title: High disease activity in ankylosing spondylitis is associated with increased serum sclerostin level and decreased wingless protein-3a signaling but is not linked with greater structural damage.
abstract: BACKGROUND
  Clinical activity of ankylosing spondylitis (AS) predicts the natural course of the disease and the response to treatment. Several molecules are involved in new bone formation resulting in structural damage in patients with AS. However, the link between the clinical and molecular phenomena has not yet been fully established. The aim of the study was to investigate the relation between markers of bone remodeling and inflammation with clinical activity and structural damage in AS.
  
  
  METHODS
  We assessed the serum levels of sclerostin, Dickkopf-1 protein, Wingless protein-3a, bone morphogenic protein-7, matrix metalloproteinase-3, osteoprotegerin, bone alkaline phosphatase and inflammatory markers in 50 AS patients with high disease activity (BASDAI ≥ 4), 28 with low disease activity (BASDAI <4), and 23 healthy controls. Cervical and lumbar spine x-rays were performed in 46 patients to measure structural damage (mSASSS).
  
  
  RESULTS
  Sclerostin level was significantly greater in high disease activity patients than in controls. Wingless protein-3a and Dikkopf-1 protein levels were significantly lower in high activity group compared to low activity group and controls. Negative correlation was found between sclerostin and Dikkopf-1 protein in high activity group (R = -0.28, P = 0.048). The median mSASSS values were not different between patient groups.
  
  
  CONCLUSIONS
  Higher disease activity in AS may not be per se associated with greater new bone formation.
authors.affiliation: Division of Rheumatology, Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Polish Spondyloarthritis Initiative, Kraków, Poland. mariuszk@mp.pl
authors.forename: Mariusz
authors.initials: M
authors.lastname: Korkosz
authors.forename: Jerzy
authors.initials: J
authors.lastname: Gąsowski
authors.forename: Piotr
authors.initials: P
authors.lastname: Leszczyński
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Pawlak-Buś
authors.forename: Sławomir
authors.initials: S
authors.lastname: Jeka
authors.forename: Ewa
authors.initials: E
authors.lastname: Kucharska
authors.forename: Tomasz
authors.initials: T
authors.lastname: Grodzicki
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000328:Adult; D015415:Biomarkers / Q000097:blood; D019485:Bone Morphogenetic Proteins / Q000097:blood*; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005819:Genetic Markers; D006801:Humans; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D015398:Signal Transduction / Q000502:physiology*; D013167:Spondylitis, Ankylosing / Q000097:blood* / Q000175:diagnosis*; D060509:Wnt3A Protein / Q000097:blood*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D015415:Biomarkers; D019485:Bone Morphogenetic Proteins; D005819:Genetic Markers; C422903:SOST protein, human; D060509:Wnt3A Protein