EDITORIAL

Structural remodelling in AS

Tumour necrosis factor blockers and structural remodelling in ankylosing spondylitis: what is reality and what is fiction?

Georg Schett¹, Robert Landewé², Désirée van der Heijde³

¹ Department of Internal Medicine 3, Institute for Clinical Immunology, University of Erlangen-Nurnberg, Erlangen, Germany
² Department of Internal Medicine & Rheumatology, University Hospital Maastricht, Maastricht, The Netherlands
³ Department of Rheumatology, Leiden University Medical Centre, Leiden, The Netherlands

Correspondence to:
Correspondence to:
Professor G Schett
Department of Internal Medicine 3, Institute for Clinical Immunology, University of Erlangen-Nuernberg, Krankenhausstrasse 12, D-91054 Erlangen, Germany;georg.schett@med3.imed.uni-erlangen.de

Accepted 14 March 2007

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A delineation of the differences in pathology between AS and RA

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The first 150 words of the full text of this article appear below.

A hallmark of spondylarthropathies (SpA), such as ankylosing spondylitis, (AS) is the fusion of joints as well as intervertebral spaces. This fusion is caused by the formation of bony spurs appearing as syndesmophytes and osteophytes in the intervertebral spaces and in the joints, respectively. Fusion of joints is based on increased endochondral ossification, which allows bone formation and bridges the joint space. Tumour necrosis factor (TNF) is a key proinflammatory cytokine in AS, but is a potent inhibitor of bone formation, and so is unlikely to explain the formation of osteophytes in AS. This is also suggested by recent clinical data showing that TNF blockade seems not to affect structural remodeling of the spinal skeleton in AS, which largely indicates changes due to increased bone apposition. Thus, molecular concepts of structural remodelling in AS need revision, and new pathways involved in bone formation, such as Wingless . . . [Full text of this article]

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Ann Rheum Dis Online, 8 Jun 2007 [Full text]