sRANKL and OPG in serum and synovial fluid of patients with rheumatoid arthritis in comparison to non-destructive chronic arthritis

被引:0
作者
Gert E. Hein
Marit Meister
Peter Oelzner
Sybille Franke
机构
[1] Friedrich-Schiller University,Department of Internal Medicine III, Section of Rheumatology and Osteology
来源
Rheumatology International | 2008年 / 28卷
关键词
Rheumatoid arthritis; Bone destruction; Osteoprotegerin; RANKL; Inflammation;
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摘要
The aim of this study was to investigate sRANKL and OPG levels in serum and synovial fluid (SF) and to evaluate their relations in patients with RA in comparison to those with non-erosive arthritis (NEA). The study included 45 unselected RA patients with knee joint effusions and 27 patients with knee joint effusions because of NEA. Serum and SF samples were investigated isochronously. OPG and sRANKL were measured by ELISA assays. In RA, sRANKL levels were higher in serum than in SF (P = 0.007). In contrast, the NEA revealed higher sRANKL in SF compared to the serum (P = 0.001). Though in RA the average levels of sRANKLser were 5.6 times and of sRANKLsyn 1.5 times higher than in NEA, the differences were not significant. The free (unbound) OPG in SF was not significantly different in RA compared to NEA. Also in serum, the measured free OPG was only slightly higher in RA. There were no significant differences between RA and NEA concerning ESR and CRP. Significant correlations could be found between sRANKLsyn and CRP (r = 0.453; P = 0.005) as well as ESR (r = 0.362; P = 0.033) in RA. Nearly a positive correlation was evident also between sRANKLsyn and CRP in NEA (r = 0.520; P = 0.08). RA and NEA differ in particular concerning their power and intensity to destruct the juxtaarticular bone. This is the most remarkable finding of this study, that in RA a high part of sRANKL seems to be OPG bound and cleared by the blood stream, but the sRANKL neutralizing capacity of produced OPG in opposite to NEA is not sufficient to prevent osteoclast activation and bone destruction in the RA joint.
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页码:765 / 769
页数:4
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[1]  
Hofbauer LC(2001)Role of receptor activator of nuclear factor-κB ligand and osteoprotegerin in bone cell biology J Mol Med 79 243-253
[2]  
Heufelder AE(1999)OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node orgenogenesis. Nature 397 315-323
[3]  
Kong Y-Y(1997)TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells J Biol Chem 272 25190-25194
[4]  
Yoshida H(1999)Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand. Nature 402 304-309
[5]  
Sarosi I(1999)Evidence for a role of a tumor necrosis factor-α (TNF-α)-converting enzyme-like protease in shedding of TRANCE, a TNF family member involved in osteoclastogenesis and dendritic cell survival J Biol Chem 274 13613-13618
[6]  
Tan H-L(2000)The osteoclast differentiation factor osteoprotegerin-ligand is essential for mammary gland development Cell 103 41-50
[7]  
Timms E(1999)Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand Proc Natl Acad Sci USA 96 3540-3545
[8]  
Capparelli C(1997)Osteoprotegerin: a novel secreted protein involved in the regulation of bone densitiy. Cell 89 309-319
[9]  
Morony S(2000)Rheumatoid arthritis synovial macrophage–osteoclast differentiation is osteoprotegerin ligand-dependent J Pathol 192 97-104
[10]  
Oliveira-dos-Santos AJ(1999)The ligand for osteoprotegerin (OPGL) directly activates mature osteoclasts. J Cell Biol 145 527-538