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Introduction • Common disease of pilosebaceous unit in adolescent(Physiologic). • Its cause is multi factorial & has pleomorphic clinical presentation. • Different modality of treatment are available, but selection of appropriate method is Vital.
Naturalhistory • Starts at adolescent-resolve by mid-twenties • 83-95% suffers - at about 14-19years of age • 8% late onset acne - 0ver 25years age
Intro Factorsduction • Genetics • Environmental • Sebum- 1.Triglycride is hydrolysed by P.acnes to free fatty acid, 2. increased squalene,& 3.decreased Linoleic acid • P.acnes- lipase, phosphatase & hyaluronate lyase • Ductal keratinocyte- IL-1,IL-1β, TNF
Special features of pilosebaceous unit • Propionibacterium acnes-unique composition of sebum • Release of IL-1,IL-1β, TNF from ductal keratinocytes • Androgen receptors – Keratinocytes of hair follicle & Basal cells of sebaceous unit • Follicular keratinocytes has – increased 17β-hydroxysteroid dehydrogenase &5-reductase activity (Type-I isoenzyme)[pivotal in development of sebaceous gland and acne]
Factors responsible for Keratinocyte hyperproliferation • Androgenic hormone Dihydrotestosterone (DHT) • Decrease Linoleic acid • Increased Interleukin (IL)-1