Effects of substrate strain and mechanical damage on osteocyte around implant

微损伤自然地包含在骨中，并被认为是引发骨重建的原因。骨细胞存在于骨基质中，形成三维的细胞-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，并参与骨重建的启动机制。本研究旨在探讨骨细胞在种植体周围破骨细胞形成的早期阶段中的作用，将骨细胞样细胞系MLO-Y 4细胞在胶原凝胶中进行三维培养，并使其受到类似咬合力的周期性牵拉。在植入后1、2和4周，处死大鼠并制作不脱钙的研磨切片。荧光染色观察骨细胞周围的微裂隙，VillanuevaGoldner染色后计算骨体积。结果表明，每个样本都显示种植体周围有新骨形成，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。在体外研究中，我们建立了一个加载装置，将骨细胞样细胞系MLO-Y 4细胞在胶原凝胶中三维培养，并在近咬合力下进行循环拉伸。机械组RANKL水平明显高于非机械组。我们的数据表明，当MLO-Y 4细胞受到机械损伤时，M-CSF和RANKL的膜结合形式被释放，因此可以作为骨重建的“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.