SAT0086 Receptor Activator of Nuclear Factor Kappa-B Ligand (Rankl) and Sclerostin are Related to Joint Destruction in Early Rheumatoid Arthritis. (9th June 2015)

• Record Type: Journal Article
• Authors: Rantapää-Dahlqvist, S.; Boman, A.; Kokkonen, H.; Berglin, E.
• Is Part Of: Annals of the rheumatic diseases. Volume 74(2015)Supplement 2
• Page Start: 679
• Page End: 680
• Publication Date: 2015-06-09
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2015-eular.3338
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Rheumatoid arthritis (RA) is a chronic disease characterized by joint inflammation and destruction of cartilage and bone. The destructive process of the joints is partly explained by presences of autoantibodies, genetic factors and markers related to inflammation and cartilage and bone metabolism. Objectives: To analyse the relationships of receptor activator of nuclear factor kappa-B ligand (RANKL) and sclerostin to joint destruction and radiological progression in early RA Methods: In this study 407 patients (69% female) with early RA (symptom duration <1 year) (ARA criteria) with radiological examinations at inclusion and after 24 months were consecutively included. Disease activity score (DAS28) including swollen (SJC) and tender (TJC) joint count, ESR and C-reactive protein (CRP) and treatment were registered regularly. Concentrations of sclerostin. (Human Sclerostin HS EIA Kit, TECOmedical group, Sissach, Switzerland), RANKL (Human sRANKL ELISA, BioVendor, Karasek, Czech Republic) and anti-CCP2 antibodies (ELISA, Euro-Diagnostica AB, Malmö, Sweden) were analysed at baseline. Results: The concentration of RANKL was significantly higher in the patients compared with controls (p<0.001). Anti-CCP positive patients had significantly higher concentration of RANKL compared with anti-CCP negatives, median (Q1-Q3) 763.7 (347.3-1325.0) pmol/L and 241.5 (137.8-474.1) pmol/L. The concentration of sclerostin was also significantly increased in the patients (median (Q1-Q3)) 0.63 (0.49-0.78) ng/mL versus controls (0.51 (0.4-0.7) ng/mL (p<0.01). After stratification for sex the difference was only significant in female patients 0.59 (0.47-0.74) ng/mL compared with female controls 0.49 (0.4-0.65) ng/mL (p<0.02). There was no difference in concentrations in anti-CCP2 positive patients vs. negative patients. RANKL concentration was related to Larsen score at baseline (β=0.001 (0.000-0.002), p<0.01), Larsen score after 24 months (β=0.002 (0.001-0.003), p<0.001) and to radiological progression after 2 years (β=0.001 (0.000-0.002), p<0.001) in simple analyses of variance. No corresponding relationships were found for the concentration of sclerostin. In multiple analyses of variance the concentration of RANKL was only related to Larsen score at baseline adjusted for age and SJC. However, the concentration of sclerostin was significantly ((β=2.55 (0.15-4.95), p<0.05) related to radiological progression after 2 years adjusted for sex, Larsen score and ESR at baseline and response to treatment after 24 months. Conclusions: The concentration of RANKL was related to Larsen score at baseline adjusted for age and baseline SJC, whilst the concentration of sclerostin at baseline was related to radiological progression during the first 2 years of disease adjusted for therapeutic response and ESR. Measurement of sclerostin at baseline could be a valuable predictor of radiological progression during the first 2 years. Disclosure of Interest: None declared