[Physiopathology of rosacea]

For a long time rosacea was thought to be mainly a vascular disorder. In the past ten years many other concepts have emerged, such as the neurovascular aspects and involvement of innate immunity. There is obviously a genetic part in rosacea, as it is much more common in people with fair skin, blue eyes and Celtic ascendance. The same persons are submitted to continental weather, with major temperature seasonal variations. Erythema and telangiectasia result from dilated superficial capillaries that have bizarre shapes, and induce constant edema of the dermis. This might be a favouring factor for Demodex colonization, which plays a major role in rosacea. Inflammation is always present, even in erythematotelangiectatic subtypes. It involves innate immunity, in response to environmental factors, like Demodex and its own biotope, resulting in overproduction of LL37, a pro-inflammatory peptide able to induce skin inflammation in an animal model, trough activation of inflammatory cells. Tool like receptors are involved in the activation of innate immunity. Demodex is the cause of ganulomas seen in papulopustular rosacea, but it is also always present in the erythematotelangiectatic subtypoe. Colonization by Demodex is nevertheless not decreased with conventional treatments of rosacea, like tetracyclins and metronizaole. This might be due to induction of inflamation by bacteria hosted by Demodex, like Bacillus oleronius, and dozens of bacteria that are being investigated. Finaly, rhinophyma is linked to both vascular changes and activation of fibrosis, involving TGF beta.