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Preface
This article is about exact acne working mechanism.
How does the acne works?
The prevalence of acne is widespread, affecting 80% of population between the ages of 12 and 25.
Although acne is generally self-limiting, the psychological effect may be profound. Current views of this disorder and its therapy have been reviewed extensively.
Causes of acne are multi-factorial and not completely understood. Sebaceous follicles of the face and upper trunk that normally produce substances to "moisturize" the skin, are predominantly involved. A cross-section view of the sebaceous follicle shows an opening to the skin (orifice or "pore"), and a long narrow canal extending into the dermis. Sebaceous glands that develop at puberty in response to androgen stimulation are attached to the follicular canal by sebaceous ducts. Sebum produced in sebaceous glands is transported through the ducts to the canal and out onto the surface of the skin. Fine keratinous material (similar to skin surface cells) and bacteria (usually Propionibacterium acnes) may also be present within the follicular canal. Acne is primarily due to derangement in structure and/or function of the normal sebaceous follicle.
Formation of a primary acne lesion, the comedo (or comedone) may be thought of simplistically as a plugging of the sebaceous follicle. As a result, the follicular canal widens and cell production is increased. Sebaceous glands may atrophy and sebum generally combines with excess loose cells in the follicular canal to form a keratinous plug. This lesion clinically appears as a "blackhead" or open comedo. Trauma or inflammatory changes in this lesion may lead to formation of a "whitehead" or closed comedo. If the follicular wall is damaged or ruptured by trauma or irritation, contents of the follicle wall may extrude into the dermis and initiate an inflammatory reaction clinically defined as a pustule or cyst. These pustules or cysts are commonly referred to as "pimples" or "zits" by many young people.
Androgens stimulate growth of sebaceous follicles and enhance sebum production. During the second decade of life, sebum production parallels androgen production and the presence of acne. Increased secretion of sebum into follicles also correlates with severity of acne.
The glyceride component of sebum is converted to free fatty acids and glycerol by lipases which are produced by acnes.
The free fatty acids presumably irritate the follicular wall and cause increased cell turnover and inflammation. This explanation perhaps is an oversimplification as glycerol has been identified as a substrate for acnes and free fatty acids act as a measure of acnes activity and viability.
Acnes play an important role in the initial development and maintenance of the inflammatory response of acne. Acnes may be responsible for increased antibody formation and levels of antibodies to acnes also are higher in patients with more severe forms of acne than normal controls.
Furthermore, acnes may activate the complement cascade via classic ant alternative pathways leading to vascular leakage, mast cell degranulation, leukocyte chemotaxis, and direct tissue damage. In addition, chemotactic factors secreted by acnes diffuse through the follicle wall and activate neutrophil chemotaxis and complement.
Clinically, acne can be mild and involve only a few open commedones, or it can be severe and involve multiple inflamed cysts, nodules, and pustules. Although these acne lesions may take as long as a month to develop and three to six weeks to completely heal, the fibrosis that accompanies healing may lead to permanent scarring. Severe forms of acne may be persistent and require advanced treatment. There is no "cure" for acne, however, aggressive therapy may modify or halt progression, and thereby prevent scaring. The choice of therapy for acne depends on both the severity of the inflammatory response and individual patient tolerance. Since acne is multifunctional process, multiple medications are available for its treatment.
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