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Annales de Dermatologie et de Vénéréologie
Volume 138, n° S3
pages 184-191 (novembre 2011)
Doi : 10.1016/S0151-9638(11)70088-6
Pathophysiology of rosacea: redness, telangiectasia, and rosacea
Physiopathologie de la rosacée. Rougeurs, couperose et rosacée
 

B. Cribier
Clinique Dermatologique, Faculté de Médecine, Université de Strasbourg et Hôpitaux, Universitaires de Strasbourg, 1, place de l’Hôpital, 67091 Strasbourg, France 

Summary

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.

The full text of this article is available in PDF format.
Résumé

La physiopathologie de la rosacée fait intervenir de nombreux éléments qu’il est parfois difficile de relier entre eux. Il n’y a ainsi pas de modèle physiopathologique unique. Néanmoins, il semble aujourd’hui établi que les deux facteurs essentiels sont des anomalies vasculaires et inflammatoires.

La maladie survient sur un terrain prédisposé, principalement le phototype clair, soumis à des variations climatiques importantes. Sur un fond d’anomalie vasculaire primitive, des facteurs externes (climat, exposition aux ultra-violets, flore cutanée…) contribuent au développement de vaisseaux superficiels anormaux, ayant une perméabilité diminuée. L’œdème qui en résulte favorise sans doute la colonisation et la multiplication de Demodex folliculorum . Ce parasite crée une inflammation, de façon directe et indirecte, qui se traduit par des lésions papulo-pustuleuses ou des granulomes.

L’inflammation de la rosacée se caractérise aussi par des anomalies de l’immunité innée, avec augmentation d’expression des protéases épidermiques et production de peptides de cathélicidine pro-inflammatoires. Il existe en outre une hypersensibilité faciale, bien que la barrière cutanée ne soit pas altérée.

Enfin, le rhinophyma reste mal expliqué; les anomalies vasculaires induisent la production locale de transforming growth factor β 1 (TGF-β1) capable de créer une fibrose, donc un épaississement cutané.

The full text of this article is available in PDF format.

Keywords : Rosacea, Facial telangiectasia, Demodex folliculorum, Innate immunity, Telangiectasias

Mots clés : Rosacée, Erythro-couperose, Demodex folliculorum, Immunité innée, Télangiectasies




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