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Regulation of bone lysis in inflammatory diseases.

作者信息

Haynes David R, Crotti Tania N

机构信息

Department of Pathology, University of Adelaide, Adelaide, S.A. 5005, Australia.

出版信息

Inflammopharmacology. 2003;11(4):323-31. doi: 10.1163/156856003322699500.

DOI:10.1163/156856003322699500
PMID:15035786
Abstract

Focal bone erosion is a major pathological feature of several common inflammatory diseases. Over the past decade there have been major advances in our understanding of the factors that regulate osteoclast formation and activity. It is now apparent that receptor activator for NFkappaB (RANK), its ligand RANKL (also known as TRANCE, osteoclast differentiation factor and osteoprotegerin (OPG) ligand) and the RANKL inhibitor OPG, are the major factors regulating osteoclast formation. These molecules influence normal bone physiology and now there is growing evidence that RANK-RANKL interactions also regulate osteoclast formation in disease. This paper reviews recent findings showing expression of RANK, RANKL and OPG in inflammatory diseases including rheumatoid arthritis, periodontal disease and peri-implant loosening. It is emerging that OPG and RANKL are key molecules regulating bone loss in disease and therapeutic intervention that targets these molecules may be helpful in treating a wide range of diseases.

摘要

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J Orthop Res. 2008 Dec;26(12):1577-84. doi: 10.1002/jor.20714.

本文引用的文献

1
Receptor activator NF kappaB ligand (RANKL) and osteoprotegerin (OPG) protein expression in periodontitis.牙周炎中核因子κB受体活化因子配体(RANKL)和骨保护素(OPG)蛋白表达
J Periodontal Res. 2003 Aug;38(4):380-7. doi: 10.1034/j.1600-0765.2003.00615.x.
2
RANKL and RANK as novel therapeutic targets for arthritis.
Curr Opin Rheumatol. 2003 May;15(3):280-7. doi: 10.1097/00002281-200305000-00016.
3
Osteoprotegerin expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathies and osteoarthritis and normal controls.类风湿关节炎、脊柱关节病、骨关节炎患者及正常对照者滑膜组织中骨保护素的表达。
Rheumatology (Oxford). 2003 Jan;42(1):123-34. doi: 10.1093/rheumatology/keg047.
4
Two distinct cellular mechanisms of osteoclast formation and bone resorption in periprosthetic osteolysis.人工关节周围骨溶解中破骨细胞形成和骨吸收的两种不同细胞机制。
J Orthop Res. 2003 Jan;21(1):73-80. doi: 10.1016/S0736-0266(02)00106-7.
5
Expression of RANKL and OPG mRNA in periodontal disease: possible involvement in bone destruction.RANKL和OPG mRNA在牙周病中的表达:可能参与骨破坏过程。
Int J Mol Med. 2003 Jan;11(1):17-21. doi: 10.3892/ijmm.11.1.17.
6
Receptor activator NF-kappaB ligand (RANKL) expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathy, osteoarthritis, and from normal patients: semiquantitative and quantitative analysis.类风湿关节炎、脊柱关节病、骨关节炎患者及正常患者滑膜组织中核因子κB受体活化因子配体(RANKL)的表达:半定量和定量分析
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7
Pathogenesis of bone lesions in rheumatoid arthritis.类风湿关节炎骨病变的发病机制。
Curr Rheumatol Rep. 2002 Jun;4(3):226-31. doi: 10.1007/s11926-002-0069-y.
8
RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-beta.核因子κB受体活化因子配体(RANKL)通过依赖于c-Fos的干扰素-β诱导来维持骨稳态。
Nature. 2002 Apr 18;416(6882):744-9. doi: 10.1038/416744a.
9
The osteoclastogenic molecules RANKL and RANK are associated with periprosthetic osteolysis.破骨细胞生成分子RANKL和RANK与假体周围骨溶解有关。
J Bone Joint Surg Br. 2001 Aug;83(6):902-11. doi: 10.1302/0301-620x.83b6.10905.
10
Osteoclast-like cells in an in vitro model of bone destruction by rheumatoid synovium.类风湿性滑膜导致骨破坏的体外模型中的破骨细胞样细胞。
Rheumatology (Oxford). 2001 Jun;40(6):673-82. doi: 10.1093/rheumatology/40.6.673.