Effects of substrate strain and mechanical damage on osteocyte around implant

骨中自然含有微损伤，并被认为会引发骨重塑。骨细胞存在于骨基质中，形成三维细胞-细胞网络，为检测微损伤附近的局部力学环境提供细胞基础，可能参与骨重塑的启动机制。这次我们展示了骨细胞在种植体周围破骨细胞发生初期的作用，在胶原凝胶中三维培养骨细胞样细胞系MLO-Y4细胞，并施加循环拉伸样咬合力。在体内研究中，取大鼠右侧上颌第一磨牙，植入3种种植体（无负荷、合理负荷、超载）。在植入后1、2、4周处死大鼠，制作未钙化的地面切片。用荧光染色法检测骨细胞周围的微裂纹，并用Villanueva Goldner染色法对标本进行染色，计算骨体积。结果，每个标本在种植体周围都有新的骨形成，但这些骨质量是矿化程度较低的骨。因此骨细胞不能显示这些观察期。未来，我们将继续对种植体周围骨重塑进行长期观察。在体外实验中，我们建立了一种加载装置，将骨细胞样细胞系MLO-Y4细胞三维培养于胶原凝胶中，并在近咬合力下进行循环拉伸。机械组RANKL水平显著高于非机械组。我们的数据表明，当mlo - y4细胞受到机械损伤时，M-CSF和RANKL的膜结合形式被释放，因此可以作为骨重塑的“靶向”信号。

Microdamage is naturally contained in bone and has been considered to trigger bone remodeling. Osteocytes, which exist in bone matrix forming 3-D cell-to-cell network, provide cellular basis to detect local mechanical environment neighboring the microdamage, and should be involved in the initiating mechanism of bone remodeling. This time we demonstrate the role of osteocytes in the initial phase of osteoclastogenesis around implant, osteocyte-like cell line MLO-Y4 cells were three-dimensionally cultured inside col- lagen gel and subjected to cyclic stretching like occlusal force.In vivo study, right maxillary first molars were extirpated from rats and implanted with 3 types of implants (non-load, reasonable-load, over loaded). At 1, 2 and 4 weeks after implantation, rats were sacrificed and undecalcified ground sections were fabricated. We examined microcracks around osteocytes by fluorescent stain and after that, the specimens were stained with the Villanueva Goldner stain and bone volume was calculated. As a results, every specimens showed new bone formation around implants, but these bone qualities were less mineralized bone. So osteocyte could not showed these observation period. In the future, we continue to examine bone remodeling around implant long period of observation.In vitro study, we established a loading apparatus in which osteocyte-like cell line MLO-Y4 cells were three-dimensionally cultured inside collagen gel and subjected to cyclic stretching in near occlusal force. According to the level of RANKL in mechanical group were significantly higher than those in the non-mechanical group. Our data suggested that when MLO-Y4cells are mechanically damaged, the membrane-bound forms of M-CSF and RANKL are released, and could thus act as a “targeting” signal to bone remodeling.