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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Publication history
Published online: December 31, 2021
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