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首页> 外文期刊>Tissue engineering, Part C. Methods >Establishment of an in vivo model for molecular assessment of titanium implant osseointegration in compromised bone.
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Establishment of an in vivo model for molecular assessment of titanium implant osseointegration in compromised bone.

机译：建立用于评估受损骨中钛植入物骨整合的分子评估的体内模型。

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Shortening of the healing time before loading risks impeding successful titanium implant anchorage into compromised bone. A thorough understanding at the genetic scale of the early phases of bone regeneration at the implant interface is required before the development of strategies to enhance implant osseointegration. In this study a new in vivo implant model to explore the mechanism by which titanium implant osseointegration is affected by the host bone properties is presented. An implant was conceptualized enabling standardized harvesting of peri-implant tissue for quantitative molecular analysis while preserving the mimicking of the clinical setting. The implant is partly indented to provide a well-defined healing compartment from where tissue differentiation and de novo bone formation can be investigated and partly screw-threaded to provide a good implant anchorage into the bone. The feasibility of the implant design was assessed in osteopenic bone conditions, evoked by simulated weightlessness. Wistar rats were either hindlimb unloaded by tail suspension (HU) for 9 days or acted as controls (CTL). The status of compromised bone tissue through 9-days HU was confirmed by micro-X-ray computed tomography. The implant was installed in the proximal tibial bone 7 days after the onset of HU or CTL. Two days postimplantation, the peri-implant regenerating tissue responses were recorded by measuring expression of inflammatory, angiogenic, and bone resorption parameters (hypoxia-inducible factor 1, alpha subunit; vascular endothelial growth factor A; angiopoietin 1; endothelial PAS domain protein 1; fibroblast growth factor 2; tumor necrosis factor; interleukin 11; acid phosphatase 5, tartrate resistant; tumor necrosis factor (ligand) superfamily, member 11/RANKL). We successfully demonstrated that HU-associated bone conditions evoked a significant alteration of expression of the angiogenic markers in the peri-implant regenerative tissue during initial implant osseointegration, whereas the expression levels of the inflammatory and bone resorption parameters remained unchanged. We concluded that this in vivo implant model provides a well-designed and controlled method to examine molecular responses in implant osseointegration to impaired bone conditions. This model may serve to explore the application of anabolic strategies in peri-implant osteogenesis.
机译：加载前缩短愈合时间可能会导致钛植入物无法成功锚定到受损骨中。在开发增强植入物骨整合的策略之前，需要对植入物界面的骨再生早期阶段的遗传尺度有一个全面的了解。在这项研究中，提出了一种新的体内植入物模型，以探索钛植入物骨整合受宿主骨特性影响的机理。对植入物进行了概念化，从而可以标准化收集植入物周围组织用于定量分子分析，同时保留模拟的临床环境。将植入物部分缩进以提供一个明确的愈合隔室，从中可以研究组织分化和从头形成的骨骼，并部分拧入螺纹以提供良好的植入物锚固到骨骼中。通过模拟失重诱发的骨质疏松骨状况评估了植入物设计的可行性。 Wistar大鼠要么通过尾部悬吊（HU）卸载9天，要么作为对照组（CTL）。通过X线计算机X线断层扫描（X射线计算机断层扫描）证实了经过9天的HU后受损的骨组织的状态。 HU或CTL发作后7天，将植入物安装在胫骨近端。植入后两天，通过测量炎症，血管生成和骨吸收参数（缺氧诱导因子1，α亚基;血管内皮生长因子A;血管生成素1;内皮PAS结构域蛋白1;抗氧化剂）的表达来记录植入物周围的再生组织反应。成纤维细胞生长因子2;肿瘤坏死因子;白介素11;酸性磷酸酶5，酒石酸耐药;肿瘤坏死因子（配体）超家族，成员11 / RANKL）。我们成功地证明，与HU相关的骨质状况引起了植入初期骨整合过程中植入物周围再生组织中血管生成标记物表达的显着改变，而炎症和骨吸收参数的表达水平却保持不变。我们得出的结论是，这种体内植入物模型提供了一种设计良好且可控的方法，可以检查植入物骨整合中对受损骨质状况的分子反应。该模型可能有助于探索合成代谢策略在种植体周围成骨中的应用。

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