Abstract

Annular lesions represent a distinct morphology which characterizes many well-known dermatologic conditions. Little is definitively known regarding the pathogenesis of annular lesions, however there a few well-regarded hypotheses. Lesions that clear centrally while enlarging peripherally may result from a local central tissue anergy, or tolerance. The central area in lesions due to dermatophyte infections or subacute cutaneous lupus erythematous may have a central immunity to the antigen that trigged the lesion. The peripheral spread of inflammatory mediators may also contribute to lesions that expand centrifugally. In a highly active immune response, some of the inflammatory mediators may spread to adjacent tissue, which can propagate the inflammatory reaction. The additional hypotheses regarding pathogenesis are disease specific with individual mechanisms having been proposed. This chapter will describe both general and disease specific mechanisms that may contribute to the formation of annular lesions.

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