Involvement of apoptosis of cementoblast in orthodontic root resorption

成牙骨质细胞凋亡参与正畸牙根吸收

• 批准号: 23593044
• 负责人: KASAI KAZUTAKA
• 金额: $ 3.33万
• 依托单位: Nihon University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23593044/
• 关键词: 歯根吸収; アポトーシス; 破歯細胞; セメント細胞; 歯根膜細胞; 歯科矯正学; 矯正治療

The effect of compression force on periodontal ligament (PDL) plays a critical role in orthodontic tooth movement. However, little is known about this effect on apoptosis and the underlying reactive mechanisms in PDL cells. This study focuses on the application of compression force associated with reactive oxygenspecies (ROS)-induced apoptosis in PDL cells.The cell cycle and apoptosis wereassessed in compression force-treated PDL cells using flow cytometry. In vivo study revealed an increased number of terminal transferase-mediated dUTP nick end labeling (TUNEL) and caspase 8-positive cells in the orthodontic force group. In our in vitro study model, the compression force increased the G1 phase and apoptotic cells. A large increase in the intracellular ROS levels in human (h) PDL cells was observed in the compression force group. These results provide new information on compression force-induced G1 arrestand apoptosis in hPDL cells.

压力对牙周膜的影响在正畸牙齿移动中起着至关重要的作用。然而，对PDL细胞中这种对细胞凋亡的影响和潜在的反应机制知之甚少。本研究旨在探讨压力对活性氧合酶(ROS)诱导的PDL细胞凋亡的影响，并用流式细胞仪检测压力对PDL细胞周期和细胞凋亡率的影响。体内研究显示，正畸力组末端转移酶介导的dUTP缺口末端标记(TUNEL)和caspase8阳性细胞数量增加。在我们的体外研究模型中，压力增加了G1期细胞和凋亡细胞。加力组人(H)PDL细胞内ROS水平显著升高。这些结果为压迫力诱导hPDL细胞G1期阻滞细胞凋亡提供了新的信息。

项目成果

Orthodontic Root Resorption was Associated with the Secretion of IL-6 and IL-8 Stimulated by IL-17in Dental Pulp Cells

• DOI: 10.5466/ijoms.11.172
• 发表时间: 2013
• 期刊: International Journal of Oral-Medical Sciences
• 作者: Mami Shimizu;M. Yamaguchi;M. Asano;S. Fujita;T. Utsunomiya;Hirotsugu Yamamoto;K. Kasai

TNF-αaggravates The Progression of OIIRR in The Presence of RANKL

RANKL 存在时 TNF-α 会加重 OIIRR 的进展

• 发表时间: 2014
• 期刊: J Hard Tissue Biol
• 影响因子: 0.4
• 作者: Yoshino T;Yamaguchi M;Shimizu M;Yamada K;Kasai K
• 通讯作者: Kasai K

Immunohistochemical localization of T-helper 17 cells, IL-17, and RANKL during root resorption induced by excessive orthodontic force in a mouse model of T cell-mediated autoimmune disease.

在 T 细胞介导的自身免疫性疾病小鼠模型中，过度正畸力诱导牙根吸收过程中 T 辅助细胞 17 细胞、IL-17 和 RANKL 的免疫组织化学定位。

• 发表时间: 2013
• 期刊: International Journal of Oral-Medical Sciences
• 作者: Yamaguchi M;Yamada M;Asano M;Fujita S;Kasai K.
• 通讯作者: Kasai K.

TNF-αはRANKLと相乗的に歯根吸収を増悪させる

TNF-α 与 RANKL 协同加剧牙根吸收

• 发表时间: 2013
• 作者: 吉野智一;山口大;清水真美;山田邦彦;菊田純;葛西一貴
• 通讯作者: 葛西一貴

根吸収はNotchシグナルを介したIL-6、RANKL発現によって誘発される

IL-6、RANKL 表达通过 Notch 信号传导诱导根吸收

• 发表时间: 2013
• 作者: 菊田純;山口大;清水真美;菊田純;葛西一貴
• 通讯作者: 葛西一貴