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REVIEW PAPER
The role of OPG/RANKL/RANK in bone destruction in rheumatoid arthritis
Online publication date: 2009-06-10
Reumatologia 2009;47(2):67-74
KEYWORDS
ABSTRACT
A decrease in bone mineral density (BMD) is common in chronic inflammatory diseases of the musculoskeletal system. So-called “inflammatory osteoporosis” concerns up to 50% of rheumatic patients. Its intensity is relevant to the disease activity and the patient’s age. In rheumatoid arthritis (RA) it is primarily caused by osteoclast activation and its most apparent manifestation is periarticular osteoporosis due to a local inflammatory process. Apart from chronic inflammation RA-related osteoporosis can be caused by glucocorticosteroid (GSS) use and immobilization. In menopausal women hormonal disturbances can contribute to the damage. RA patients are at increased risk of low-energy fractures. The questions are whether it is inflammation per se or GSS that affects bones most in this disease, and whether accelerated bone loss results in increased susceptibility to osteoporotic fractures in RA patients.
REFERENCES (62)
1.
Haugeberg G, Green MJ, Conaghan PG, et al. Hand bone densytometry: a more sensitive standard for the assessment of early bone damage in rheumatoid arthritis. Ann Rheum Dis 2007; 66: 1513-1517. .
2.
Dequeker J, Maenaut J, Verwilghen J, et al. Osteoporosis in rheumatoid arthritis. Clin Exp Rheumatol 1995; 13 (Suppl 12) S21-S26. .
3.
Supronik J. Próba oceny mineralizacji i metabolizmu kości u kobiet chorych na reumatoidalne zapalenie stawów. Praca doktorska, Białystok 1992. .
4.
Leszczyński P, Hrycaj P, Mackiewicz SH. Osteoporoza u chorych na reumatoidalne zapalenie stawów – realny problem czy fikcja? Ocena występowania złamań trzonów kręgowych u kobiet z reumatoidalnym zapaleniem stawów w wieku do 50 lat. Reumatologia 2007; 45: 362-368. .
5.
Lodder MC, De Jong Z, Kostence PJ, et al. Bone mineral density in patients with rheumatoid arthritis: relation between disease severity and low bone mineral density. Ann Rheum Dis 2004; 63: 1576-1580. .
6.
Leszczyński P, Łącki JK, Mackiewicz SH. Osteoporoza posteroidowa u chorych na reumatoidalne zapalenie stawów. Przegl Lek 2000; 57: 108-110. .
7.
Guler-Yuksel M, Bijsterbosch J, Goekoop-Ruiterman YP, et al. Bone mineral density in patients with recently diagnosed, active rheumatoid arthritis. Ann Rheum Dis 2007; 66: 1508-1512. .
8.
Huusko TM, Korpella M, Karpi P, et al. Threefold increased risk of hip fractures with rheumatoid arthritis in central Finland. Ann Rheum Dis 2001; 60: 521-522. .
9.
Chapurlat RD, Garnelo P, Breat G, et al. Serum type I collagen break down product (serum Ctx) predicts hip fracture risk in elderly women: the EPIDOS study. Bone 2000; 27: 283-286. .
10.
Badurski J, Sawicki A, Boczoń S. Osteoporoza. Osteoprint, Białystok 1994; 61-69. .
11.
Orstavik RE, Haugeberg G, Uhlig T, et al. Incidence of vertebral deformities in 255 female rheumatoid arthritis patients measured by morphometric X-ray absorptiometry. Osteoporosis Int 2005; 16: 35-42. .
12.
Keller C, Hafstrom I, Svensson B. BARFOT study group. Bone mineral density in women and men with early rheumatoid arthritis. Scand J Rheumatol 2001; 30: 213-220. .
13.
Badurski JE, Czerwiński E, Marcinowska-Suchowierska E. Osteoporoza – ocena ryzyka złamania. Status Quo Arte Anno 2007/2008: Przegląd stanowisk: Światowej Organizacji Zdrowia (WHO), Europejskiej Agencji Medycznej (EMEA), Europejskiego Towarzystwa Klinicznych i Ekonomicznych Aspektów Osteoporozy (ESEAO), Międzynarodowej Fundacji Osteoporozy (IOF), Polskiej Fundacji Osteoporozy (PFO) i Polskiego Towarzystwa Osteoartrologii (PTOA). Postępy Nauk Medycznych 2008; 21: 335-359. .
15.
Garnero P, Sornay-Rendu E, Claustrar B, et al. Biochemical markers of bone turnover, endogenous hormones and the risk of fracture in postmenopausal women: the OFFLEY study. J Bone Miner Res 2000; 15: 1526-1536. .
16.
Cortet B, Filipo RM, Pigny P, et al. Is bone turnover a determinant of bone mass in rheumatoid arthritis? J Rheumatol 1998; 25: 2339-2344. .
