School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
School of Oral Hygiene, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
Int Endod J. 2019 Jan;52(1):28-43. doi: 10.1111/iej.12962. Epub 2018 Jun 27.
To investigate whether static magnetic fields (SMFs) have a positive effect on the migration and dentinogenesis of dental pulp stem cells (DPSCs) to promote reparative dentine formation.
In vitro scratch assays and a traumatic pulp exposure model were performed to evaluate the effect of 0.4-Tesla (T) SMF on DPSC migration. The cytoskeletons of the DPSCs were identified by fluorescence immunostaining and compared with those of a sham-exposed group. Dentinogenic evaluation was performed by analysing the expressions of DMP-1 and DSPP marker genes using a quantitative real-time polymerase chain reaction (qRT-PCR) process. Furthermore, the formation of calcified deposits was examined by staining the dentinogenic DPSCs with Alizarin Red S dye. Finally, the role played by the p38 MAPK signalling pathway in the migration and dentinogenesis of DPSCs under 0.4-T SMF was investigated by incorporating p38 inhibitor (SB203580) into the in vitro DPSC experiments. The Student's t-test and the Kruskal-Wallis test followed by Dunn's post hoc test with a significance level of P < 0.05 were used for statistical analysis.
The scratch assay results revealed that the application of 0.4-T SMF enhanced DPSCs migration towards the scratch wound (P < 0.05). The cytoskeletons of the SMF-treated DPSCs were found to be aligned perpendicular to the scratch wound. After 20 days of culture, the SMF-treated group had a greater number of out-grown cells than the sham-exposed group (nonmagnetized control). For the SMF-treated group, the DMP-1 (P < 0.05) and DSPP genes (P < 0.05), analysed by qRT-PCR, exhibited a higher expression. The distribution of calcified nodules was also found to be denser in the SMF-treated group when stained with Alizarin Red S dye (P < 0.05). Given the incorporation of p38 inhibitor SB203580 into the DPSCs, cell migration and dentinogenesis were suppressed. No difference was found between the SMF-treated and sham-exposed cells (P > 0.05).
0.4-T SMF enhanced DPSC migration and dentinogenesis through the activation of the p38 MAPK-related pathway.
研究静磁场（SMF）是否对牙髓干细胞（DPSCs）的迁移和牙本质生成有积极作用，以促进修复性牙本质形成。
采用体外划痕试验和创伤性牙髓暴露模型，评估 0.4 特斯拉（T）SMF 对 DPSC 迁移的影响。通过荧光免疫染色鉴定 DPSCs 的细胞骨架，并与假暴露组进行比较。通过定量实时聚合酶链反应（qRT-PCR）过程分析 DMP-1 和 DSPP 标记基因的表达，进行牙本质生成评价。此外，通过茜素红 S 染料对牙本质生成的 DPSCs 进行染色，检查钙化沉积物的形成。最后，通过将 p38 抑制剂（SB203580）加入体外 DPSC 实验，研究 0.4-T SMF 下 p38 MAPK 信号通路在 DPSCs 迁移和牙本质生成中的作用。采用 Student's t 检验和 Kruskal-Wallis 检验，随后进行 Dunn 事后检验，显著性水平 P<0.05。
划痕试验结果表明，应用 0.4-T SMF 增强了 DPSCs 向划痕伤口的迁移（P<0.05）。SMF 处理的 DPSCs 的细胞骨架被发现垂直于划痕伤口排列。培养 20 天后，与假暴露组（非磁化对照）相比，SMF 处理组有更多的细胞向外生长。对于 SMF 处理组，通过 qRT-PCR 分析，DMP-1（P<0.05）和 DSPP 基因（P<0.05）表达更高。用茜素红 S 染料染色时，也发现 SMF 处理组的钙化结节分布更密集（P<0.05）。由于将 p38 抑制剂 SB203580 加入到 DPSCs 中，细胞迁移和牙本质生成受到抑制。SMF 处理组和假暴露组之间没有差异（P>0.05）。
0.4-T SMF 通过激活 p38 MAPK 相关途径增强 DPSC 的迁移和牙本质生成。
