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Biochemical markers of ongoing joint damage in rheumatoid arthritis - current and future applications, limitations and opportunities

Morten A Karsdal12*, Thasia Woodworth3, Kim Henriksen1, Walter P Maksymowych4, Harry Genant5, Philippe Vergnaud5, Claus Christiansen1, Tanja Schubert5, Per Qvist1, Georg Schett6, Adam Platt7 and Anne-Christine Bay-Jensen1

Author Affiliations

1 Nordic Bioscience, Herlev Hovedgade 207, DK-2730 Herlev, Denmark

2 Southern University of Denmark (SDU), Campusvej 55DK-5230 Odense M Denmark

3 Leading Edge Clinical Research LLC, 3901 SE St Lucie Blvd unit 20, Stuart, Florida 34997, USA

4 University of Alberta, 562 Heritage Medical Research Building, Edmonton, AB T6G 2S2, Canada

5 Synarc, 16 Rue Montbrillant, 69003 Lyon, France

6 University of Erlangen-Nurnberg Department of Internal Medicine, Krankenhausstra├če 12, 91054 Erlangen, Germany

7 Roche Products Limited, 6 Falcon Way, Shire Park, Welwyn Garden City, AL7 1TW, UK

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Arthritis Research & Therapy 2011, 13:215  doi:10.1186/ar3280

Published: 28 April 2011


Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease associated with potentially debilitating joint inflammation, as well as altered skeletal bone metabolism and co-morbid conditions. Early diagnosis and aggressive treatment to control disease activity offers the highest likelihood of preserving function and preventing disability. Joint inflammation is characterized by synovitis, osteitis, and/or peri-articular osteopenia, often accompanied by development of subchondral bone erosions, as well as progressive joint space narrowing. Biochemical markers of joint cartilage and bone degradation may enable timely detection and assessment of ongoing joint damage, and their use in facilitating treatment strategies is under investigation. Early detection of joint damage may be assisted by the characterization of biochemical markers that identify patients whose joint damage is progressing rapidly and who are thus most in need of aggressive treatment, and that, alone or in combination, identify those individuals who are likely to respond best to a potential treatment, both in terms of limiting joint damage and relieving symptoms. The aims of this review are to describe currently available biochemical markers of joint metabolism in relation to the pathobiology of joint damage and systemic bone loss in RA; to assess the limitations of, and need for additional, novel biochemical markers in RA and other rheumatic diseases, and the strategies used for assay development; and to examine the feasibility of advancement of personalized health care using biochemical markers to select therapeutic agents to which a patient is most likely to respond.