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A basic research on coupling factors between bone resorption and bone formation

骨吸收与骨形成耦合因素的基础研究

基本信息

批准号：
16592072
负责人：
HARA Yoshitaka
金额：
$ 2.24万
依托单位：
Nagasaki University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-16592072/
关键词：
B cell Bone resorption TNF-α RANKL OPG Immunohistological study Osteoclast 病理組織学的研究 Tリンパ球好中球 LPS

项目摘要

The involvement of RANKL and OPG in lipopolysaccharide-induced bone resorption is not well understood. So in the first study, we examined changes in the number of RANKL- and OPG-expressing cells when bone resorption was increased by repeated injections of LPS and decreased by additional injection of PBS. The number of RANKL-expressing inflammatory cells increased and OPG-expressing non-inflammatory cells decreased with enhancement of bone resorption. On the other hand, the number of OPG-expressing inflammatory cells increased with decrease of bone resorption. Of the inflammatory cells assay, RANKL-expressing T cells were detected in the lesions of mice with increased bone resorption and OPG-expressing polymorphonuclear leukocytes (PMN) were detected in the lesions of mice with decreased bone resorption. These results suggested that T cells and PMNs play important roles in the regulation of inflammatory bone resorption.The aim of the second study was to examine whether B cells truly influence inflammatory bone resorption in vivo. Alveolar bone resorption in normal mice, in SCID mice that lack both B and T cells, and in B cell-reconstituted SCID mice were compared histopathologically after repeated injections of lipopolysaccharide into mouse gingival. Furthermore, we examined whether the B cells that are stimulated by lipopolysaccharide are involved in osteoclastogenesis in vitro. As a result, the B cell-reconstituted SCID mice group showed stronger inflammatory bone resorption than the SCID mice group. Also, in vitro, lipopolysaccharide-stimulated B cells enhanced osteoclastogenesis and anti-TNF-α antibody completely blocked osteoclastogenesis induced by lipopolysaccharide-stimulated B cells. These results suggest that B cells promote inflammatory bone resorption through TNF-α.

RANKL 和 OPG 在脂多糖诱导的骨吸收中的作用尚不清楚。因此，在第一项研究中，我们检查了当重复注射 LPS 增加骨吸收并通过额外注射 PBS 减少骨吸收时，表达 RANKL 和 OPG 的细胞数量的变化。随着骨吸收的增强，表达RANKL的炎症细胞数量增加，表达OPG的非炎症细胞数量减少。另一方面，表达 OPG 的炎症细胞数量随着骨吸收的减少而增加。在炎症细胞测定中，在骨吸收增加的小鼠的病灶中检测到表达RANKL的T细胞，在骨吸收减少的小鼠的病灶中检测到表达OPG的多形核白细胞（PMN）。这些结果表明T细胞和PMN在炎症性骨吸收的调节中发挥重要作用。第二项研究的目的是检查B细胞是否真正影响体内炎症性骨吸收。将脂多糖重复注射到小鼠牙龈中后，对正常小鼠、缺乏 B 细胞和 T 细胞的 SCID 小鼠以及 B 细胞重建 SCID 小鼠的牙槽骨吸收进行组织病理学比较。此外，我们在体外检查了脂多糖刺激的 B 细胞是否参与破骨细胞生成。结果，B细胞重建的SCID小鼠组表现出比SCID小鼠组更强的炎性骨吸收。此外，在体外，脂多糖刺激的 B 细胞增强破骨细胞生成，抗 TNF-α 抗体完全阻断脂多糖刺激的 B 细胞诱导的破骨细胞生成。这些结果表明 B 细胞通过 TNF-α 促进炎症性骨吸收。