Pathophysiology of Rosacea: Introduction

Abstract

Several considerations prompt investigative dermatologists to study rosacea: it is common; its etiology remains unknown; its pathophysiology is poorly understood; and it has a significant impact on quality of life, all of which leave considerable space for investigation. Rosacea includes several distinct clinical subtypes, which lead to questions addressed by research that takes advantage of several of the disciplines within experimental dermatology, including immunology, inflammation, neuroimmunology, neuroscience, matrix biology and fibrosis, genetics, and vascular biology. Although epidemiological studies favor a genetic component in rosacea, no ‘‘rosacea predisposing’’ gene(s) have been identified. Rosacea can be triggered by any one of several environmental ‘‘insults’’, including UVR, spicy foods, alcohol, ‘‘stress’’, exercise, and temperature change, just to name a few. As a facial, chronic disease, rosacea has been characterized as having different clinical and histopathological expressions. These include erythema (vasodilation), telangiectasia, lymphedema, lympho-monocytic infiltrates with occasional appearance of neutrophils, and as a late stage, fibrosis. The pathophysiology of rosacea appears to be complex, as virtually all cutaneous cells, including immune cells, appear to have roles. Ultimately, rosacea is a good ‘‘model’’ through which investigators can learn more about the complexities of neuroimmune communication, inflammation, and immunity, as well as about chronic inflammation and the development of fibrosis. Indeed, accumulating evidence now leads to the conclusion that in chronic inflammatory diseases, there is close molecular and cellular interaction among innate immune defense mechanisms, innervation, immunity, and vascular biology. Ultimately, treatment is an important goal, and it is revealing to acknowledge that none of the several treatments for rosacea is satisfactory. The aim of this collection of reports is to focus on understanding each element in its pathogenesis in order to aid the development of novel treatment strategies for this and other inflammatory and fibrotic skin diseases.