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SAT0046 Role of C-Reactive Protein in Osteoclastogenesis in Rheumatoid Arthritis
  1. H.-R. Kim1,
  2. S.-H. Lee1,
  3. S.-H. Lee2,
  4. H.-Y. Kim1
  1. 1Konkuk University School of Medicine
  2. 2Kyung Hee University School of Medicine, SEOUL, Korea, Republic of


Background C-reactive protein (CRP) is one of the biomarkers for the diagnosis and assessment of disease activity in rheumatoid arthritis (RA). CRP is not only the by-product of inflammatory response, but also plays pro-inflammatory and pro-thrombotic roles.

Objectives This study aims to determine the role of CRP on bone destruction in RA.

Methods CRP levels in RA synovial fluid (SF) and serum were measured using the immunoturbidimetric method. The expression of CRP in RA synovium was assessed using immunohistochemical staining. CD14+ monocytes from peripheral blood were cultured with CRP, and RANKL expression and osteoclast differentiation were evaluated by using real-time PCR, counting TRAP-positive multinucleated cells and assessing bone resorbing function. CRP-induced osteoclast differentiation was also examined after inhibition of Fcgamma receptors.

Results There was a significant correlation between CRP levels serum and SF in RA patients. The SF CRP level was correlated with interleukin (IL)-6 levels, but not with RANKL levels. Immunohistochemical staining revealed that, compared with the osteoarthritis synovium, CRP was more abundantly expressed in the lining and sublining areas of the RA synovium. CRP stimulated RANKL production in monocytes, and it induced osteoclast differentiation from monocytes and bone resorption in the absence of RANKL.

Conclusions CRP could plays an important role in the bony destructive process in RA through the induction of RANKL expression and direct differentiation of osteoclast precursors into mature osteoclasts. In the treatment of RA, lowering CRP levels is a significant parameter not only for improving disease activity but also for preventing bony destruction.

Acknowledgements This work was supported by Konkuk University Medical Center Research Grant 2013.

Disclosure of Interest None declared

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