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The role of the chondrocyte in osteoarthritis

The role of the chondrocyte in osteoarthritis MARY B. GOLDRING Introduction Osteoarthritis (OA) is a slowly progressive degenerative disease characterized by gradual loss of articular cartilage. Since the OA lesion is often localized to weight-bearing cartilage or to sites of trauma, repetitive mechanical injury has been proposed as the critical signal for the initiation and progression of OA. It is now generally accepted that the chondrocyte is the target of these abnormal biomechanical factors, and that biochemical and genetic factors also contribute to alterations in the normal functional activities of these cells. Although OA has been regarded primarily as a noninflammatory arthropathy, symptoms of local inflammation and synovitis are present in many patients and have been observed in animal models of OA. Even in the absence of classic inflammation, which is characterized by infiltration of neutrophils and macrophages into joint tissues, elevated levels of inflammatory cytokines have been measured in OA synovial fluid. Although the OA cartilage lesion is present at sites remote from the synovium, the fibroblast- and macrophage-like synovial cells, as well as the chondrocyte itself, are potential sources of cytokines that could induce chondrocytes to synthesize and secrete cartilagedegrading proteases, cytokines, and other inflammatory mediators. These synovium- and chondrocyte-derived products represent potential http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arthritis & Rheumatism Wiley

The role of the chondrocyte in osteoarthritis

Goldring, Mary B.
Arthritis & Rheumatism , Volume 43 (9) – Sep 1, 2000
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References (108)

Publisher
Wiley
Copyright
Copyright © 2000 by the American College of Rheumatology
ISSN
0004-3591
eISSN
1529-0131
DOI
10.1002/1529-0131(200009)43:9<1916::AID-ANR2>3.0.CO;2-I
pmid
11014341
Publisher site
See Article on Publisher Site

Abstract

MARY B. GOLDRING Introduction Osteoarthritis (OA) is a slowly progressive degenerative disease characterized by gradual loss of articular cartilage. Since the OA lesion is often localized to weight-bearing cartilage or to sites of trauma, repetitive mechanical injury has been proposed as the critical signal for the initiation and progression of OA. It is now generally accepted that the chondrocyte is the target of these abnormal biomechanical factors, and that biochemical and genetic factors also contribute to alterations in the normal functional activities of these cells. Although OA has been regarded primarily as a noninflammatory arthropathy, symptoms of local inflammation and synovitis are present in many patients and have been observed in animal models of OA. Even in the absence of classic inflammation, which is characterized by infiltration of neutrophils and macrophages into joint tissues, elevated levels of inflammatory cytokines have been measured in OA synovial fluid. Although the OA cartilage lesion is present at sites remote from the synovium, the fibroblast- and macrophage-like synovial cells, as well as the chondrocyte itself, are potential sources of cytokines that could induce chondrocytes to synthesize and secrete cartilagedegrading proteases, cytokines, and other inflammatory mediators. These synovium- and chondrocyte-derived products represent potential

Journal

Arthritis & Rheumatism – Wiley

Published: Sep 1, 2000

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