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

虽然许多研究报道了功能障碍状态下牙周韧带（PDL）的结构变化，但细胞因子生长因子的相关性尚不清楚。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。为了研究功能减退的PDL及其恢复情况，我们重点研究了白细胞介素-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出现萎缩变化，IL-1上调，FGF-2表达降低，而在恢复过程中，IL-1降低，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不同于炎症反应愈合过程中的调节。我们的研究还发现，咬合刺激促进了PDL细胞的增殖和分化，增强了一氧化氮（NO）的合成，而缺乏咬合刺激减少了一氧化氮的合成，引起PDL细胞的萎缩变化，导致牙槽关节强直。这些结果表明，咬合力等机械刺激是PDL再生的重要因素，可受NO和细胞因子生长因子的调控。

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.