The pathophysiology of rosacea involves a large number of factors that are at times difficult to correlate. There is not a single physiopathological model. Nevertheless, today it seems to have been established that two essential factors are involved: vascular and inflammatory. The disease occurs in individuals with a predisposition, mainly a light phototype subjected to substantial variations in climate. On a background of primary vascular anomaly, external factors (climate, exposure to ultraviolet rays, cutaneous flora, etc.) contribute to the development of abnormal superficial blood vessels, with a low permeability. The edema that results undoubtedly favors the colonization and multiplication of Demodex folliculorum. This parasite creates inflammation, directly and indirectly, which is seen in the papules and pustules as well as granulomas. Inflammation from rosacea is also characterized by innate immune system anomalies, with an increase in the expression of epidermal proteases and production of pro-inflammatory cathelicidin peptides. In addition, facial hypersensitivity exists, even though the cutaneous barrier is not altered. Finally, rhinophyma remains poorly explained; the vascular abnormalities induce local production of transforming growth factor β1 (TGF-β1) capable of creating fibrosis and therefore cutaneous thickening.