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Elucidation of molecular mechanism of alveolar bone remodeling induced by orthodontic force.

阐明正畸力诱导牙槽骨重塑的分子机制。

基本信息

批准号：
17592155
负责人：
KURIHARA Saburo
金额：
$ 2.24万
依托单位：
Matsumoto Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17592155/
关键词：
Osteoclast Albeolar bone resorption Human osteoclasts PGE_2 EP2 EP4 CD14-positive cells Osteoclast progenitors BMP 骨芽細胞 RANKL op opマウスリゼドロネート OPG カルシトニンビスフォスホネート

项目摘要

We have performed three experiments to elucidate the molecular mechanism by which alveolar bone remodeling induced by orthodontic force. The role of prostaglandin E2 (PGE_2) in osteoclastic bone resorption was carefully examined in this program.Exp. 1 : PGE_2 synergistically enhances RANKL-induced osteoclastic differentiation of the precursor cells. We investigated the mechanisms of the stimulatory effect of PGE_2 on osteoclast differentiation. The stimulatory effect of PGE_2 on the RANKL-induced osteoclast differentiation of the precursor cells was mediated through EP2 and EP4. TAK1 acted as an adapter molecule linking PKA-induced signals and RANKL-and TNFα-induced such signals in osteoclast precursors. Furthermore, TAK1 is involved in the synergistic effect of cAMP/PKA signals on TNF receptor-and Toll-like receptor 4 (TLR4)-induced signaling pathways. The cAMP/PKA signal may enhance bone resorption induced by RANKL and TNFα through TAK1 in osteoclast precursors.Exp. 2 : PGE_2 itself … More has been shown to directly inhibit bone-resorbing activity of osteoclasts. We explored the mechanism of PGE_2 action in the osteoclastic differentiation of precursor cells. The stimulatory effect of PGE_2 on the RANKL-induced osteoclast differentiation of the precursor cells was mediated through EP2 and EP4. TAK1 acted as an adapter molecule linking PKA-induced signals and RANKL-and TNFα-induced such signals in osteoclast precursors. Furthermore, TAK1 is involved in the synergistic effect of cAMP/PKA signals on TNF receptor-and Toll like receptor 4 (TLR4)-induced signaling pathways. The cAMP/PKA signal may enhance bone resorption induced by RANKL and TNFα through TAK1 in osteoclast precursors.Exp. 3 : We explored the role of PGE_2 in human osteoclast differentiation in more detail. Unlike mouse macrophage cultures, PGE_2 strongly inhibited RANKL-induced osteoclast formation in human CD14^+ cell cultures. Human osteoclast progenitors produced a soluble unidentified factor(s) in response to PGE_2, which strongly inhibited RANKL-induced osteoclast formation in not only human CD14^+ cell cultures but also mouse macrophage cultures. These results suggest that COX-2 inhibitors may not be suitable therapeutic agents to suppress osteoclastic bone resorption in inflammatory bone diseases. Less

