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Highly Accessed Review

Cartilage homeostasis in health and rheumatic diseases

Mary B Goldring1* and Kenneth B Marcu23

Author Affiliations

1 Research Division, Hospital for Special Surgery, affiliated with Weill College of Medicine of Cornell University, Caspary Research Building, 535 E. 70th Street, New York, NY 10021, USA

2 Biochemistry and Cell Biology Department, Stony Brook University, Life Sciences Rm #330, Stony Brook, NY 11794, USA

3 Centro Ricerca Biomedica Applicata, S. Orsola-Malpighi University Hospital, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy

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Arthritis Research & Therapy 2009, 11:224  doi:10.1186/ar2592

Published: 19 May 2009

Abstract

As the cellular component of articular cartilage, chondrocytes are responsible for maintaining in a low-turnover state the unique composition and organization of the matrix that was determined during embryonic and postnatal development. In joint diseases, cartilage homeostasis is disrupted by mechanisms that are driven by combinations of biological mediators that vary according to the disease process, including contributions from other joint tissues. In osteoarthritis (OA), biomechanical stimuli predominate with up-regulation of both catabolic and anabolic cytokines and recapitulation of developmental phenotypes, whereas in rheumatoid arthritis (RA), inflammation and catabolism drive cartilage loss. In vitro studies in chondrocytes have elucidated signaling pathways and transcription factors that orchestrate specific functions that promote cartilage damage in both OA and RA. Thus, understanding how the adult articular chondrocyte functions within its unique environment will aid in the development of rational strategies to protect cartilage from damage resulting from joint disease. This review will cover current knowledge about the specific cellular and biochemical mechanisms that regulate cartilage homeostasis and pathology.