, rather than testosterone, may be the end-organ effector and is formed within the target cells where it stimulates lipogenesis as well as mitosis. Eunuchs do not develop acne. Estrogens reduce the size of sebaceous glands and sebum production is diminished.
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