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Curr Rheumatol Rep. 2013 Nov;15(11):375. doi: 10.1007/s11926-013-0375-6.

Homeostatic mechanisms in articular cartilage and role of inflammation in osteoarthritis.

Author information

1
UPMC, Univ Paris 06, UR4 "Ageing, Stress and Inflammation", Labex Transimmunom, Inflammation- Immunopathology-Biotherapy department (I2B), F-75252, Cedex 5, Paris, France.

Abstract

Osteoarthritis (OA) is a whole joint disease, in which thinning and disappearance of cartilage is a critical determinant in OA progression. The rupture of cartilage homeostasis whatever its cause (aging, genetic predisposition, trauma or metabolic disorder) induces profound phenotypic modifications of chondrocytes, which then promote the synthesis of a subset of factors that induce cartilage damage and target other joint tissues. Interestingly, among these factors are numerous components of the inflammatory pathways. Chondrocytes produce cytokines, chemokines, alarmins, prostanoids, and adipokines and express numerous cell surface receptors for cytokines and chemokines, as well as Toll-like receptors. These receptors activate intracellular signaling pathways involved in inflammatory and stress responses of chondrocytes in OA joints. This review focuses on mechanisms responsible for the maintenance of cartilage homeostasis and highlights the role of inflammatory processes in OA progression.

PMID:
24072604
PMCID:
PMC3989071
DOI:
10.1007/s11926-013-0375-6
[Indexed for MEDLINE]
Free PMC Article

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