Over 50% of NeoGen treatments currently performed in Asia are for the treatment of acne vulgaris, and, anecdotally, excellent results have been reported. There is a huge unmet need for new, non-drug treatments in inflammatory acne. There may be several methods by which NeoGen may be improving acne, one of which is anti-bacterial activity.
Acne pathogenesis and treatment
Acne is estimated to affect 9.4% of the population globally, making it the 8th most prevalent disease worldwide. Acne affects the face and upper torso, where there are high numbers of sebaceous glands, which secrete lipids in the form of sebum.
The aetiology of acne has four major features:
Androgen-induced seborrhoea (excess grease). The more sebum (grease) the greater degree of acne, evidence suggests that in most patients the seborrhoea is due to increased response of the sebaceous glands to normal levels of plasma androgens (male hormones).
Comedone formation (blackheads, whiteheads and microcomedones). Known as comedogenesis, this is due to an abnormal proliferation and differentiation of ductal keratinocytes. It is controlled, in part, by androgens. In pre-pubertal subjects comedones are seen early and they precede the development of inflammatory lesions.
Colonisation of the pilosebaceous duct with Propionibacterium acnes (P.acnes) is a later stage in the development of acne lesions (especially inflammatory lesions). The seborrhoea and comedone formation alter the ductal microenvironment, which results in colonisation of the duct. P.acnes (sometimes described as Cutibacterium acnes, or C.acnes), is an aerotolerant, anerobic, Gram positive bacterium. It is a common skin bacterium, and is mainly considered as beneficial to skin health, helping to keep a low pH by releasing free fatty acids onto the skin. Its role in acne pathogenesis is still unclear, although it seems to aggravate inflammation, promote comedone formation and cause other biochemical changes within the sebaceous gland.
Production of inflammation. This is a complex process involving an interaction between biological changes occurring in the duct as a result of comedone formation and P.acnes colonisation of the duct and the patients cellular (especially lymphocytes) response within the dermis, which responds to pro-inflammatory cytokines spreading from the duct to the dermis.
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