J Korean Orthop Assoc.
2004 Dec;39(7):729-735.
Expression of RANKL/OPG in Joint Fluids of Periprosthetic Osteolysis
- Affiliations
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- 1Department of Orthopaedic Surgery, St. Paul's Hospital, The Catholic University of Korea, Seoul, Korea. hnsukku@catholic.ac.kr
- 2Department of Orthopaedic Surgery, KangNam St. Mary's Hospital, The Catholic University of Korea, Seoul, Korea.
- 3Department of Orthopaedic Surgery, Washington University School of Medicine Barnes Jewish Hospital, St. Lewis, MO, USA
Abstract
- PURPOSE
This study evaluated the expression level of Receptor Activator of NF-kappaB Ligand (RANKL), Osteoprotegerin (OPG)and other pro-inflammatory cytokines in the osteoarthritic and periprosthetic joint fluid in order to characterize the role of these regulatory proteins in periprosthetic osteolysis. MATERIALS AND METHODS: Joint fluid specimens taken from 47 patients undergoing hip or knee reconstructive surgery were analyzed by enzyme-linked immunoassay (ELISA)in order to determine the relative protein expression level of RANKL, OPG, IL-1beta, IL-6 and TNF-alpha. The fluid from joints with osteoarthritis (15 cases, Group I), implants revised without associated osteolysis (15 cases, Group II)and failed implants with radiographically moderate to severe osteolysis (17 cases, Group III) were compared. The fluids from all cases with implants (Group II and III) was combined (Group IV)and compared with the osteoarthritic joint fluids. RESULTS: RANKL was present in all the fluids at similar concentrations. The OPG levels were significantly lower (2.2-3.9 fold)in Groups II and III than in Group I (p<0.0001). The IL-1beta concentration was significantly higher in Groups II, III and IV and with Group III being the highest (12.1 fold)(p<0.0001). The IL-6 expression level was significantly higher in Group III (2.0 fold)than in Groups I and II (p<0.0001). The TNF-alpha levels were 2.0 times higher in Group III and significantly higher in all implant cases (Group IV)are analyzed (p=0.03). CONCLUSION: Permissive RANKL protein expression coupled with suppressed OPG levels and enhanced osteoclastogenic cytokine expression results in periprosthetic osteolysis.
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