Advances in understanding and managing rosacea: part 1: connecting the dots between pathophysiological mechanisms and common clinical features of rosacea with emphasis on vascular changes and facial erythema.

Rosacea is a common inflammatory facial dermatoses affecting primarily adults with fair skin, although all skin types may be affected. The diagnostic term "rosacea" reflects a spectrum of clinical features with the more common presentations characterized by increased blood flow and vasodilation during disease flares, which accentuate central facial erythema. Inflammatory lesions, usually papules and/or pustules are present in some cases. Variations in magnitude of the associated features of rosacea are noted clinically. Over time, other clinical features emerge or may be further accentuated, such as diffuse facial erythema and telangiectasias, as fixed changes in cutaneous vasculature occur. These later findings account for persistent diffuse facial erythema usually accentuated centrally on the inner cheeks, chin, nose, and/or medial forehead. Some patients may also develop phymatous changes and/or have concurrent ocular rosacea. Augmented innate immune response to certain triggers (often exogenous) and neurovascular/neuroimmune dysregulation appear to be involved early in the pathophysiological sequence of cutaneous rosacea and appear to signal other downstream inflammatory or physiochemical cascades that contribute to the pathogenesis of the disorder. In this article, Part 1 of a two-part series, emphasis is placed upon the correlation of clinical features and underlying pathophysiological changes in the more common presentations of rosacea encountered by the clinician. The importance of this information is that some of these pathogenic mechanisms are modulated by available therapies, and others remain as targets for the development of new therapeutic agents or modalities.