X Baraliakos1, F Heldmann1, J Callhoff2, J Listing2, T Appelboom3, J Brandt4, F Van den Bosch5, M Breban6, Gr Burmester7, M Dougados8, P Emery9, H Gaston10, M Grunke11, I E Van Der Horst-Bruinsma12, R Landewé13, M Leirisalo-Repo14, J Sieper15, K De Vlam16, D Pappas17, U Kiltz1, D Van Der Heijde18, J Braun1. 1. Rheumazentrum Ruhrgebiet Herne, Ruhr-University Bochum, Germany. 2. Epidemiology Unit, German Rheumatism Research Center, Berlin, Germany. 3. Hopital Erasme, Brussels, Belgium. 4. Rheumapraxis Steglitz/Charité, Berlin, Germany. 5. Department of Rheumatology, Universitair Ziekenhuis Ghent, Gent, Belgium. 6. Department of Rheumatology, Hopital Ambroise Paré, University of Versailles Saint-Quentin-en-Yvelines, Boulogne, France. 7. Department of Rheumatology and Clinical Immunology, Charité University Medicine Berlin, Campus Mitte, Berlin, Germany. 8. Department of Rheumatology B, Paris-Descartes University; AP-HP, Cochin Hospital, Paris, France. 9. Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Chapel Allerton Hospital, Leeds, and NIHR Leeds Musculoskeletal Biomedical Research Unit, Leeds Teaching Hospitals NHS Trust, Leeds, UK. 10. Department of Rheumatology, Addenbrookes Hospital, University of Cambridge, Cambridge, UK. 11. Medizinische Klinik und Poliklinik IV, University of Munich, Munich, Germany. 12. Department of Rheumatology, VU Medical Center, Amsterdam, The Netherlands. 13. Department of Clinical immunology & Rheumatology, AMC Amsterdam, Academisch Ziekenhuis Maastricht, Amsterdam, The Netherlands. 14. Department of Medicine, Division of Rheumatology, University Central Hospital Helsinki, Helsinki, Finland. 15. Medical Department I, Rheumatology, Charité University Medicine Berlin, Campus Steglitz, Berlin, Germany. 16. University Hospital Leuven, Leuven, Belgium. 17. Center for Orthopaedics and Traumatology, St. Anna Hospital, Herne, Germany. 18. Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands.
Abstract
OBJECTIVE: To study the relationship of spinal inflammation and fatty degeneration (FD) as detected by MRI and new bone formation seen on conventional radiographs (CRs) in ankylosing spondylitis (AS). METHODS: CRs at baseline, 2 years and 5 years and spinal MRIs at baseline and 2 years of 73 AS patients treated with infliximab in European AS Infliximab Cohort were available. Relative risks (RR) were calculated with a general linear model after adjustment for within-patient variation. RESULTS: In a total of 1466 vertebral edges (VEs) without baseline syndesmophytes, 61 syndesmophytes developed at 5 years, the majority of which (57.4%) had no corresponding detectable MRI lesions at baseline. VEs with both inflammation and FD at baseline had the highest risk (RR 3.3, p=0.009) for syndesmophyte formation at 5 years, followed by VEs that developed new FD or did not resolve FD at 2 years (RR=2.3, p=0.034), while inflammation at baseline with no FD at 2 years had the lowest risk for syndesmophyte formation at 5 years (RR=0.8). Of the VEs with inflammation at baseline, >70% resolved completely, 28.8% turned into FD after 2 years, but only 1 syndesmophyte developed within 5 years. CONCLUSIONS: Parallel occurrence of inflammation and FD at baseline and development of FD without prior inflammation after 2 years were significantly associated with syndesmophyte formation after 5 years of anti-tumour necrosis factor (TNF) therapy. However, the sequence 'inflammation-FD-new bone formation' was rarely observed, an argument against the TNF-brake hypothesis. Whether an early suppression of inflammation leads to a decrease of the risk for new bone formation remains to be demonstrated. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
OBJECTIVE: To study the relationship of spinal inflammation and fatty degeneration (FD) as detected by MRI and new bone formation seen on conventional radiographs (CRs) in ankylosing spondylitis (AS). METHODS: CRs at baseline, 2 years and 5 years and spinal MRIs at baseline and 2 years of 73 AS patients treated with infliximab in European AS Infliximab Cohort were available. Relative risks (RR) were calculated with a general linear model after adjustment for within-patient variation. RESULTS: In a total of 1466 vertebral edges (VEs) without baseline syndesmophytes, 61 syndesmophytes developed at 5 years, the majority of which (57.4%) had no corresponding detectable MRI lesions at baseline. VEs with both inflammation and FD at baseline had the highest risk (RR 3.3, p=0.009) for syndesmophyte formation at 5 years, followed by VEs that developed new FD or did not resolve FD at 2 years (RR=2.3, p=0.034), while inflammation at baseline with no FD at 2 years had the lowest risk for syndesmophyte formation at 5 years (RR=0.8). Of the VEs with inflammation at baseline, >70% resolved completely, 28.8% turned into FD after 2 years, but only 1 syndesmophyte developed within 5 years. CONCLUSIONS: Parallel occurrence of inflammation and FD at baseline and development of FD without prior inflammation after 2 years were significantly associated with syndesmophyte formation after 5 years of anti-tumour necrosis factor (TNF) therapy. However, the sequence 'inflammation-FD-new bone formation' was rarely observed, an argument against the TNF-brake hypothesis. Whether an early suppression of inflammation leads to a decrease of the risk for new bone formation remains to be demonstrated. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
Entities:
Keywords:
Ankylosing Spondylitis; Anti-TNF; Magnetic Resonance Imaging