The approach to acne treatment underwent significant changes during the twentieth century. Retinoids were introduced as a medical treatment for acne in 1943. Benzoyl peroxide was first proposed as a treatment in 1958 and has been routinely used for this purpose since the 1960s. Acne treatment was modified in the 1950s with the introduction of oral tetracycline antibiotics (such as minocycline). These reinforced the idea amongst dermatologists that bacterial growth on the skin plays an important role in causing acne. Subsequently, in the 1970s tretinoin (original trade name Retin A) was found to be an effective treatment. The development of oral isotretinoin (sold as Accutane and Roaccutane) followed in 1980. After its introduction in the United States it was recognized as a medication highly likely to cause birth defects if taken during pregnancy. In the United States, more than 2,000 women became pregnant while taking isotretinoin between 1982 and 2003, with most pregnancies ending in abortion or miscarriage. About 160 babies were born with birth defects.
A major mechanism of acne-related skin inflammation is mediated by C. acnes's ability to bind and activate a class of immune system receptors known as toll-like receptors (TLRs), especially TLR2 and TLR4. Activation of TLR2 and TLR4 by C. acnes leads to increased secretion of IL-1α, IL-8, and TNF-α. Release of these inflammatory signals attracts various immune cells to the hair follicle including neutrophils, macrophages, and Th1 cells. IL-1α stimulates increased skin cell activity and reproduction, which in turn fuels comedo development. Furthermore, sebaceous gland cells produce more antimicrobial peptides, such as HBD1 and HBD2, in response to binding of TLR2 and TLR4.
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Acne appears to be strongly inherited with 81% of the variation in the population explained by genetics. Studies performed in affected twins and first-degree relatives further demonstrate the strongly inherited nature of acne. Acne susceptibility is likely due to the influence of multiple genes, as the disease does not follow a classic (Mendelian) inheritance pattern. Several gene candidates have been proposed including certain variations in tumor necrosis factor-alpha (TNF-alpha), IL-1 alpha, and CYP1A1 genes, among others. The 308 G/A single nucleotide polymorphism variation in the gene for TNF is associated with an increased risk for acne. Acne can be a feature of rare genetic disorders such as Apert's syndrome. Severe acne may be associated with XYY syndrome.
Cystic Acne: The most severe type of acne, cystic acne requires dermatological care and prescription acne medication to treat. Even the best acne products available over the counter are no match for this painful condition in which the area of the outbreak becomes inflamed, but not infected. Cystic acne can result in permanent scarring. However, it's important to know that all acne lesions can scar. Scarring is related to size, amount of inflammation, genetics and delay in therapy.
Retinoids are medications which reduce inflammation, normalize the follicle cell life cycle, and reduce sebum production. They are structurally related to vitamin A. Studies show they are underprescribed by primary care doctors and dermatologists. The retinoids appear to influence the cell life cycle in the follicle lining. This helps prevent the accumulation of skin cells within the hair follicle that can create a blockage. They are a first-line acne treatment, especially for people with dark-colored skin, and are known to lead to faster improvement of postinflammatory hyperpigmentation.
Acne appears when a pore in our skin clogs. This clog begins with dead skin cells. Normally, dead skin cells rise to surface of the pore, and the body sheds the cells. When the body starts to make lots of sebum (see-bum), oil that keeps our skin from drying out, the dead skin cells can stick together inside the pore. Instead of rising to the surface, the cells become trapped inside the pore.