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Current Concepts of the Pathogenesis of Acne

Implications for Drug Treatment

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Abstract

The pathogenesis of acne is complex, with strong evidence supporting the involvement of sebaceous hyperplasia, follicular hyperkeratinisation, bacterial hypercolonisation, as well as immune reactions and inflammation. High sebum concentrations and follicular hyperkeratinisation lead to a change of the follicular milieu with consecutive proliferation of bacteria, chiefly Propionibacterium acnes. This leads to further increased production of the pro-inflammatory cytokines interleukin-1α and tumour necrosis factor α by T cells and keratinocytes, leading to proliferation of both cell types. Follicular keratinocytes fail to differentiate by apoptosis and produce hypergranulosis similar to the impermeable skin outer layer, resulting in the formation of microcomedones. Further inflammatory responses lead to the development of increasing degrees of severity in inflammatory forms of acne.

Retinoids aid the differentiation and reduce the hyperproliferation of keratinocytes, and can inhibit the migration of leucocytes. Combination therapy using retinoids plus benzoyl peroxide or antibacterials can treat existing acne lesions faster than the individual agents alone and can also prevent the development of new lesions. The new retinoids (e.g. adapalene) have not only the typical potent comedolytic activity but also anti-inflammatory effects. When added to antibacterial therapy, topical retinoids demonstrate faster and significantly greater reduction of inflammatory acne lesions and comedones than antibacterials alone.

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Acknowledgements

Professor Gollnick has conducted clinical studies for Galderma, Schering Berlin (AG), Yamanouchi, Hoffmann-la Roche and Hermal Company. Preparation of this manuscript was supported by Galderma International.

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Correspondence to Harald Gollnick.

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Gollnick, H. Current Concepts of the Pathogenesis of Acne. Drugs 63, 1579–1596 (2003). https://doi.org/10.2165/00003495-200363150-00005

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