title: Focal fat lesions at vertebral corners on magnetic resonance imaging predict the development of new syndesmophytes in ankylosing spondylitis.
abstract: OBJECTIVE
  Focal fat infiltration is frequently visible on magnetic resonance imaging (MRI) of the spine in patients with ankylosing spondylitis (AS) and likely reflects postinflammatory tissue metaplasia. To support the concept of coupling between inflammation and new bone formation, we tested the hypothesis that focal fat infiltration at a vertebral corner is more likely to evolve into a de novo syndesmophyte.
  
  
  METHODS
  MRI scans were obtained at baseline and radiographs were obtained at baseline and 2 years in 100 AS patients from 2 cohorts: a clinical trial cohort (n = 38) and an observational cohort (n = 62). In the clinical trial cohort, patients were randomized to receive anti-tumor necrosis factor (anti-TNF) therapy or placebo for 12-24 weeks and then open-label treatment for 2 years. In the observational cohort, patients received either standard therapy (n = 36) or anti-TNF therapy (n = 26) for 2 years. Vertebral corner inflammation and fat infiltration were assessed independently by pairs of readers who were blinded with regard to the radiographic findings.
  
  
  RESULTS
  New syndesmophytes developed significantly more frequently in vertebral corners with fat in both the clinical trial (10.2%) and the observational (6.5%) cohort as compared to those without either feature on baseline MRI (3.1% [P = 0.008] and 1.4% [P = 0.0002], respectively). Adjusting for within-patient variations in baseline syndesmophytes/ankylosis, vertebral corners that were fat-positive/inflammation-positive significantly predicted new syndesmophytes, with an odds ratio (OR) of 7.6 (95% confidence interval [95% CI] 1.5-38.5 [P = 0.01]), while a model that included baseline variations in both fat and inflammation showed an OR of 5.8 (95% CI 2.2-15.3 [P < 0.001]) for inflammation and an OR of 1.9 (95% CI 0.9-4.1 [P = 0.1]) for fat.
  
  
  CONCLUSIONS
  Our data lend support to the hypothesis that inflammatory lesions evolve into new bone through a process of tissue metaplasia that includes fat infiltration.
authors.affiliation: University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Praveena
authors.initials: P
authors.lastname: Chiowchanwisawakit
authors.forename: Robert G W
authors.initials: RG
authors.lastname: Lambert
authors.forename: Barbara
authors.initials: B
authors.lastname: Conner-Spady
authors.forename: Walter P
authors.initials: WP
authors.lastname: Maksymowych
mesh_terms: D000273:Adipose Tissue / Q000473:pathology*; D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D018450:Disease Progression; D005260:Female; D006801:Humans; D007249:Inflammation / Q000000981:diagnostic imaging / Q000473:pathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011859:Radiography; D013131:Spine / Q000000981:diagnostic imaging / Q000473:pathology*; D013167:Spondylitis, Ankylosing / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology*; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D014409:Tumor Necrosis Factor-alpha; C529000:golimumab