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Acne vulgaris, the most common skin disease, affects 80% of the population between the ages of 12 and 25.(1) It is generally self-limiting, however, may persist for years and in severe cases, may potentially lead to scarring and disfigurement. The lesions of acne are generally classified as inflammatory or noninflammatory, and include comedones, papules, pustules, and nodules, or cysts, and occur most frequently on the face, neck, chest, and back.
The pathogenesis of acne is proving to be increasingly complex. It involves the interaction of enzymatic, immunologic, and chemotactic effects on normal cutaneous microflora; hormonal influences; abnormal keratinization of the sebaceous follicular duct wall; increased sebum production; follicular fragility; and host responsiveness.(2)
One of the pathogenic factors in acne is sebum, produced by sebaceous glands. Sebaceous glands are located throughout the body except for the palms of the hands, soles and dorsa of the feet, and the lower lip. Each person has approximately 5,000 sebaceous follicles. These glands are the largest and most numerous on the face, back, chest, and upper outer arms. Sebaceous glands are large at birth, and then reduce in size until adolescence. They once again enlarge during pre-puberty with changes in hormone levels influencing sebaceous gland secretion. The expression of the disease during puberty is due to increased production and release of sebum by the sebaceous glands. Comedones, or small cysts, appear as a result of the blockage of hair follicles by excess sebum and keratinous material. The activity of lipophilic yeast (P. orbiculare) and bacteria (Proprionobacterium acnes) within the comedones releases free fatty acids from sebum, causes inflammation within the cyst, and results in rupture of the cyst wall.(3)
The hormonal mechanism by which sebum levels are increased occurs as testosterone is converted to dihydrotestosterone in the skin, which acts directly on the sebaceous gland to increase its size and metabolic rate. Estrogens, however, have a less well-defined mechanism, and decrease sebaceous gland secretion. Sebaceous cells mature, die, fragment, and extrude into the sebaceous duct, where they combine with desquamating cells of the lower hair follicle, and finally arrive at the surface of the skin as sebum. Early acne lesions result from blockage of the follicular canal. Increased amounts of keratin, also induced by hormonal changes, mix with sebum, which has been modified by the action of resident flora (P.acnes). This increases the number of cornified cells which remain adherent to the follicular canal. This is known as retention keratosis and occurs just above the opening of the sebaceous gland duct to form a plug.
The importance of altered keratinization of cells within the follicle is not completely understood. It has been observed, though, that increased production of loosely adherent keratin cells has been correlated with obstruction of the follicles seen in comedo formation. It is unknown whether this activity is inherent or secondary to irritation and other factors.(4)
Proprionobacterium acnes, the resident flora of which we have spoken is an anaerobic diphtheroid. As it interacts with the increased amount of sebum, it produces lipases, proteases, hyaluronidase, and chemotactic factors. The interaction creates free fatty acids, which are primary irritants and are very comedogenic. Also, chemotactic factors attract neutrophils. Neutrophils release hydrolases that weaken the follicular wall. As a result, the wall thins, becomes inflamed (red papule), and ruptures, releasing part of the comedo into the dermis. If this occurs, an intense foreign body inflammatory reaction occurs, resulting in the formation of a pustule or cyst.
The earliest lesions most often seen in adolescence are mildly inflamed or non-inflamed comedones on the<
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