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Cellular characterization of magnetic resonance imaging (MRI) bone edema in rheumatoid arthritis; implications for pathogenesis of erosive disease
  1. Nicola Dalbeth (n.dalbeth{at}auckland.ac.nz)
  1. University of Auckland, New Zealand
    1. Timothy Smith
    1. University of Auckland, New Zealand
      1. Samuel Gray
      1. University of Auckland, New Zealand
        1. Anthony Doyle
        1. University of Auckland, New Zealand
          1. Pam Antill
          1. University of Auckland, New Zealand
            1. Maria Lobo
            1. University of Auckland, New Zealand
              1. Elizabeth Robinson
              1. University of Auckland, New Zealand
                1. Alan King
                1. University of Auckland, New Zealand
                  1. Jillian Cornish
                  1. University of Auckland, New Zealand
                    1. Gareth Shalley
                    1. University of Auckland, New Zealand
                      1. Angela Gao
                      1. University of Auckland, New Zealand
                        1. Fiona M McQueen (f.mcqueen{at}auckland.ac.nz)
                        1. University of Auckland, New Zealand

                          Abstract

                          Aims: MRI bone edema is an important predictor of bone erosion in rheumatoid arthritis (RA). This study aimed to determine the cellular components of MRI bone edema, and clarify the relationship between bone erosion and MRI bone edema.

                          Methods: Twenty-eight bones from 11 patients with RA undergoing orthopedic surgery were analyzed by quantitative and semi-quantitative immunohistochemistry. Pre-operative contrast-enhanced MRI scans were analyzed for bone edema.

                          Results: The density of osteoclasts was higher in those samples with MRI bone edema than those without MRI bone edema (p=0.01). Other cells identified within bone marrow included macrophages and plasma cells, and these were more numerous in samples with MRI bone edema (p=0.02 and 0.05 respectively). B cells were present in lower numbers, but B cell aggregates were identified in some samples with MRI bone edema. There was a trend to increased RANKL expression in samples with MRI bone edema (p=0.09). Expression of RANKL correlated with the number of osteoclasts (r=0.592, p=0.004).

                          Summary: The increased number of osteoclasts and RANKL expression in samples with MRI bone edema supports the hypothesis that bone erosion in RA occurs through activation of local bone resorption mechanisms within subchondral bone as well as through synovial invasion into bone.

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