Inflammatory bone loss: pathogenesis and therapeutic intervention

被引:779
作者
Redlich, Kurt [1 ]
Smolen, Josef S. [1 ]
机构
[1] Med Univ Vienna, Div Rheumatol, Dept Med 3, A-1090 Vienna, Austria
关键词
TUMOR-NECROSIS-FACTOR; RHEUMATOID-ARTHRITIS PATIENTS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; BLOOD MONONUCLEAR-CELLS; TNF-ALPHA; OSTEOBLAST DIFFERENTIATION; MINERAL DENSITY; OSTEOCLAST DIFFERENTIATION; TRANSCRIPTION FACTOR; PARATHYROID-HORMONE;
D O I
10.1038/nrd3669
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 [微生物学]; 090105 [作物生产系统与生态工程];
摘要
Bone is a tissue undergoing continuous building and degradation. This remodelling is a tightly regulated process that can be disturbed by many factors, particularly hormonal changes. Chronic inflammation can also perturb bone metabolism and promote increased bone loss. Inflammatory diseases can arise all over the body, including in the musculoskeletal system (for example, rheumatoid arthritis), the intestine (for example, inflammatory bowel disease), the oral cavity (for example, periodontitis) and the lung (for example, cystic fibrosis). Wherever inflammatory diseases occur, systemic effects on bone will ensue, as well as increased fracture risk. Here, we discuss the cellular and signalling pathways underlying, and strategies for therapeutically interfering with, the inflammatory loss of bone.
引用
收藏
页码:234 / 250
页数:17
相关论文
共 265 条
[1]
Tumor necrosis factor-α inhibits pre-osteoblast differentiation through its type-1 receptor [J].
Abbas, S ;
Zhang, YH ;
Clohisy, JC ;
Abu-Amer, Y .
CYTOKINE, 2003, 22 (1-2) :33-41
[2]
Lipopolysaccharide-stimulated osteoclastogenesis is mediated by tumor necrosis factor via its P55 receptor [J].
AbuAmer, Y ;
Ross, FP ;
Edwards, J ;
Teitelbaum, SL .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (06) :1557-1565
[3]
Clinical utility of denosumab for treatment of bone loss in men and women [J].
Adler, Robert A. ;
Gill, Ranjodh S. .
CLINICAL INTERVENTIONS IN AGING, 2011, 6 :119-124
[4]
Physical disability in rheumatoid arthritis is associated with cartilage damage rather than bone destruction [J].
Aletaha, Daniel ;
Funovits, Julia ;
Smolen, Josef S. .
ANNALS OF THE RHEUMATIC DISEASES, 2011, 70 (05) :733-739
[5]
Osteoporosis in Inflammatory Bowel Disease [J].
Ali, Tauseef ;
Lam, David ;
Bronze, Michael S. ;
Humphrey, Mary Beth .
AMERICAN JOURNAL OF MEDICINE, 2009, 122 (07) :599-604
[6]
ACTION OF RECOMBINANT HUMAN INTERLEUKIN-6, INTERLEUKIN-1-BETA AND TUMOR NECROSIS FACTOR-ALPHA ON THE MESSENGER-RNA INDUCTION OF ACUTE-PHASE PROTEINS [J].
ANDUS, T ;
GEIGER, T ;
HIRANO, T ;
KISHIMOTO, T ;
HEINRICH, PC .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1988, 18 (05) :739-746
[7]
[Anonymous], ANN RHEUM DIS S3
[8]
Aringer M., 2011, AUTOIMMUNITY RE 0518, DOI [10.1016/j.autrev.2011.05.001.2011, DOI 10.1016/J.AUTREV.2011.05.001.2011]
[9]
THE AMERICAN-RHEUMATISM-ASSOCIATION 1987 REVISED CRITERIA FOR THE CLASSIFICATION OF RHEUMATOID-ARTHRITIS [J].
ARNETT, FC ;
EDWORTHY, SM ;
BLOCH, DA ;
MCSHANE, DJ ;
FRIES, JF ;
COOPER, NS ;
HEALEY, LA ;
KAPLAN, SR ;
LIANG, MH ;
LUTHRA, HS ;
MEDSGER, TA ;
MITCHELL, DM ;
NEUSTADT, DH ;
PINALS, RS ;
SCHALLER, JG ;
SHARP, JT ;
WILDER, RL ;
HUNDER, GG .
ARTHRITIS AND RHEUMATISM, 1988, 31 (03) :315-324
[10]
A generalized skeletal hyperostosis in two siblings caused by a novel mutation in the SOST gene [J].
Balemans, W ;
Cleiren, E ;
Siebers, U ;
Horst, J ;
Van Hul, W .
BONE, 2005, 36 (06) :943-947