Pathogenesis of Cystic Acne
Pathogenesis of cystic acne is related to abnormal follicular differentiation, increased cornification, enhanced sebaceous gland activity and hyper seborrhea, bacterial hyper colonization, inflammation and immunological host reaction.With respect to classical aspects, acne is a chronic inflammatory disease affecting sebaceous gland follicles located on face, chest, shoulders and back.
Acne is the most common disease affecting all ages and ethnic groups. Not less than 15-30% of acne patients require medical treatment due to severity of their clinical condition, 2-7% of them experience life long post acne scars.
With respect to modern aspects, androgens, skin lipids, inflammatory signaling and regulatory neuropeptides and chemokines or cytokines seem to be involved in this multifactorial process. Hereditary factors also play an important but indirect role in acne.
The hereditary evidence with association of androgen and lipid abnormalities has been reported. The association of smoking with acne formation has also been reported .
Current concepts of pathogenesis of acne prove involvement of sebaceous hyperplasia, follicular hyperkeratinisation, bacterial hyper colonization as well as immune reactions and inflammation.
High sebum concentrations and follicular hyperkeratinisation lead to the follicular milieu with consecutive proliferation and bacteria chiefly Propionibacterium acnes.
This leads to further increased production of the pro-inflammatory cytokines interleukin-1 (alpha) and tumor necrosis factor (alpha) by T-cells and keratinocytes leading to proliferation of both cell types.
Follicular keratinocytes fail to differentiate by apoptosis and produce hyperganulosis similar to impermeable skin outer layer resulting in formation of microcomedones.
Further inflammatory responses lead to development of increasing degrees of severity in inflammatory focus of acne [63(15)].
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