Pathways for Bone Loss in Inflammatory Disease

被引：168

作者：

Braun, Tobias ^{[1
,2
]}

Schett, Georg ^{[1
,2
]}

机构：

[1] Univ Erlangen Nurnberg, Dept Internal Med 3, D-91054 Erlangen, Germany

[2] Univ Erlangen Nurnberg, Inst Clin Immunol, D-91054 Erlangen, Germany

来源：

CURRENT OSTEOPOROSIS REPORTS | 2012年 / 10卷 / 02期

关键词：

Bone loss; Inflammatory disease; Osteoporosis; NF-KAPPA-B; INDUCED OSTEOCLAST FORMATION; NECROSIS-FACTOR-ALPHA; RHEUMATOID-ARTHRITIS; NUCLEAR-FACTOR; T-CELLS; AUTOIMMUNE ARTHRITIS; RECEPTOR ACTIVATOR; RANKL EXPRESSION; INTERFERON-GAMMA;

D O I：

10.1007/s11914-012-0104-5

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

Chronic inflammation including autoimmune disease is an important risk factor for the development of osteoporosis. Receptor activator of nuclear factor-kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) play a central role in osteoclast differentiation and function, and the molecular pathways by which M-CSF and RANKL induce osteoclast differentiation have been analyzed in detail. Proinflammatory cytokines directly or indirectly regulate osteoclastogenesis and bone resorption providing a link between inflammation and osteoporosis. Tumor necrosis factor-a, interleukin (IL)-1, IL-6, and IL-17 are the most important proinflammatory cytokines triggering inflammatory bone loss. Inhibition of these cytokines has provided potent therapeutic effects in the treatment of diseases such as rheumatoid arthritis. Further investigation is needed to understand the pathophysiology and to develop new strategies to treat inflammatory bone loss. This review summarizes new data on inflammatory bone loss obtained in 2011.

引用

页码：101 / 108

页数：8

共 96 条

[91]

Adenylate Cyclase and Calmodulin-Dependent Kinase Have Opposite Effects on Osteoclastogenesis by Regulating the PKA-NFATc1 Pathway [J].