title: Biochemical markers of ongoing joint damage in rheumatoid arthritis--current and future applications, limitations and opportunities.
abstract: 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.
authors.affiliation: Nordic Bioscience, Herlev Hovedgade 207, DK-2730 Herlev, Denmark. MK@nordicbioscience.com
authors.forename: Morten A
authors.initials: MA
authors.lastname: Karsdal
authors.forename: Thasia
authors.initials: T
authors.lastname: Woodworth
authors.forename: Kim
authors.initials: K
authors.lastname: Henriksen
authors.forename: Walter P
authors.initials: WP
authors.lastname: Maksymowych
authors.forename: Harry
authors.initials: H
authors.lastname: Genant
authors.forename: Philippe
authors.initials: P
authors.lastname: Vergnaud
authors.forename: Claus
authors.initials: C
authors.lastname: Christiansen
authors.forename: Tanja
authors.initials: T
authors.lastname: Schubert
authors.forename: Per
authors.initials: P
authors.lastname: Qvist
authors.forename: Georg
authors.initials: G
authors.lastname: Schett
authors.forename: Adam
authors.initials: A
authors.lastname: Platt
authors.forename: Anne-Christine
authors.initials: AC
authors.lastname: Bay-Jensen
mesh_terms: D001172:Arthritis, Rheumatoid / Q000175:diagnosis* / Q000276:immunology / Q000378:metabolism*; D015415:Biomarkers / Q000032:analysis* / Q000378:metabolism; D006801:Humans
chemical_list: D015415:Biomarkers