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Corrigendum to: What is the current status of chondroitin sulfate and glucosamine for the treatment of knee osteoarthritis? Maturitas 78 (2014) 184–187

  • Yves Henrotin
    Correspondence
    Corresponding author.
    Affiliations
    Bone and Cartilage Research Unit, Arthropôle Liège, University of Liège, Institute of Pathology, CHU Sart-Tilman, 4000 Liège, Belgium
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  • Marc Marty
    Affiliations
    Rheumatology Department, Teaching Hospital H Mondor, Creteil, France
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  • Ali Mobasheri
    Affiliations
    School of Veterinary Medicine, Faculty of Health and Medical Sciences, University of Surrey, Duke of Kent Building, Guildford, Surrey GU2 7XH, United Kingdom

    Arthritis Research UK Centre for Sport, Exercise and Osteoarthritis, Arthritis Research UK Pain Centre, Medical Research Council and Arthritis Research UK Centre for Musculoskeletal Ageing Research, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, United Kingdom

    Center of Excellence in Genomic Medicine Research (CEGMR), King Fahd Medical Research Center (KFMRC), King AbdulAziz University, Jeddah 21589, Kingdom of Saudi Arabia
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      The authors regret that the Competing Interest in the original paper was not accurate. The correct Competing Interest is as below:
      YH received honoraria from Artialis, Bioiberica, Danone, Expanscience, Ibsa, Merck; Pierre Fabre, Synolyne Pharma, Tilman. YH is the founder and chairman of Artialis SA and Synolyne Pharma, two spin-off company of the University of Liège. YH also received unrestricted educational grant from Bioiberica, Expanscience, Royal Canin, Artialis, and Nestle.
      The authors would like to apologise for any inconvenience caused.

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      • What is the current status of chondroitin sulfate and glucosamine for the treatment of knee osteoarthritis?
        MaturitasVol. 78Issue 3
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          Chondroitin sulfate and glucosamine sulfate exert beneficial effects on the metabolism of in vitro models of cells derived from synovial joints: chondrocytes, synoviocytes and cells from subchondral bone, all of which are involved in osteoarthritis (OA). They increase type II collagen and proteoglycan synthesis in human articular chondrocytes and are able to reduce the production of some pro-inflammatory mediators and proteases, to reduce the cellular death process, and improve the anabolic/catabolic balance of the extracellular cartilage matrix (ECM).
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