Huang Chun-Yi, Le Huynh Hoai Thuong, Tsai Hsiao-Chi, Tang Chih-Hsin, Yu Jian-Hong
School of Dentistry, College of Dentistry, China Medical University, Taichung, Taiwan.
Department of Orthodontics, China Medical University Hospital Medical Center, Taichung, Taiwan.
J Dent Sci. 2024 Jul;19(3):1452-1460. doi: 10.1016/j.jds.2024.03.023. Epub 2024 Mar 30.
BACKGROUND/PURPOSE: Osteoclast differentiation is crucial for orchestrating both tooth movement and the maintenance of bone density. Therefore, the current study sought to explore the impact of low-level laser therapy (LLLT) on osteoclast differentiation, functional gene expression, molecular signaling pathways, and orthodontic tooth movement in clinical settings.
The RAW 264.7 cell line served as the precursor for osteoclasts, and these cells underwent irradiation using a 808-nm LLLT. Osteoclast differentiation was assessed through tartrate-resistant acid phosphatase (TRAP) staining. Functional gene expression levels were evaluated using real-time quantitative polymerase chain reaction (RT-qPCR) while signaling molecules were examined through Western blot analysis. In the clinical study, 12 participants were enrolled. Their tooth movement was monitored using a TRIOS desktop scanner. Bone density measurements were conducted using Mimics software, which processed cone-beam computed tomography (CBCT) images exported in Digital Imaging and Communications in Medicine (DICOM) format.
We found that LLLT effectively promoted receptor activator of nuclear factor-κB ligand (RANKL)-dependent osteoclast differentiation and the expression of osteoclast functional genes, including matrix metallopeptidase 9 (MMP9), nuclear factor of activated T-cells cytoplasmic 1(NFATc1), tartrate-resistant acid phosphatase (TRAP) and cathepsin K (CTSK) in RAW264.7 cells. Clinically, the cumulative tooth movement over 90 days was significantly higher in the laser group than in the control group.
Our research demonstrates that LLLT not only significantly promotes osteoclast differentiation but is also a valuable adjunct in orthodontic therapy.
背景/目的：破骨细胞分化对于协调牙齿移动和维持骨密度至关重要。因此，本研究旨在探讨低强度激光疗法（LLLT）在临床环境中对破骨细胞分化、功能基因表达、分子信号通路和正畸牙齿移动的影响。
RAW 264.7细胞系用作破骨细胞的前体，这些细胞接受808nm低强度激光疗法照射。通过抗酒石酸酸性磷酸酶（TRAP）染色评估破骨细胞分化。使用实时定量聚合酶链反应（RT-qPCR）评估功能基因表达水平，同时通过蛋白质印迹分析检测信号分子。在临床研究中，招募了12名参与者。使用TRIOS台式扫描仪监测他们的牙齿移动。使用Mimics软件进行骨密度测量，该软件处理以医学数字成像和通信（DICOM）格式导出的锥形束计算机断层扫描（CBCT）图像。
我们发现低强度激光疗法有效地促进了RAW264.7细胞中核因子κB受体活化因子配体（RANKL）依赖性破骨细胞分化以及破骨细胞功能基因的表达，包括基质金属肽酶9（MMP9）\、活化T细胞核因子细胞质1（NFATc1）、抗酒石酸酸性磷酸酶（TRAP）和组织蛋白酶K（CTSK）。临床上，激光组90天内的累计牙齿移动明显高于对照组。
我们的研究表明，低强度激光疗法不仅能显著促进破骨细胞分化，也是正畸治疗中有价值的辅助手段。
