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Journal of the American Academy of Dermatology
Volume 69, n° 6S1
pages 15-26 (décembre 2013)
Doi : 10.1016/j.jaad.2013.04.045
accepted : 21 April 2013
New insights into rosacea pathophysiology: A review of recent findings

Martin Steinhoff, MD, PhD a, , Jürgen Schauber, MD b, James J. Leyden, MD c
a Department of Dermatology, University of California, San Francisco, California 
b Department of Dermatology and Allergy, Ludwig Maximilian University, Munich, Germany 
c Department of Dermatology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 

Reprint requests: Martin Steinhoff, MD, PhD, Department of Dermatology, University of California, San Francisco, 1701 Divisadero St, Third Floor, San Francisco, CA 94115.

Rosacea is a common, chronic inflammatory skin disease of poorly understood origin. Based on its clinical features (flushing, chronic inflammation, fibrosis) and trigger factors, a complex pathobiology involving different regulatory systems can be anticipated. Although a wealth of research has shed new light over recent years on its pathophysiology, the precise interplay of the various dysregulated systems (immune, vascular, nervous) is still poorly understood. Most authors agree on 4 major clinical subtypes of rosacea: erythematotelangiectatic rosacea, papulopustular rosacea, phymatous rosacea, and ocular rosacea. Still, it needs to be elucidated whether these subtypes develop in a consecutive serial fashion or if any subtypes may occur individually as part of a syndrome. Because rosacea often affects multiple family members, a genetic component is also suspected, but the genetic basis of rosacea remains unclear. During disease manifestation and early stage, the innate immune system and neurovascular dysregulation seem to be driving forces in rosacea pathophysiology. Dissection of major players for disease progression and in advanced stages is severely hampered by the complex activation of the innate and adaptive immune systems, enhanced neuroimmune communication, profound blood vessel and possibly lymphatic vessel changes, and activation of almost every resident cell in the skin. This review discusses some of the recent findings and aims to build unifying hypotheses for a modern understanding of rosacea pathophysiology.

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

Key words : adaptive immunity, antimicrobial peptides, cytokines, fibrosis, innate immunity, mast cells, neurovascular system

Abbreviations used : AMP, CAMP, CCL2, CXCL8, ER, ETR, H2R, HTR3A, IL, KLK, MMP, NF-κB-C/EBPa, NK, PACAP, PhR, PPR, SP, TGF, Th1, TLR, TRP, TRPA1, TRPV, TRPV1, UV, VEGF-A

 Publication of this article was supported by a grant from Galderma International. Editorial support provided by Galderma International.
 Disclosure: Dr Steinhoff has served on an advisory board and as speaker for Galderma, and as a consultant for Leo and Galderma and received grants and equipment in compensation. Dr Schauber has served as a speaker for Galderma, Astellas, and La Roche Posay, and as a consultant for Leo and received honoraria as compensation. Dr Leyden has served as consultant for Galderma, Allergan, and Medicis and received honoraria in compensation.

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