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  • Open Access

PReS-FINAL-2071: Anti-type II collagen antibodies, anti-CCP, IgA-RF and IgM-RF are associated with joint damage eight years after onset of juvenile idiopathic arthritis (JIA)

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Pediatric Rheumatology201311 (Suppl 2) :P83

  • Published:


  • Public Health
  • Collagen
  • Arthritis
  • Serum Sample
  • Median Time


Antibodies specific for native human type II collagen (anti-CII) characterize an early inflammatory/destructive phenotype in adults with RA. There are no data presented so far on this antibody and its possible influence on disease course/outcome in children with JIA.


We wanted to relate occurrence of anti-CII, IgM-RF, IgA-RF and anti-CCP to assessment of joint damage, outcome and ILAR categories after eight years of disease in children with JIA.


From the Nordic JIA database 192 patients with available sera were included. Serum samples were collected at a median time of 4 months (IQR 2-7) after disease onset. Patients were followed prospectively for a median of 97 months (IQR 95-105). At the 8-year follow-up visit, data on remission according to the preliminary criteria of C. Wallace et al as well as joint damage according to JADI were collected. Frozen and stored sera were analyzed with enzyme immunoassays for anti-CII, IgM-RF, IgA-RF and anti-CCP. Reference values for adults were used.


Anti-type II collagen antibodies occurred in 3.1% of patients sera, IgM-RF in 3.6%, IgA-RF in 3.1%, anti-CCP in 2.6% of the patients. Occurrence of RF and anti-CCP did to some extent overlap, but rarely with anti-CII. The polyarticular and oligoarticular extended categories were overrepresented in patients with any of the four autoantibodies. All four autoantibodies were significantly associated with joint damage after eight years, but we found no association with ongoing disease activity after eight years.


- Occurrence of anti-CII did rarely overlap with anti-CCP, IgA-RF and IgM-RF, but all four were associated with joint damage after 8 years of disease in patients with JIA.

- Further studies on anti-CII in patients with JIA are needed.

Disclosure of interest

None declared.

Authors’ Affiliations

Dept of Paediatrics, Uppsala University Hospital, Uppsala, Sweden
Dept of Paediatrics, Helsinki University Hospital, Helsinki, Finland
Dept of Paediatrics, University of Gothenburg, Gothenburg, Sweden
Dept of Paediatrics, Århus University Hospital, Århus, Denmark
Pediatric Rheumatology Department, Pediatric Clinic II, Copenhagen University Hospital, Copenhagen, Denmark
Dept of Paediatrics, University Hospital of North Norway, Tromsø, Tromsø, Norway
Department of Laboratory Medicine, Children's and Women's Health, and Department of Pediatrics, Norwegian University of Science and Technology and St.Olav's Hospital, Trondheim, Norway
Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden


© Berntson et al.; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.