Rheumatic diseases: the effects of inflammation on bone

被引:295
作者
Walsh, NC [1 ]
Crotti, TN [1 ]
Goldring, SR [1 ]
Gravallese, EM [1 ]
机构
[1] Harvard Univ, Beth Israel Deaconess Med Ctr, Inst Med, New England Baptist Bone & Joint Inst, Boston, MA 02115 USA
关键词
D O I
10.1111/j.0105-2896.2005.00338.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Rheumatoid arthritis, juvenile idiopathic arthritis, the seronegative spondyloarthropathies including psoriatic arthritis, and systemic lupus erythematosus are all examples of rheumatic diseases in which inflammation is associated with skeletal pathology. Although some of the mechanisms of skeletal remodeling are shared among these diseases, each disease has a unique impact on articular bone or on the axial or appendicular skeleton. Studies in human disease and in animal models of arthritis have identified the osteoclast as the predominant cell type mediating bone loss in arthritis. Many of the cytokines and growth factors implicated in the inflammatory processes in rheumatic diseases have also been demonstrated to impact osteoclast differentiation and function either directly, by acting on cells of the osteoclast-lineage, or indirectly, by acting on other cell types to modulate expression of the key osteoclastogenic factor receptor activator of nuclear factor (NF) kappa B ligand (RANKL) and/or its inhibitor osteoprotegerin (OPG). Further elucidation of the mechanisms responsible for inflammation-induced bone loss will potentially lead to the identification of novel therapeutic strategies for the prevention of bone loss in these diseases. In this review, we provide an overview of the cell types, inflammatory mediators, and mechanisms that are implicated in bone loss and new bone formation in inflammatory joint diseases.
引用
收藏
页码:228 / 251
页数:24
相关论文
共 329 条
[91]  
Harada S, 1999, ARTHRITIS RHEUM, V42, P1508, DOI 10.1002/1529-0131(199907)42:7<1508::AID-ANR26>3.0.CO
[92]  
2-L
[94]   Regulation of receptor activator of NF-κB ligand-induced osteoclastogenesis by endogenous interferon-β (INF-β) and suppressors of cytokine signaling (SOCS) -: The possible counteracting role of SOCSs in IFN-β-inhibited osteoclast formation [J].
Hayashi, T ;
Kaneda, T ;
Toyama, Y ;
Kumegawa, M ;
Hakeda, Y .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (31) :27880-27886
[95]   Osteoprotegerin expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathies normal controls [J].
Haynes, DR ;
Barg, E ;
Crotti, TN ;
Holding, C ;
Weedon, H ;
Atkins, GJ ;
Zannetino, A ;
Ahern, MJ ;
Coleman, M ;
Roberts-Thomson, PJ ;
Kraan, M ;
Tak, PP ;
Smith, MD .
RHEUMATOLOGY, 2003, 42 (01) :123-134
[96]   Osteoprotegerin and receptor activator of nuclear factor kappaB ligand (RANKL) regulate osteoclast formation by cells in the human rheumatoid arthritic joint [J].
Haynes, DR ;
Crotti, TN ;
Loric, M ;
Bain, GI ;
Atkins, GJ ;
Findlay, DM .
RHEUMATOLOGY, 2001, 40 (06) :623-630
[97]   Cytosolic phospholipase A2α-deficient mice are resistant to collagen-induced arthritis [J].
Hegen, M ;
Sun, LH ;
Uozumi, N ;
Kume, K ;
Goad, ME ;
Nickerson-Nutter, CL ;
Shimizu, T ;
Clark, JD .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (10) :1297-1302
[98]   Principles of interleukin (IL)-6-type cytokine signalling and its regulation [J].
Heinrich, PC ;
Behrmann, I ;
Haan, S ;
Hermanns, HM ;
Müller-Newen, G ;
Schaper, F .
BIOCHEMICAL JOURNAL, 2003, 374 (01) :1-20
[99]   Zoledronic acid protects against local and systemic bone loss in tumor necrosis factor-mediated arthritis [J].
Herrak, P ;
Görtz, B ;
Hayer, S ;
Redlich, K ;
Reiter, E ;
Gasser, J ;
Bergmeister, H ;
Kollias, G ;
Smolen, JS ;
Schett, G .
ARTHRITIS AND RHEUMATISM, 2004, 50 (07) :2327-2337
[100]   Interleukin-1β and tumor necrosis factor-α, but not interleukin-6, stimulate osteoprotegerin ligand gene expression in human osteoblastic cells [J].
Hofbauer, LC ;
Lacey, DL ;
Dunstan, CR ;
Spelsberg, TC ;
Riggs, BL ;
Khosla, S .
BONE, 1999, 25 (03) :255-259