17.
Momohara S, Okamoto H, Yago T, et al. The study of bone mineral density and bone turnover markers in postmenopausal women with active rheumatoid arthritis. Mod Rheumatol 2005; 15: 410-414. .
18.
Dias A, Lopes Vaz A, Hargreaves M, et al. Biomarkers in secondary osteoporosis. Clin Rheum 1989 (suppl 2): 89-94. .
19.
Manrique F, Gamaro P, de Elguezabal N. Abnormalities of bone mineral density and bone metabolism in Venezuelan patients with rheumatoid arthritis. J Clin Rheumatol 2003; 9: 219-227. .
20.
Turner CH. Biomechanics of bone. Determinants of skeletal fragility and bone quality. Osteoporosis Int 2002; 13: 97-104. .
21.
Paschalis EP, Shane E, Lyritis G, et al. Bone fragility and collagen cross-links. J Bone Miner Res 2004; 19: 2000-2004. .
23.
Takayanagi H, Iizuka H, Juji T, et al. Involvement of receptor activator of nuclear factor kappa B ligand/osteoclast differentiation factor in osteoclastogenesis from synoviocytes in rheumatoid arthritis. Arthritis Rheum 2000; 43: 259-269. .
24.
Gough A, Sambroock P, Delvin J, et al. Osteoclastic activation is the principial mechanism leading to secondary osteoporosis in rheumatoid arthritis. J Rheumatol 1998; 25: 1282-1298. .
25.
Kong YY, Yoshida H, Sarosi I, et al. OPG is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis. Nature 1999; 397: 315-323. .
26.
Łukaszkiewicz J, Lorenc SR. Udział czynników endokrynnych i parakrynnych w etiopatogenezie osteoporozy. Terapia 2008; 5 (209). .
27.
Lacey DL, Timms E, Tan HL, et al. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation. Cell 1998; 93: 165-176. .
28.
Kim N, Odgren PR, Kim DK, et al. Diverse roles of the tumor necrosis factor family member TRANCE in skeletal physiology revealed by TRANCE deficiency and partial rescue by a lymphocyte-expressed TRANCE transgene. Proc Natl Acad Sci U S A 2000; 97: 10905-10910.
29.
Hofdbauer LC, Khosla S, Dunstan CR, et al. The roles of osteoprotegerin and osteoprotegerin ligand in the paracrine regulation of bone resorption. J Bone Miner Res 2000; 15: 2-12. .
30.
Wong BR, Rho J, Arron J, et al. 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 1997; 272: 25190-25194. .
31.
Hsu H, Lacey DL, Dunstan CR, et al. Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand. Proc Natl Acad Sci U S A 1999; 96: 3540-3545. .
32.
Fata JE, Kong YY, Li J, et al. The osteoclast differentiation factor osteoprotegerin-ligand is Essentials for mammary gland development. Cell 2000; 103: 41-50. .
33.
Boyle WJ, Simonet WS, Lacey DL. Osteoclast differentiation and activation. Nature 2003; 423: 337-342. .
34.
Ishida N, Hayashi K, Hoshijima M, et al. Large scale gene expression analysis of osteoclastogenesis in vitro and elucidation of NFAT2 as a key regulator. J Biol Chem 2002; 277: 41147-41156. .
35.
Wong BR, Besser D, Kim N, et al. TRANCE, a TNF family member, activates Akt/PKB through a signaling complex involving TRAF6 and c-Src. Moll Cell 1999; 4: 1041-1049. .
36.
Morony S, Capparelli C, Lee R, et al. A chimeric form of osteoprotegerin inhibits hypercalcemia and bone resorption induced by IL-1 beta, TNF-αlpha, PTH, PTHrP, and 1,25(OH)2D3. J Bone Miner Res 1999; 14: 1478-1485. .
37.
Bucay N, Sarosi I, Dunstan CR, et al. Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification. Genes Dev 1998; 12: 1260-1268. .
38.
Ziółkowska M, Kurowska M, Radzikowska A, et al. High levels of osteoprotegerin and soluble receptor activator of nuclear factor kappa B ligand in serum of rheumatoid arthritis patients and their normalization after anti-tumor necrosis factor alpha treatment. Arthritis Rheum 2002; 46: 1744-1753. .
39.
Shigeyama Y, Pap T, Kunzler P, et al. Expression of osteoclast differentiation factor in rheumatoid arthritis. Arthritis Rheum 2000; 43: 2523-2530. .
40.
Nakashima T, Wada T, Penninger JM. RANKL and RANK as novel therapeutic targets for arthritis. Curr Opin Rheumatol 2003; 15: 280-287. .
41.
Vidal NO, Brandstrom H, Jonsson KB, et al. Osteoprotegerin mRNA is expressed in primary human osteoblast-like cells: down-regulation by glucocorticoids. J Endocrinol 1998; 159: 191-195. .
