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Regulation of cytokine growth factor inhibits anakylosis and root resorption in transplanted teeth

细胞因子生长因子的调节抑制移植牙的强直和牙根吸收

基本信息

批准号：
17592129
负责人：
KANNO Zuisei
金额：
$ 2.11万
依托单位：
Tokyo Medical and 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-17592129/
关键词：
autotransplantation hypofunctional PDL inflammatory cytokine ankylosis root resorption regeneration of PDL

项目摘要

While many studies reported the structural changes in the periodontal ligament (PDL) under hypofunctional conditions, the associations of cytokine growth factors are still unclear. They are known to take part in inflammation, and may affect the biological properties of hypofunctional tooth. To investigate the hypofunctional PDL and the recovery from this condition, we focused on interleukin-1 beta (IL-1) and basic fibroblast growth factor (FGF-2). The lack of occlusal stimuli caused atrophic changes in the PDL with the upregulation of IL-1 and decreased expression of FGF-2, while decreased IL-1 and enhanced FGF-2 expression were observed in the recovery process. These results suggest that occlusal stimuli regulate IL-1 and FGF-2 expression, and the nature of this regulation may differ from that in the healing process of an inflammatory reaction.Our study also revealed that the occlusal stimuli promote the proliferation and differentiation of PDL cells with enhanced nitric oxide (NO) synthesis, while the lack of occlusal stimuli reduced the NO synthesis and induced atrophic changes in PDL which resulted in the dentoalveolar ankylosis.Those results clarified that the mechanical stimulus, such as occlusal force, is an important factor for the regeneration of PDL, which could be regulated by NO and cytokine growth factors.

虽然许多研究报告了功能低下条件下牙周膜（PDL）的结构变化，但细胞因子生长因子的关联仍不清楚。已知它们参与炎症，并可能影响功能低下牙齿的生物学特性。为了研究 PDL 功能低下及其恢复情况，我们重点关注白细胞介素 1 β (IL-1) 和碱性成纤维细胞生长因子 (FGF-2)。缺乏咬合刺激导致PDL萎缩性变化，IL-1上调，FGF-2表达减少，而在恢复过程中观察到IL-1减少和FGF-2表达增强。这些结果表明，咬合刺激调节IL-1和FGF-2的表达，这种调节的性质可能与炎症反应愈合过程中的调节不同。我们的研究还发现，咬合刺激促进PDL细胞的增殖和分化，增强一氧化氮（NO）合成，而咬合刺激的缺乏则减少NO合成并诱导PDL萎缩性变化。结果表明，咬合力等机械刺激是PDL再生的重要因素，NO和细胞因子生长因子可以调节牙槽骨再生。