• Frank C Powell.
• Regional Centre of Dermatology, Mater Misercordiae Hospital, Dublin, Ireland.
• Cutis. 2004 Sep 1; 74 (3 Suppl): 9-12, 32-4.

AbstractThe pathophysiology of rosacea remains unknown. A leading theory suggests a vascular basis; however, clinical observations and histopathologic studies suggest that inflammation of the pilosebaceous follicle may be central to the pathogenesis of rosacea. Demodex folliculorum is a frequently seen commensal in the follicles of facial skin. According to evidence from biopsies of the skin surface, individuals with rosacea have a higher density of this parasite. This increased mite density may play a role in the pathophysiology of rosacea by triggering inflammatory or specific immune reactions, mechanically blocking the follicles, or acting as a vector for bacteria. Ongoing research has shown that bacteria from patients with rosacea may behave differently at the higher skin temperature that may be present in patients with rosacea. Another group has isolated bacteria from the Demodex mites; these bacteria may play a pathogenic role in papulopustular rosacea by facilitating follicular-based inflammatory changes.

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