Uncoupling of collagen II metabolism in newly diagnosed, untreated rheumatoid arthritis is linked to inflammation and antibodies against cyclic citrullinated peptides

J Rheumatol. 2010 Jun;37(6):1113-20. doi: 10.3899/jrheum.091265. Epub 2010 May 1.

Abstract

Objective: To investigate the relationship between markers of collagen II synthesis and degradation with disease activity measures, autoantibodies, and radiographic outcomes in a 4-year protocol on patients with early rheumatoid arthritis (RA) who are naïve to disease-modifying antirheumatic drugs.

Methods: One hundred sixty patients with newly diagnosed, untreated RA entered the Cyclosporine, Methotrexate, Steroid in RA (CIMESTRA) trial. Disease activity and radiograph status were measured at baseline and 4 years. The N-terminal propeptide of collagen IIA (PIIANP) and the cross-linked C-telopeptide of collagen II (CTX-II) were quantified at baseline by ELISA. PIIANP was also assayed at 2 and 4 years. Anticyclic citrullinated peptide (anti-CCP) was recorded at baseline. An uncoupling index for cartilage collagen metabolism was calculated from PIIANP and CTX-II measurements.

Results: PIIANP was low at diagnosis and 4 years on (p < 0.001), irrespective of treatment and disease activity. PIIANP was lowest in anti-CCP positive patients (p = 0.006), and there was a negative correlation between PIIANP and anti-CCP titers (rho = -0.25, p 0.002). CTX-II was increased (p < 0.001) and correlated positively with disease activity and radiographic progression, but not with anti-CCP (p = 0.93). The uncoupling index was not superior to CTX-II in predicting radiographic changes.

Conclusion: These results suggest that cartilage collagen formation and degradation are unbalanced when RA is diagnosed. The different associations of collagen II anabolism (PIIANP) and collagen II degradation (CTX-II) with anti-CCP, synovitis, and radiographic progression indicate that at this early stage of RA, cartilage collagen degradation is mainly driven by synovitis, while anti-CCP antibodies may interfere with cartilage regeneration by inhibiting collagen IIA formation. Trial registration j.nr NCT00209859.

Publication types

  • Multicenter Study
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Arthritis, Rheumatoid / immunology
  • Arthritis, Rheumatoid / metabolism*
  • Arthritis, Rheumatoid / physiopathology
  • Autoantibodies / blood
  • Autoantibodies / immunology
  • Biomarkers / metabolism
  • Cartilage, Articular / metabolism
  • Collagen Type II / biosynthesis*
  • Collagen Type II / blood
  • Collagen Type II / immunology
  • Disease Progression
  • Female
  • Humans
  • Male
  • Middle Aged
  • Peptide Fragments / biosynthesis*
  • Peptide Fragments / blood
  • Peptide Fragments / immunology
  • Peptides, Cyclic / blood
  • Peptides, Cyclic / immunology*
  • Procollagen / biosynthesis*
  • Procollagen / blood
  • Procollagen / immunology
  • Severity of Illness Index
  • Synovitis / metabolism
  • Young Adult

Substances

  • Autoantibodies
  • Biomarkers
  • Collagen Type II
  • Peptide Fragments
  • Peptides, Cyclic
  • Procollagen
  • collagen II C-telopeptide
  • cyclic citrullinated peptide
  • procollagen type IIA amino-terminal peptide

Associated data

  • ClinicalTrials.gov/NCT00209859