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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >Endosseous implant anchorage is critically dependent on mechanostructural determinants of peri-implant bone trabeculae.
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Endosseous implant anchorage is critically dependent on mechanostructural determinants of peri-implant bone trabeculae.

机译:骨内植入物的锚固严重取决于植入物周围骨小梁的机械结构决定因素。

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摘要

Low bone mass is highly prevalent among patients receiving endosseous implants. In turn, the implantation prognosis in low-density skeletal sites is poor. However, little is known about the mechanostructural determinants of implant anchorage. Using metabolic manipulations that lead to low bone density and to its rescue, we show here that anchorage is critically dependent on the peri-implant bone (PIB). Titanium implants were inserted horizontally into the proximal tibial metaphysis of adult rats 6 weeks after orchiectomy (ORX) or sham ORX. Systemic intermittent administration of human parathyroid hormone (1-34) [iahPTH(1-34)] or vehicle commenced immediately thereafter for 6 weeks. The bone-implant apparatus was then subjected to image-guided failure assessment, which assesses biomechanical properties and microstructural deformation concomitantly. Anchorage failure occurred mainly in PIB trabeculae, 0.5 to 1.0 mm away from the implant. Mechanically, the anchorage performed poorly in ORX-induced low-density bone, attributable mainly to decreased trabecular number. iahPTH(1-34) rescued the PIB density and implant mechanical function by augmenting trabecular thickness (Tb.Th). However, implant biomechanical properties in low-density bone were relatively insensitive to implant surface treatment that affected only the osseointegration (%bone-implant contact). These results support a model wherein anchorage failure involves buckling of the weakest trabecular struts followed by sequential failure of the stronger trabeculae. Treatment with iahPTH(1-34) induced thicker struts, which were able to delay and even prevent failure of individual elements, thus implicating trabecular thickness as a prime target for enhancing implant anchorage by systemic bone anabolic therapy.
机译:低骨量在接受骨内植入物的患者中非常普遍。反过来,低密度骨骼部位的植入预后很差。但是,关于植入物锚固的机械结构决定因素知之甚少。使用导致低骨密度及其抢救的代谢操作,我们在这里表明锚固严重依赖于种植体周围骨(PIB)。睾丸切除术(ORX)或假ORX术后6周,将钛植入物水平插入成年大鼠的胫骨近端干physi端。此后立即开始系统性间歇性给予人甲状旁腺激素(1-34)[iahPTH(1-34)]或媒介,持续6周。然后,对骨植入设备进行图像引导的失效评估,该评估同时评估了生物力学性能和微结构变形。锚固失败主要发生在距植入物0.5至1.0 mm的PIB小梁中。在机械方面,ORX诱导的低密度骨的锚固性能较差,主要归因于小梁数目减少。 iahPTH(1-34)通过增加小梁厚度(Tb.Th)挽救了PIB密度和植入物的机械功能。但是,低密度骨中的植入物生物力学特性对仅影响骨整合(%骨-植入物接触)的植入物表面处理相对不敏感。这些结果支持了一个模型,其中锚固破坏包括最弱的小梁支撑屈曲,随后是强小梁的连续破坏。用iahPTH(1-34)进行治疗可引起较粗的支杆,这些支杆能够延迟甚至防止单个元件的失效,因此暗示小梁厚度是通过全身骨合成代谢疗法增强植入物锚固的主要目标。

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