4.3 Article

Micro-osteoperforations accelerate orthodontic tooth movement by stimulating periodontal ligament cell cycles

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MOSBY-ELSEVIER
DOI: 10.1016/j.ajodo.2018.01.023

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  1. Japan Society for the Promotion of Science [15H06648, 16K11795, 16K11796, 16K20656, 17K17339]

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Introduction: 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-alpha), proliferating cell nuclear antigen (PCNA), and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) during experimental tooth movement. Methods: 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 inves-tigated tooth movement and alveolar bone microstructure using microcomputed tomography (n = 5). We also determined the expression of TNF-alpha and PCNA in the pressure sides of periodontal ligaments via an immuno-histochemical analysis. The expression of apoptotic cells was also determined by the TUNEL method. Results: 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-alpha 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. Conclusions: These results suggest that MOPs may accelerate tooth movement through activation of cell proliferation and apoptosis of periodontal ligament cells.

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