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This article is part of the supplement: The evolution of anti-TNF therapy in rheumatic disease: experience, insights and advances

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Structural damage in rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis: traditional views, novel insights gained from TNF blockade, and concepts for the future

Georg Schett1*, Laura C Coates2, Zoe R Ash3, Stefanie Finzel1 and Phillip G Conaghan4

Author Affiliations

1 Department of Internal Medicine 3, Institute for Clinical Immunology, University of Erlangen-Nuremberg, Krankenhausstrasse 12, 91054 Erlangen, Germany

2 LIMM, Section of Musculoskeletal Disease, University of Leeds, Chapel Allerton Hospital, Leeds LS9 7TF, UK

3 Section of Musculoskeletal Disease, Leeds Institute of Molecular Medicine, University of Leeds, Leeds LS9 7TF, UK

4 Section of Musculoskeletal Disease, University of Leeds, and NIHR Leeds Musculoskeletal Biomedical Research Unit, Leeds LS9 7TF, UK

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Arthritis Research & Therapy 2011, 13(Suppl 1):S4  doi:10.1186/1478-6354-13-S1-S4

Published: 25 May 2011


Structural changes of bone and cartilage are a hallmark of inflammatory joint diseases such as rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS). Despite certain similarities – in particular, inflammation as the driving force for structural changes – the three major inflammatory joint diseases show considerably different pathologies. Whereas RA primarily results in bone and cartilage resorption, PsA combines destructive elements with anabolic bone responses, and AS is the prototype of a hyper-responsive joint disease associated with substantial bone and cartilage apposition. In the present review we summarize the clinical picture and pathophysiologic processes of bone and cartilage damage in RA, PsA, and AS, we describe the key insights obtained from the introduction of TNF blockade, and we discuss the future challenges and frontiers of structural damage in arthritis.