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Current Rheumatology Reports

, 15:375 | Cite as

Homeostatic Mechanisms in Articular Cartilage and Role of Inflammation in Osteoarthritis

  • Xavier Houard
  • Mary B. Goldring
  • Francis Berenbaum
OSTEOARTHRITIS (MB GOLDRING, SECTION EDITOR)
Part of the following topical collections:
  1. Topical Collection on Osteoarthritis

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.

Keywords

Chondrocytes Homeostatic mechanisms Articular Cartilage Osteoarthritis Inflammation Mechanical stress Homeostasis Cartilage matrix degradation Alarmins Toll-like receptors Chemokines Adipokines Mechanotransduction 

Notes

Acknowledgments

Research related to this work was supported by French state funds managed by the ANR within the Investissements d'Avenir programme under reference ANR11-IDEX-0004-02 (to F.B. and X.H.), and by National Institutes of Health grants R01-AG022021 and RC4-AR060546 (to M.B.G.).

Compliance with Ethics Guidelines

Conflict of Interest

Xavier Houard, Mary B. Goldring, and Francis Berenbaum declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • Xavier Houard
    • 1
  • Mary B. Goldring
    • 2
  • Francis Berenbaum
    • 1
    • 3
    • 4
  1. 1.UPMC, Univ Paris 06, UR4 “Ageing, Stress and Inflammation”, Labex Transimmunom, Inflammation- Immunopathology-Biotherapy department (I2B)ParisFrance
  2. 2.Tissue Engineering, Regeneration and Repair Program, Research Division, The Hospital for Special Surgery and Department of Cell and Developmental BiologyWeill Cornell Medical CollegeNew YorkUSA
  3. 3.Department of Rheumatology, AP-HP Saint-Antoine hospital, Labex Transimmunom, Inflammation-Immunopathology-Biotherapy Department (I2B)ParisFrance
  4. 4.Pierre & Marie Curie University (UR-4)Paris Cedex 5France

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