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Fibroblasts express RANKL and support osteoclastogenesis in a COX-2-dependent manner after stimulation with titanium particles.成纤维细胞在受到钛颗粒刺激后,以COX-2依赖的方式表达核因子κB受体活化因子配体(RANKL)并支持破骨细胞生成。
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IL-1 mediates TNF-induced osteoclastogenesis.白细胞介素-1介导肿瘤坏死因子诱导的破骨细胞生成。
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RANKL regulates Fas expression and Fas-mediated apoptosis in osteoclasts.核因子κB受体活化因子配体(RANKL)调节破骨细胞中Fas的表达和Fas介导的细胞凋亡。
J Bone Miner Res. 2005 Jan;20(1):107-16. doi: 10.1359/JBMR.041022. Epub 2004 Oct 25.
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Osteoclasts enhance myeloma cell growth and survival via cell-cell contact: a vicious cycle between bone destruction and myeloma expansion.破骨细胞通过细胞间接触促进骨髓瘤细胞的生长和存活:骨破坏与骨髓瘤增殖之间的恶性循环。
Blood. 2004 Oct 15;104(8):2484-91. doi: 10.1182/blood-2003-11-3839. Epub 2004 Jun 8.
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Regulation of osteoclast activity in peri-implant tissues.种植体周围组织中破骨细胞活性的调节
Biomaterials. 2004 Sep;25(20):4877-85. doi: 10.1016/j.biomaterials.2004.01.003.
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Joint erosion in rheumatoid arthritis: interactions between tumour necrosis factor alpha, interleukin 1, and receptor activator of nuclear factor kappaB ligand (RANKL) regulate osteoclasts.类风湿关节炎中的关节侵蚀:肿瘤坏死因子α、白细胞介素1和核因子κB受体激活剂配体(RANKL)之间的相互作用调节破骨细胞。
Ann Rheum Dis. 2004 Apr;63(4):354-9. doi: 10.1136/ard.2003.008458.
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NF-kB signaling blockade abolishes implant particle-induced osteoclastogenesis.核因子-κB信号通路阻断可消除植入物颗粒诱导的破骨细胞生成。
J Orthop Res. 2004 Jan;22(1):13-20. doi: 10.1016/S0736-0266(03)00156-6.
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Imbalance of RANKL/RANK/OPG system in interface tissue in loosening of total hip replacement.
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10
Mitogen-activated protein (MAP) kinases mediate PMMA-induction of osteoclasts.丝裂原活化蛋白(MAP)激酶介导聚甲基丙烯酸甲酯(PMMA)诱导破骨细胞生成。
J Orthop Res. 2003 Nov;21(6):1041-8. doi: 10.1016/S0736-0266(03)00081-0.

聚甲基丙烯酸甲酯颗粒在体外刺激成熟破骨细胞的骨吸收。

Polymethylmethacrylate particles stimulate bone resorption of mature osteoclasts in vitro.

作者信息

Zhang Hao, Ricciardi Benjamin F, Yang Xu, Shi Yuexian, Camacho Nancy P, Bostrom Mathias G

机构信息

The Hospital for Special Surgery, New York, NY, USA.

出版信息

Acta Orthop. 2008 Apr;79(2):281-8. doi: 10.1080/17453670710015166.

DOI:10.1080/17453670710015166
PMID:18484256
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2662348/
Abstract

BACKGROUND

Interaction between wear particle debris and the cells at the implant-bone interface is an important contributory factor to periprosthetic bone loss seen in arthroplasties.

METHOD

To investigate the effect of this particle-induced response on different stages of osteoclast maturation, polymethylmethacrylate (PMMA) particles were added to a murine osteoclastogenic bone marrow cell culture system at either day 0, day 4, or day 8 of culture, which represented PMMA particle stimulation of precursor osteoclasts, mature osteoclasts, or end-stage osteoclasts, respectively. The number of TRAP-posi-tive multinucleate cells (MNCs) and the degree of bone resorption in culture were measured

RESULTS

Treatment of precursor osteoclasts with PMMA particles resulted in a statistically significant increase in TRAP-positive MNCs that persisted for 4 days, but there was no significant increase in bone resorption. Addition of particles to mature osteoclasts resulted in a significant increase in the number of TRAP-positive MNCs that lasted for 8 days, and also a significant increase in bone resorption. Treatment of end-stage osteoclasts with PMMA particles did not result in an increased number of TRAP-positive MNCs and there was no increase in bone resorption.

INTERPRETATION

Treatment of mature osteoclasts with PMMA particles resulted in an elevated number of TRAP-positive cells. This persisted over a longer period of time than at the other stages of osteoclast development, and there was also a greater increase in bone resorption.

摘要

背景

磨损颗粒碎片与植入物-骨界面处的细胞之间的相互作用是关节置换术中假体周围骨丢失的一个重要促成因素。

方法

为了研究这种颗粒诱导反应对破骨细胞成熟不同阶段的影响,在培养的第0天、第4天或第8天,将聚甲基丙烯酸甲酯(PMMA)颗粒添加到小鼠破骨细胞生成骨髓细胞培养系统中,分别代表对破骨细胞前体、成熟破骨细胞或终末期破骨细胞的PMMA颗粒刺激。测量培养物中抗酒石酸酸性磷酸酶(TRAP)阳性多核细胞(MNCs)的数量和骨吸收程度。

结果

用PMMA颗粒处理破骨细胞前体导致TRAP阳性MNCs数量在统计学上显著增加,并持续4天,但骨吸收没有显著增加。向成熟破骨细胞中添加颗粒导致TRAP阳性MNCs数量显著增加,持续8天,同时骨吸收也显著增加。用PMMA颗粒处理终末期破骨细胞并未导致TRAP阳性MNCs数量增加,骨吸收也没有增加。

解读

用PMMA颗粒处理成熟破骨细胞导致TRAP阳性细胞数量增加。这比破骨细胞发育的其他阶段持续的时间更长,并且骨吸收也有更大的增加。