Analysis of periodontal ligament cells derived from permanent teeth and primary teeth on tooth root resorption.
恒牙和乳牙来源的牙周膜细胞对牙根吸收的影响分析。
基本信息
- 批准号:18592239
- 负责人:
- 金额:$ 2.49万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2006
- 资助国家:日本
- 起止时间:2006 至 2007
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Although root resorption of deciduous teeth occurs physiologically in periods of permanent tooth eruption, abnormal root resorption frequently occurs when bacterial infection in the root canal caused inflammation around the root apex. Moreover, root resorption of a deciduous tooth sometimes occurs spontaneously when the succeeding permanent tooth is lacking. Therefore, it is possible that periodontal ligament (PDL) cells can play a role in root resorption by regulating osteoclastogenesis.This study investigated the effect of amelogenin on osteoclastogenesis. In co-cultures with calvaria osteoblasts and purified bone marrow cells, amelogenin inhibited osteoclastogenesis. Futhermore, amelogenin inhibited the expression of receptor activator of nuclear factor kappaB ligand (RANKL) ,macrophage-colony stimulating factor (M-CSF) and fibronectin in osteoblasts, while RANKL expression was induced by fibronectin and inhibited by treatment with fibronectin small interfering RNA. These results suggest that the inhibitory effect of amelogenin on osteoclastogenesis lead to downregulation of RANKL, M-CSF and fibronectin production in osteoblasts.Therefore, these data suggest that PDL cells which contain the epithelial rests of Malassez may inhibit root resorption.
虽然乳牙的牙根吸收发生在恒牙萌出的生理时期,但当根管中的细菌感染引起根尖周围的炎症时,经常发生异常牙根吸收。此外,乳牙的牙根吸收有时会在后续恒牙缺失时自发发生。因此,牙周膜细胞可能通过调节破骨细胞的生成而在牙根吸收中发挥作用。在与颅骨成骨细胞和纯化的骨髓细胞共培养中,釉原蛋白抑制破骨细胞的生成。氟替卡松、釉原蛋白抑制成骨细胞核因子κ B受体激活因子配体(RANKL)、巨噬细胞集落刺激因子(M-CSF)和纤连蛋白的表达,而RANKL的表达被纤连蛋白诱导,被纤连蛋白小干扰RNA抑制。这些结果表明,釉原蛋白抑制破骨细胞的生成,导致成骨细胞RANKL、M-CSF和FN的表达下调,因此,含有Malassez上皮剩余物的PDL细胞可能抑制牙根吸收。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Current topics in pharmacological research on bone metabolism : , osteoclast differentiation regulated by glycosphingolipids. Review
骨代谢药理学研究的当前主题:鞘糖脂调节的破骨细胞分化。
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Fukumoto,S.,Iwamoto;T.;Sakai;E.;Yuasa,K.;Fukumoto,E.;Yamada,A.;Hasegawa,T.;Nonaka,K.;KatoY
- 通讯作者:KatoY
Amelogenin is a negative regulator of osteoclastogenesis via downregulation of RANKL, M-CSF and fibronectin expression in osteoblasts
- DOI:10.1016/j.archoralbio.2006.09.016
- 发表时间:2007-03-01
- 期刊:
- 影响因子:3
- 作者:Nishiguchi, Miyuki;Yuasa, Kenji;Fukumoto, Satoshi
- 通讯作者:Fukumoto, Satoshi
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HASEGAWA Tomokazu其他文献
HASEGAWA Tomokazu的其他文献
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{{ truncateString('HASEGAWA Tomokazu', 18)}}的其他基金
Effect of CCL11 derived from deciduous tooth on pulp and root resorption
乳牙来源的CCL11对牙髓和牙根吸收的影响
- 批准号:
20K10205 - 财政年份:2020
- 资助金额:
$ 2.49万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
homeostatic regulation and regeneration of periodontal ligament tissues
牙周膜组织的稳态调节和再生
- 批准号:
16K11804 - 财政年份:2016
- 资助金额:
$ 2.49万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Study of periodontal ligament tissue function about maintaining homeostasis and regeneration in periodontal tissues, and development of new regeneration therapy in periodontal tissues.
研究牙周膜组织对维持牙周组织稳态和再生的功能,开发新的牙周组织再生疗法。
- 批准号:
25463182 - 财政年份:2013
- 资助金额:
$ 2.49万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Establishment of periodontal ligament (PDL) cells derived from deciduous teeth and periodontal tissue regeneration with PDL cells.
乳牙来源的牙周膜(PDL)细胞的建立以及PDL细胞的牙周组织再生。
- 批准号:
22592296 - 财政年份:2010
- 资助金额:
$ 2.49万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Analysis of genetic risk factors in periodontal diseses ― Effect of cellular aging on damage of cells ―
牙周病遗传危险因素分析―细胞衰老对细胞损伤的影响―
- 批准号:
12557178 - 财政年份:2000
- 资助金额:
$ 2.49万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Establishment of Human Fibroblasts deribed from Dental Pulp Tissues of Primary Teeth and Permanent Teeth, and Development of Systems of Cytotoxicity Tests for Dental Materials
乳牙和恒牙牙髓组织中人成纤维细胞的建立以及牙科材料细胞毒性测试系统的开发
- 批准号:
08672378 - 财政年份:1996
- 资助金额:
$ 2.49万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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