Xu Yang, Wang Lufei, Sun Yao, Han Xianglong, Gao Tian, Xu Xin, Chen Tian, Zhao Xuefeng, Zeng Huan, Wang Yanmin, Bai Ding
Department of Orthodontics, State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Department of Oral Implantology, Dental Transformation Medical Center, College of Stomatology, Tongji University, Shanghai 200011, P.R. China.
Exp Ther Med. 2016 May;11(5):1812-1818. doi: 10.3892/etm.2016.3124. Epub 2016 Mar 2.
Bone loss is caused by occlusal hypofunction and is a serious health concern. This is particularly true of tooth loss, which is common in the elderly. However, the cellular and molecular mechanisms underlying bone loss have yet to be fully elucidated. Sclerostin and Wnt/β-catenin signaling have previously been reported to serve important roles in regulating bone remodeling. Therefore, the present study aimed to investigate the involvement of sclerostin and Wnt/β-catenin signaling in occlusal hypofunction-induced alveolar bone remodeling. The unilateral maxillary molars of 14 male Sprague-Dawley rats were extracted in order to establish a model of occlusal hypofunction. For each rat, the non-extraction side was treated as the control group for comparisons with the extraction side. At 8 weeks after tooth extraction, the rats were sacrificed and alveolar bone specimens were harvested for X-ray radiography, micro-computed tomography (CT) and histological and immunohistochemical examinations. Bone loss and architecture deterioration were observed at the occlusal hypofunction side. The bone mineral density was markedly decreased and the ratio of bone volume to total volume was significantly decreased at the hypofunction side, as compared with the control side (P<0.001). In addition, the number of osteoclasts at the hypofunction side were significantly increased compared with that in the control side (P<0.001), as demonstrated using tartrate-resistant acid phosphatase staining. Furthermore, the protein expression levels of sclerostin and receptor activator of nuclear factor-κB ligand were increased, whereas those of β-catenin were decreased, at the hypofunction side when compared with the control side. In conclusion, the results of the present study suggested that occlusal hypofunction-induced bone loss may be associated with upregulated expression of sclerostin, which, in turn, may inhibit the activity of the Wnt/β-catenin signaling pathway.
咬合功能减退会导致骨质流失，这是一个严重的健康问题。牙齿缺失的情况尤其如此，在老年人中很常见。然而，骨质流失背后的细胞和分子机制尚未完全阐明。此前有报道称，硬化蛋白和Wnt/β-连环蛋白信号通路在调节骨重塑中发挥重要作用。因此，本研究旨在探讨硬化蛋白和Wnt/β-连环蛋白信号通路在咬合功能减退诱导的牙槽骨重塑中的作用。为建立咬合功能减退模型，拔除了14只雄性Sprague-Dawley大鼠的单侧上颌磨牙。对于每只大鼠，将未拔牙侧作为对照组，与拔牙侧进行比较。拔牙后8周，处死大鼠，采集牙槽骨标本进行X线摄影、显微计算机断层扫描（CT）以及组织学和免疫组织化学检查。在咬合功能减退侧观察到骨质流失和结构破坏。与对照组相比，功能减退侧的骨矿物质密度显著降低，骨体积与总体积之比也显著降低（P<0.001）。此外，使用抗酒石酸酸性磷酸酶染色显示，功能减退侧的破骨细胞数量与对照组相比显著增加（P<0.001）。此外，与对照组相比，功能减退侧的硬化蛋白和核因子κB受体活化因子配体的蛋白表达水平升高，而β-连环蛋白的表达水平降低。总之，本研究结果表明，咬合功能减退诱导的骨质流失可能与硬化蛋白表达上调有关，而硬化蛋白又可能抑制Wnt/β-连环蛋白信号通路的活性。
