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Extended report
MRI vertebral corner inflammation followed by fat deposition is the strongest contributor to the development of new bone at the same vertebral corner: a multilevel longitudinal analysis in patients with ankylosing spondylitis
  1. Pedro M Machado1,2,
  2. Xenofon Baraliakos3,
  3. Désirée van der Heijde1,
  4. Jürgen Braun3,
  5. Robert Landewé4,5
  1. 1Rheumatology Department, Leiden University Medical Center, Leiden, The Netherlands
  2. 2Clínica Universitária de Reumatologia, Faculty of Medicine, University of Coimbra, Portugal
  3. 3Rheumatology Department, Rheumazentrum Ruhrgebiet Herne, Ruhr-University Bochum, Bochum, Germany
  4. 4Department of Rheumatology & Clinical Immunology, Amsterdam Rheumatology & Clinical Immunology Center, Amsterdam, The Netherlands
  5. 5Rheumatology Department, Atrium Medical Center, Heerlen, The Netherlands
  1. Correspondence to Dr Pedro Machado, Department of Rheumatology, Leiden University Medical Center, PO Box 9600, Leiden 2300 RC, The Netherlands; pedrommcmachado{at}


Objectives To study the sequential relationship between MRI vertebral corner inflammation (VCI), vertebral corner fat deposition (VCFD) and the development/growth of radiographic syndesmophytes at the same vertebral corner (VC).

Methods Baseline, 24 and 102 weeks spinal MRIs were assessed for the presence/absence of VCI and VCFD. Anterior VCs of lateral radiographs of the cervical and lumbar spine (baseline and 102 weeks) were assessed for the development of new bone (syndesmophyte formation or syndesmophyte formation/growth combined). Data from 161 to 177 patients were analysed at the VC level using two-way and multilevel analyses adjusting for within-patient correlation and MRI reader (generalised estimating equations for binomial outcomes).

Results The presence of VCI (adjusted (adj) OR 1.75 to 1.98) as well as the presence of VCFD (adjOR 1.60 to 2.32) at any time point (TP) were significantly associated with the development of new bone. The combination of VCI and VCFD at the same VC increased the strength of the association, both for the sequential or simultaneous presence of VCI and VCFD across the three TPs (adjOR 2.12 to 2.73), as well as for the development of new VCFD preceded by VCI at a previous TP (adjOR 2.12 to 3.01). The complete absence of both VCI and VCFD across the three TPs ‘protected’ against new bone formation (adjOR 0.45 to 0.62). However, 40–66% of new bone still developed in VCs without MRI inflammation or fat degeneration at any of the three TPs.

Conclusions Both VCI and VCFD contribute to new bone formation in ankylosing spondylitis (AS), especially if VCI precedes VCFD. However, VCI, VCFD and this particular sequence of events only partially explain the development of new bone in AS.

  • Ankylosing Spondylitis
  • Magnetic Resonance Imaging
  • Spondyloarthritis
  • Outcomes research
  • Inflammation

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