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Autoantibodies to osteoprotegerin are associated with increased bone resorption in rheumatoid arthritis
  1. Barbara Hauser1,
  2. Philip L Riches1,
  3. Tamara Gilchrist1,
  4. Micaela R Visconti1,
  5. James F Wilson2,
  6. Stuart H Ralston1
  1. 1Rheumatic Diseases Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK
  2. 2Centre for Population Health Sciences, University of Edinburgh, Edinburgh, UK
  1. Correspondence to Professor Stuart H Ralston, Rheumatic Diseases Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh EH4 2XU, UK; stuart.ralston{at}ed.ac.uk

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Periarticular and systemic bone loss are important complications of rheumatoid arthritis (RA).1 The pathogenesis is complex involving local and systemic release of cytokines which promote osteoclastic bone resorption2; production of receptor activator of nuclear factor κB (NFκB) ligand (RANKL) by activated T cells3 and immobility, corticosteroid use4 and the direct osteoclast activating effects of antibodies directed against citrullinated proteins (ACPA).5 ,6 We previously reported the occurrence of severe osteoporosis in a patient with autoimmune disease who had developed autoantibodies to the bone protective protein osteoprotegerin (OPG).7 In this study, we screened for the presence of similar autoantibodies in RA and evaluated their clinical significance. We developed an ELISA for autoantibodies to OPG, by coating 96-well plates with recombinant human OPG as the capture antigen. Following the addition of patient samples to each well and multiple wash steps, bound OPG antibodies were detected by a peroxidase conjugated, anti-human IgG antibody (Jackson Immuno Research Labs , 109-035-127). Concentrations of OPG antibody were then …

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