Ikeda Masaaki, Yoshimura Yoshitaka, Kikuiri Takashi, Matsuno Mino, Hasegawa Tomokazu, Fukushima Kumu, Hayakawa Takako, Minamikawa Hajime, Suzuki Kuniaki, Iida Junichiro
Department of Orthodontics, Hokkaido University Graduate School of Dental Medicine, Sapporo, Hokkaido 060‑8586, Japan.
Department of Molecular Cell Pharmacology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Hokkaido 060‑8586, Japan.
Mol Med Rep. 2016 Nov;14(5):4699-4705. doi: 10.3892/mmr.2016.5801. Epub 2016 Oct 5.
Bone remodeling is an important factor in orthodontic tooth movement. During orthodontic treatment, osteoclasts are subjected to various mechanical stimuli, and this promotes or inhibits osteoclast differentiation and fusion. It has been previously reported that the release from tensile force induces osteoclast differentiation. However, little is known about how release from compressive force affects osteoclasts. The present study investigated the effects of release from compressive force on osteoclasts. The number of tartrate‑resistant acid phosphatase (TRAP)‑positive multinucleated osteoclasts derived from RAW264.7 cells was counted, and gene expression associated with osteoclast differentiation and fusion in response to release from compressive force was evaluated by reverse transcription‑quantitative polymerase chain reaction. Osteoclast number was increased by optimal compressive force application. On release from this force, osteoclast differentiation and fusion were suppressed. mRNA expression of NFATc1 was inhibited for 6 h subsequent to release from compressive force. mRNA expression of the other osteoclast‑specific genes, TRAP, RANK, matrix metalloproteinase‑9, cathepsin‑K, chloride channel 7, ATPase H+ transporting vacuolar proton pump member I, dendritic cell‑specific transmembrane protein and osteoclast stimulatory transmembrane protein (OC‑STAMP) was significantly inhibited at 3 h following release from compressive force compared with control cells. These findings suggest that release from optimal compressive force suppresses osteoclast differentiation and fusion, which may be important for developing orthodontic treatments.
骨重塑是正畸牙齿移动的一个重要因素。在正畸治疗过程中，破骨细胞受到各种机械刺激，这会促进或抑制破骨细胞的分化和融合。此前有报道称，拉力释放会诱导破骨细胞分化。然而，关于压力释放如何影响破骨细胞却知之甚少。本研究调查了压力释放对破骨细胞的影响。对源自RAW264.7细胞的抗酒石酸酸性磷酸酶（TRAP）阳性多核破骨细胞数量进行计数，并通过逆转录定量聚合酶链反应评估与压力释放反应中破骨细胞分化和融合相关的基因表达。施加最佳压力会增加破骨细胞数量。当从该压力释放时，破骨细胞的分化和融合受到抑制。在从压力释放后的6小时内，NFATc1的mRNA表达受到抑制。与对照细胞相比，在从压力释放后3小时，其他破骨细胞特异性基因TRAP、RANK、基质金属蛋白酶-9、组织蛋白酶-K、氯离子通道7、ATP酶H +转运液泡质子泵成员I、树突状细胞特异性跨膜蛋白和破骨细胞刺激跨膜蛋白（OC-STAMP）的mRNA表达显著受到抑制。这些发现表明，从最佳压力释放会抑制破骨细胞的分化和融合，这可能对开发正畸治疗方法很重要。
