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APOPTOSIS OF OSTEOCLASTS AND INFLAMMATORY BONE

破骨细胞和炎症骨的凋亡

基本信息

批准号：
10557203
负责人：
OKAHASHI Nobuo
金额：
$ 3.2万
依托单位：
NATIONAL INSTITUTE OF INFECTIOUS DISEASES
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10557203/
关键词：
OSTEOCLAST APOPTOSIS PERIODONTITIS LIPOPOLYSACCHARIDE リポ多糖サイトカイン

项目摘要

Periodontitis often results in tooth loss due to inflammatory bone resorption. Bone resorption is mediated by osteoclasts. Although the differentiation pathway of osteoclasts is not well known at present, various inflammatory mediators are known to trigger the production of osteoclasts. We have found that lipopolysaccharides (LPS) of various periodontophatic bacteria mediate osteoclast formation and stimulate bone resorption in vitro. In this project, we investigate the mechanism of osteoclast differentiation mediated by LPS from a periodontophatic bacteria Actinobacillus actinomycetemcomitans.In mouse bone marrow cultures, LPS of A. actinomycetemocomitans induced osteoclast formation. Indomethacin and anti-IL-1 antibodies significantly inhibited the osteoclast formation, suggesting that prostaglandin E2 (PGE2) and IL-1 were involved in LPS-mediated osteoclast formation. We also found that LPS from A. actinomycetemcomitans induced expression of osteoclast differentiation factor (ODF) on cells of osteoblastic lineage. These results indicated that LPS of A. actinomycetemcomitans mediated osteoclast formation through upregulation of PGE2, IL-1 and ODF in periodontal tissues. Furthermore, we found that taurine, a sulfer containing amino acid, inhibited the osteoclast formation mediated by LPS from A. actinomycetemcomitans. Taurine was also found to inhibit the experimental bone resorption in ligature-mediated periodontitis in hamsters.

牙周炎常因炎症性骨吸收而导致牙齿脱落。破骨细胞介导骨吸收。虽然破骨细胞的分化途径目前还不清楚，但已知各种炎症介质可触发破骨细胞的产生。我们已经发现，各种牙周细菌的脂多糖（LPS）介导破骨细胞的形成和刺激骨吸收在体外。本课题旨在研究伴放线放线杆菌（Actinobacillusactinomycetemcomitans）的脂多糖（LPS）诱导破骨细胞分化的机制。放线菌共生菌诱导破骨细胞形成。吲哚美辛和抗IL-1抗体显着抑制破骨细胞的形成，表明前列腺素E2（PGE 2）和IL-1参与LPS介导的破骨细胞的形成。我们还发现A.伴放线菌可诱导成骨细胞系破骨细胞分化因子（ODF）的表达。这些结果表明，A.伴放线菌通过上调牙周组织中PGE 2、IL-1和ODF介导破骨细胞的形成。此外，我们发现含硫氨基酸牛磺酸可抑制LPS介导的破骨细胞形成。伴放线菌牛磺酸还被发现抑制仓鼠结扎介导的牙周炎的实验性骨吸收。