我们通过三个实验来阐明正畸力诱导牙槽骨改建的分子机制。本研究旨在探讨前列腺素E_2（PGE_2）在骨细胞骨吸收中的作用。1：PGE_2协同增强RANKL诱导的前体细胞成骨分化。本研究探讨了PGE_2促进破骨细胞分化的机制。PGE_2对RANKL诱导的破骨细胞前体细胞分化的促进作用是通过EP 2和EP 4介导的。TAK 1作为连接破骨细胞前体中PKA诱导信号与RANKL和TNFα诱导的此类信号的衔接分子。此外，TAK 1参与cAMP/PKA信号对TNF受体和Toll样受体4（TLR 4）诱导的信号传导途径的协同作用。cAMP/PKA信号可能通过TAK 1增强RANKL和TNFα诱导的破骨细胞骨吸收。2：PGE_2本身 ...更多信息已显示直接抑制破骨细胞的骨再吸收活性。本研究探讨了PGE_2在前体细胞向成骨细胞分化中的作用机制。PGE_2对RANKL诱导的破骨细胞前体细胞分化的促进作用是通过EP 2和EP 4介导的。在破骨细胞前体中，TAK 1作为连接PKA诱导的信号和RANKL和TNFα诱导的信号的衔接分子。此外，TAK 1参与cAMP/PKA信号对TNF受体和Toll样受体4（TLR 4）诱导的信号传导途径的协同作用。cAMP/PKA信号可能通过TAK 1增强RANKL和TNFα诱导的破骨细胞骨吸收。3、进一步探讨PGE_2在人破骨细胞分化中的作用。与小鼠巨噬细胞培养物不同，PGE_2在人CD 14 ^+细胞培养物中强烈抑制RANKL诱导的破骨细胞形成。人破骨细胞祖细胞对PGE_2产生一种可溶性未知因子，这种因子不仅在人CD 14 ^+细胞培养物中，而且在小鼠巨噬细胞培养物中，都能强烈抑制RANKL诱导的破骨细胞形成。这些结果表明，考克斯-2抑制剂可能不是合适的治疗药物，以抑制骨吸收的炎性骨疾病。少

项目成果

期刊论文数量（18）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Cephalometric study of elderly with nearly intact dental arches.

牙弓几乎完整的老年人的头影测量研究。

DOI：
发表时间：
2006
期刊：
Gerodontology 23・(1)
影响因子：
0
作者：
Kataoka K. et al.;Misawa Y et al.;Kataoka K. et al.;Okafuji N et al.;Okafuji N et al.;Hagiwara Y. et al.;Hagiwara Y. et al.;Shimizu T et al.
通讯作者：
Shimizu T et al.

Nurse-like cells from patients with rheumatoid arthritis support survival of osteoclast precursors via macrophage-colony stimulating factor production.

来自类风湿性关节炎患者的护士样细胞通过巨噬细胞集落刺激因子的产生支持破骨细胞前体的存活。

DOI：
发表时间：
2005
期刊：
Arthritis Rheum 52・12
影响因子：
0
作者：
Nakamichi Y et al.;Tsukiyama K et al.;Itoh S et al.;Yamamoto Y et al.;Udagawa N et al.;Okumura S et al.;Nakamichi Y et al.;Tsukiyama K et al.;Itoh S et al.;Yamamoto Y et al.;Udagawa N et al.;Okumura S et al.;Takahashi N et al.;Yamaki M;Kobayashi Y;Kobayashi Y;Yang S;Take I;Tsuboi H
通讯作者：
Tsuboi H

Prostaglandin E2 receptors EP2 and EP4 are down-regulated during differentiation of mouse osteoclasts from their precursors

DOI：
10.1074/jbc.m500926200
发表时间：
2005-06-24
期刊：
JOURNAL OF BIOLOGICAL CHEMISTRY
影响因子：
4.8
作者：
Kobayashi, Y;Take, I;Takahashi, N
通讯作者：
Takahashi, N

Tissue reaction to poly (lactic-co-glycolic acid) copolymer membrane in rhBMP used rabbit experimental mandibular reconstruction

rhBMP 中聚乳酸-乙醇酸共聚物膜的组织反应用于兔实验性下颌骨重建

DOI：
发表时间：
2006
期刊：
Eur J Med Res 11・(9)
影响因子：
0
作者：
Kataoka K. et al.;Misawa Y et al.;Kataoka K. et al.;Okafuji N et al.;Okafuji N et al.;Hagiwara Y. et al.;Hagiwara Y. et al.;Shimizu T et al.;Hagiwara Yukari et al.;Okafuji N et al.;Terao Yutaka;Okafuji N et al.;Hino Ayako;Shimizu T et al.;Okafuji N et al.
通讯作者：
Okafuji N et al.

Effect of age on alveolar bone turnover adjacent to maxillary molar roots in male rats: A histomorphometric study