title: Corticosteroid treatment of experimental arthritis retards cartilage destruction as determined by histology and serum COMP.
abstract: OBJECTIVE
  To examine if changes in serum cartilage oligomeric matrix protein (COMP) correlate with the development of cartilage damage, as measured by histological grading, in corticosteroid-treated animals with collagen-induced arthritis (CIA).
  
  
  METHODS
  DA rats with established CIA were treated with corticosteroids (betamethasone, 0.1 mg/kg body weight) or placebo (saline) intraperitoneally once daily after reaching an arthritis score exceeding 1. The treatment continued throughout the study. Arthritis progression was monitored by clinical scoring of paws, serial measurements of serum COMP and fibrinogen, and histological grading of paws.
  
  
  RESULTS
  Corticosteroid treatment reduced clinical signs of arthritis compared with placebo (arthritis score reduced, P < 0.01 at day 25). Corticosteroid treatment also reduced fibrinogen levels compared with placebo (P < 0.01). The morphological changes in the joint were less severe in the corticosteroid-treated animals (median cartilage score 4 in the placebo group, 0 in the corticosteroid-treated group; P < 0.01). The levels of COMP remained unchanged during treatment in the corticosteroid-treated arthritic animals, whereas an increase in levels of COMP was observed in rats treated with placebo (P < 0.01). There was a correlation between serum COMP and the extent of cartilage destruction at day 25 after immunization (r = 0.77, P < 0.001).
  
  
  CONCLUSIONS
  Corticosteroids given therapeutically to arthritic rats diminish joint destruction histologically, and stable serum COMP levels reflect this effect.
authors.affiliation: Rheumatology Unit, Department of Medicine, Karolinska Hospital, Stockholm, Sweden. esbjorn.larsson@ks.se
authors.forename: E
authors.initials: E
authors.lastname: Larsson
authors.forename: H
authors.initials: H
authors.lastname: Erlandsson Harris
authors.forename: A
authors.initials: A
authors.lastname: Larsson
authors.forename: B
authors.initials: B
authors.lastname: Månsson
authors.forename: T
authors.initials: T
authors.lastname: Saxne
authors.forename: L
authors.initials: L
authors.lastname: Klareskog
mesh_terms: D000818:Animals; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001169:Arthritis, Experimental / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D001623:Betamethasone / Q000031:analogs & derivatives* / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002358:Cartilage, Articular / Q000473:pathology*; D004305:Dose-Response Relationship, Drug; D016903:Drug Monitoring / Q000379:methods; D016326:Extracellular Matrix Proteins / Q000097:blood*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005938:Glucocorticoids / Q000627:therapeutic use*; D006023:Glycoproteins / Q000097:blood*; D064235:Matrilin Proteins; D051381:Rats
chemical_list: D018501:Antirheumatic Agents; D015415:Biomarkers; D016326:Extracellular Matrix Proteins; D005938:Glucocorticoids; D006023:Glycoproteins; D064235:Matrilin Proteins; C028994:betamethasone sodium phosphate; D005340:Fibrinogen; D001623:Betamethasone