42.
Josien R, Li HL, Ingulli E, et al. TRANCE, a tumor necrosis factor family member, enhances the longevity and adjuvant properties of dendric cells in vivo. J Exp Med 2000; 191: 495-502. .
43.
Kotake S, Udagawa N, Hakoda M, et al. Activated human T cells directly induce osteoclastogenesis from human monocytes: possible role of T cells in bone destruction in rheumatoid arthritis patients. Arthritis Rheum 2001; 44: 1003-1012. .
44.
Josien R, Wong BR, Li HL, et al. TRANCE, a TNF family member, is differentially expressed on T cell subsets and induces cytokine production in dendric cells. J Immunol 1999; 162: 2562-2568. .
45.
Saidenberg-Kermanach N, Cohen-Solal M, Bessis N, et al. Role for osteoprotegerin in rheumatoid inflammation. Joint Bone Spine 2004; 71: 9-13. .
46.
Goldring SR, Gravallese EM. Pathogenesis of bone erosions in rheumatoid arthritis. Curr Opin Rheumatol 2000; 12: 195-199. .
47.
Kotake S, Sato K, Kim KJ, et al. Interleukin-6 and soluble interleukin-6 receptors in the synovial fluids from rheumatoid arthritis patients are responsible for osteoclast-like cell formation. J Bone Miner Res 1996; 11: 88-95. .
48.
Lubberts E, Koenders MI, van den Berg WB. The role of T cell interleukin-17 in conducting destructive arthritis: lessons from animal models. Arthritis Res Ther 2005; 7: 29-37. .
49.
Kamel Mohamed SG, Sugiyama E, Shinoda K, et al. Interleukin-4 inhibits RANKL-induced expression of NFATc1 and c-Fos: a possible mechanism for downregulation of osteoclastogenesis. Biochem Biophys Res Commun 2005; 329: 839-845. .
50.
Romas E, Bakharevski O, Hards DK, et al. Expression of osteoclast differentiation factor at sites of bone erosion in collagen-induced arthritis. Arthritis Rheum 2000; 43: 821-826. .
51.
Haynes DR, Crotti TN, Loric M, et al Osteoprotegerin and receptor activator of nuclear factor kappa B ligand (RANKL) regulate osteoclast formation by cells in the human rheumatoid arthritic joint. Rheumatology (Oxford) 2001; 40: 623-630. .
52.
Pettit AR, Ji H, von Stechow D, et al. TRANCE/RANKL knockout mice are protected from bone erosion in a serum transfer model of arthritis. Am J Pathol 2001; 159: 1689-1699. .
53.
Kong YY, Feige U, Sarosi I, et al. Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand. Nature 1999; 402: 304-309. .
54.
Mori H, Kitazawa R, Mizuki S, et al. RANK ligand, RANK, and OPG expression in type II collagen-induced arthritis Mouse. Histochem Cell Biol 2002; 117: 283-292. .
55.
Schett G, Redlich K, Hayer S, et al. Osteoprotegerin protects against generalized bone loss in tumor necrosis factor-transgenic mice. Arthritis Rheum 2003; 48: 2042-2051. .
56.
Wu Y, Liu J, Feng X, et al. Synovial fibroblasts promote osteoclast formation by RANKL in a novel model of spontageous arthritis. Arthritis Rheum 2005; 52: 3257-3268. .
57.
Bekker PJ, Holloway D, Nakanishi A, et al. The effect of a single dose of osteoprotegerin in postmenopausal women. J Bone Miner Res 2001; 16: 348-360. .
58.
Kamijo S, Nakajima A, Ikeda K, et al. Amelioration of bone loss in collagen-induced arthritis by neutralizing anti-RANKL monoclonal antibody. Bioche Biophys Res Commun 2006; 347: 124-132. .
59.
Romas E, Gillespie MT. Inflammation-induced bone loss: can it be prevented? Rheum Dis Clin North Am 2006, 32: 759-773. .
60.
Catrina AI, af Klint E, Ernestam S, et al. Anti-tumor necrosis factor therapy increases synovial osteoprotegerin expression in rheumatoid arthritis. Arthritis Rheum 2006; 54: 76-81. .
61.
Lee CK, Lee EY, Chung SM, et al. Effects of disease-modifying antirheumatic drugs and antiinflammatory cytokines on human osteoclastogenesis through interaction with receptor activator of nuclear factor kappa B, osteoprotegerin, and receptor activator of nuclear factor kappa B ligand. Arthritis Rheum 2004; 50: 3831-3843. .
62.
Van Lieshout AW, Barrera P, Smeets RL, et al. Inhibition of TNF alpha during maturation of dendritic cells results in the development of semi-mature cells: a potential mechanism for the beneficial effects of TNF alpha blockade in rheumatoid arthritis. Ann Rheum Dis 2005; 64: 408-414.
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