Although the exact aetiological mechanism is unknown, it is accepted that acne is the result of the interaction of several processes, which centre on pathological changes in the pilosebaceous duct (PSD) in response to an as yet unidentified trigger mechanism. Thickening of the follicular stratum corneum (hypercornification) leads to blockage and accumulation of sebum, which is produced in large quantities in response to the androgen surges that accompany puberty. The resident skin commensal Propionibacterium acnes then proliferates in the lipid-rich sebaceous follicles and there is a build up of bacteria and their metabolites, sebum and dead cellular material. This cannot be discharged because of the blockage at the follicle opening and there is therefore an inflammatory response. The extent and duration of the inflammation, and hence the severity of the acne, may be determined by individual variation in the immune response to P. acnes, its metabolic products or any component of the blocked PSD contents. The relative roles of the various contributory factors will also differ between individuals and possibly between sites in any individual.
The onset of acne is generally associated with adrenarche, although androgen markers and mild comedonal acne have been detected in children under 10 years of age,4,5 particularly in girls who have an earlier onset of puberty.6 Although the overall incidence tends to be equivalent in both sexes, with the peak rates occurring at 17 years of age,7 boys tend to have more severe disease.8 There is no evidence that ethnic or racial differences influence the development of acne, although Caucasians have been reported to have a higher incidence of disease.9 Whilst genetic factors are also thought to influence susceptibility to acne,10,11 the mode of inheritance has not been determined.
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