Department of Orthodontics, School of Dentistry, Nihon University, Matsudo, Chiba, Japan.
Department of Orthodontics, School of Dentistry, Nihon University, Matsudo, Chiba, Japan.
Am J Orthod Dentofacial Orthop. 2018 Dec;154(6):788-796. doi: 10.1016/j.ajodo.2018.01.023.
The aim of this study was to investigate the mechanism of how micro-osteoperforations (MOPs) accelerate tooth movement. We focused on inflammation, cell proliferation, and apoptosis of periodontal ligament cells and performed immunostaining of MOPs exposed to tumor necrosis factor-alpha (TNF-α), proliferating cell nuclear antigen (PCNA), and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) during experimental tooth movement.
Eleven-week-old male Wistar rats were divided into 2 groups: (1) 10 g of orthodontic force applied to the maxillary first molar (TM) and (2) force application plus 3 small perforations of the cortical plate (TM + MOPs). On days 1, 4, 7, 10, and 14 after force application, we investigated tooth movement and alveolar bone microstructure using microcomputed tomography (n = 5). We also determined the expression of TNF-α and PCNA in the pressure sides of periodontal ligaments via an immunohistochemical analysis. The expression of apoptotic cells was also determined by the TUNEL method.
The tooth movement in the TM + MOPs group was significantly greater on days 4 to 14 than in the TM group. The TM + MOPs group showed statistically significant decreases in bone volume/tissue volume ratio and bone mineral density compared with the TM group. The ratios of TNF-α positive cells in the TM + MOPs group were increased on days 1, 4. 7, and 10 compared with the TM group. The ratios of PCNA positive cells in the TM + MOPs group were increased on days 1, 4, and 7 compared with the TM group, and the ratios of TUNEL positive cells in the TM + MOPs group were increased on days 1 and 7 compared with the TM group.
These results suggest that MOPs may accelerate tooth movement through activation of cell proliferation and apoptosis of periodontal ligament cells.
本研究旨在探讨微骨开窗(MOPs)加速牙齿移动的机制。我们关注牙周膜细胞的炎症、增殖和凋亡,并对暴露于肿瘤坏死因子-α(TNF-α)、增殖细胞核抗原(PCNA)和末端脱氧核苷酸转移酶 dUTP 缺口末端标记(TUNEL)的 MOPs 进行免疫染色,以研究实验性牙齿移动过程中的细胞反应。
将 11 周龄雄性 Wistar 大鼠分为 2 组:(1)上颌第一磨牙(TM)施加 10g 正畸力;(2)施加力加 3 个皮质板小穿孔(TM+MOPs)。在力施加后第 1、4、7、10 和 14 天,通过微计算机断层扫描(n=5)研究牙齿移动和牙槽骨微观结构。我们还通过免疫组织化学分析确定了牙周膜压力侧 TNF-α和 PCNA 的表达。通过 TUNEL 方法还确定了凋亡细胞的表达。
TM+MOPs 组在第 4 至 14 天的牙齿移动明显大于 TM 组。TM+MOPs 组的骨体积/组织体积比和骨密度与 TM 组相比均有统计学显著降低。与 TM 组相比,TM+MOPs 组在第 1、4、7 和 10 天 TNF-α阳性细胞比例增加。与 TM 组相比,TM+MOPs 组在第 1、4 和 7 天 PCNA 阳性细胞比例增加,TM+MOPs 组在第 1 和 7 天 TUNEL 阳性细胞比例增加。
这些结果表明,MOPs 可能通过激活牙周膜细胞的增殖和凋亡来加速牙齿移动。