Inflammatory osteolysis: a conspiracy against bone

被引：195

作者：

Mbalaviele, Gabriel ^{[1
]}

Novack, Deborah V. ^{[1
,2
]}

Schett, Georg ^{[3
]}

Teitelbaum, Steven L. ^{[1
,2
]}

机构：

[1] Washington Univ, Sch Med, Dept Med, Div Bone & Mineral Dis, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Dept Pathol & Immunol, Div Anat & Mol Pathol, St Louis, MO 63110 USA

[3] Univ Erlangen Nurnberg, Dept Internal Med 3, Rheumatol & Immunol, Erlangen, Germany

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2017年 / 127卷 / 06期

关键词：

NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; INTERLEUKIN-1 RECEPTOR ANTAGONIST; FAMILIAL MEDITERRANEAN FEVER; C-REACTIVE PROTEIN; RHEUMATOID-ARTHRITIS; OSTEOCLAST DIFFERENTIATION; PORPHYROMONAS-GINGIVALIS; FACTOR-ALPHA; TNF-ALPHA;

D O I：

10.1172/JCI93356

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

There are many causes of inflammatory osteolysis, but regardless of etiology and cellular contexts, the osteoclast is the bone-degrading cell. Thus, the impact of inflammatory cytokines on osteoclast formation and function was among the most important discoveries advancing the treatment of focal osteolysis, leading to development of therapeutic agents that either directly block the bone-resorptive cell or do so indirectly via cytokine arrest. Despite these advances, a substantial number of patients with inflammatory arthritis remain resistant to current therapies, and even effective anti-inflammatory drugs frequently do not repair damaged bone. Thus, insights into events such as those impacted by inflammasomes, which signal through cytokine-dependent and -independent mechanisms, are needed to optimize treatment of inflammatory osteolysis.

引用

页码：2030 / 2039

页数：10

共 185 条

[21] osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification [J].

Bucay, N ;

Sarosi, I ;

Dunstan, CR ;

Morony, S ;

Tarpley, J ;

Capparelli, C ;

Scully, S ;

Tan, HL ;

Xu, WL ;

Lacey, DL ;

Boyle, WJ ;

Simonet, WS .

GENES & DEVELOPMENT, 1998, 12 (09) :1260-1268

[22] A Bone Anabolic Effect of RANKL in a Murine Model of Osteoporosis Mediated Through FoxP3+ CD8 T Cells [J].

Buchwald, Zachary S. ;

Yang, Chang ;

Nellore, Suman ;

Shashkova, Elena V. ;

Davis, Jennifer L. ;

Cline, Anna ;

Ko, Je ;

Novack, Deborah V. ;

DiPaolo, Richard ;

Aurora, Rajeev .

JOURNAL OF BONE AND MINERAL RESEARCH, 2015, 30 (08) :1508-1522

[23] Osteoclast-induced Foxp3+ CD8 T-cells limit bone loss in mice [J].

Buchwald, Zachary S. ;

Kiesel, Jennifer R. ;

Yang, Chang ;

DiPaolo, Richard ;

Novack, Deborah V. ;

Aurora, Rajeev .

BONE, 2013, 56 (01) :163-173

[24] Osteoclast Activated FoxP3+ CD8+ T-Cells Suppress Bone Resorption in vitro [J].

Buchwald, Zachary S. ;

Kiesel, Jennifer R. ;

DiPaolo, Richard ;

Pagadala, Meghana S. ;

Aurora, Rajeev .

PLOS ONE, 2012, 7 (06)

[25] Orthopedic wear debris mediated inflammatory osteolysis is mediated in part by NALP3 inflammasome activation [J].

Burton, Lyndsey ;

Paget, Daniel ;

Binder, Nikolaus B. ;

Bohnert, Krista ;

Nestor, Bryan J. ;

Sculco, Thomas P. ;

Santambrogio, Laura ;

Ross, F. Patrick ;

Goldring, Steven R. ;

Purdue, P. Edward .

JOURNAL OF ORTHOPAEDIC RESEARCH, 2013, 31 (01) :73-80

[26] Increasing both CoCrMo-alloy particle size and surface irregularity induces increased macrophage inflammasome activation in vitro potentially through lysosomal destabilization mechanisms [J].

Caicedo, Marco S. ;

Samelko, Lauryn ;

McAllister, Kyron ;

Jacobs, Joshua J. ;

Hallab, Nadim J. .

JOURNAL OF ORTHOPAEDIC RESEARCH, 2013, 31 (10) :1633-1642

[27] 21st Century Storm Chasers: Defining Macrophage Activation Syndrome [J].

Canna, Scott W. ;

Nigrovic, Peter A. .

ARTHRITIS & RHEUMATOLOGY, 2016, 68 (03) :557-560

[28] An activating NLRC4 inflammasome mutation causes autoinflammation with recurrent macrophage activation syndrome [J].

Canna, Scott W. ;

de Jesus, Adriana A. ;

Gounil, Sushanth ;

Brooks, Stephen R. ;

Marrero, Bernadette ;

Liu, Yin ;

DiMattia, Michael A. ;

Zaal, Kristien J. M. ;

Sanchez, Gina A. Montealegre ;

Kim, Hanna ;

Chapelle, Dawn ;

Plass, Nicole ;

Huang, Yan ;

Villarinol, Alejandro V. ;

Biancotto, Angelique ;

Fleisher, Thomas A. ;

Duncan, Joseph A. ;

O'Shea, John J. ;

Benseler, Susanne ;

Grom, Alexei ;

Deng, Zuoming ;

Laxer, Ronald M. ;

Goldbach-Mansky, Raphaela .

NATURE GENETICS, 2014, 46 (10) :1140-1146

[29] Inflammasome-independent IL-1β mediates autoinflammatory disease in Pstpip2-deficient mice [J].

Cassel, Suzanne L. ;

Janczy, John R. ;

Bing, Xinyu ;

Wilson, Shruti P. ;

Olivier, Alicia K. ;

Otero, Jesse E. ;

Iwakura, Yoichiro ;

Shayakhmetov, Dmitry M. ;

Bassuk, Alexander G. ;

Abu-Amer, Yousef ;

Brogden, Kim A. ;

Burns, Trudy L. ;

Sutterwala, Fayyaz S. ;

Ferguson, Polly J. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2014, 111 (03) :1072-1077

[30] Gain-of-Function Pyrin Mutations Induce NLRP3 Protein-Independent Interleukin-1β Activation and Severe Autoinflammation in Mice [J].

Chae, Jae Jin ;

Cho, Young-Hun ;

Lee, Geun-Shik ;

Cheng, Jun ;

Liu, P. Paul ;

Feigenbaum, Lionel ;

Katz, Stephen I. ;

Kastner, Daniel L. .

IMMUNITY, 2011, 34 (05) :755-768

← 1 2 3 4 5 6 7 8 9 10 →