The Physiology of Rosacea

The precise pathophysiology of rosacea remains unknown. In the clinical picture, rosacea manifests itself primarily as a cutaneous vascular disorder; however, inflammatory changes are a hallmark of severe rosacea.

Therefore rosacea may be thought of as a disease spectrum with 2 primary etiologic components, vascular and inflammatory. The earliest manifestations of the disease are cutaneous vascular dilatory changes with subsequent increased blood flow in the form of telangiectasias and erythema. Sunlight-induced small vessel damage may contribute to this underlying vascular instability.

In its later stages, the rosacea picture is marked by inflammatory changes in the form of papules and pustules in the midface, rhinophyma (bullous nose), blepharitis and meibomitis, and corneal vascularization. A type 4, cell-mediated hypersensitivity reaction has been hypothesized as a possible mechanism.

Demodex mites also have been implicated as a possible inflammatory stimulus in the overall picture of rosacea.

Added to the picture, Helicobacter pylori has been postulated to be a causative factor in a subset of patients. Whatever the underlying mechanism, there is a fundamental abnormality in the sebaceous glands of the face and eyelids, which leads to the inflammatory changes exhibited.

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