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首页> 外文会议>ASME Bioengineering Conference >MICROMOTIONS AT THE BONE IMPLANT INTERFACE UP-REGULATE OSTEOBLASTS-MEDIATED ACTIVATION OF OSTEOCLASTS IN EX VIVO HUMAN SAMPLES
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MICROMOTIONS AT THE BONE IMPLANT INTERFACE UP-REGULATE OSTEOBLASTS-MEDIATED ACTIVATION OF OSTEOCLASTS IN EX VIVO HUMAN SAMPLES

机译：骨植入界面的微调上调成骨细胞介导的骨液活化在离体人样品中的破骨细胞活化

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摘要

A radiolucent zone at the interface of bone and implants in total joint prosthesis is frequently observed in uncemented and cemented implants. This radiolucent zone, representing a fibrous tissue, is the result of the progressive deterioration of the bone surrounding implants. Fibrous tissues affect the implant fixation, increasing then the risk of aseptic loosening. Today, aseptic loosening is the most common cause of arthroplasties revisions. Bone resorption around implants precedes the formation of fibrous tissue, therefore there is a need to understand its activation pathways. There are different hypothesis to explain bone resorption around implants. Mounting evidence shows that the debris, after implant wear, induce inflammatory reactions at the bone-implant interface. Upon accumulation of the foreign debris, a chain of cellular events is triggered within the tissue leading to periprosthetic osteolysis, fibrous tissue formation and implant loosening [1, 2]. It was observed that bone resorption around the implant is associated with high peak stresses at the interface immediately post-op [3]. Numerical models have been used to evaluate micromotions amplitude at bone-implant interfaces. It has been calculated that micromotions between 5 and more than 150 μm occur at the bone implant interface during normal gait cycles for hip implants. Jasty et al., found that micromotions lower than 40μm favor bone formation, while micromotions higher than 100μm lead to peri-implant osteolysis and the creation of a fibrous tissue [4]. These data were collected on animal models, and, to our knowledge, no human data are available to confirm these results. We hypothesize that micromotions at the bone implant interface may induce direct activation of bone lysis, around the implant through osteoblastic cells signalling toward osteoclasts in human bone, and tested our hypothesis with an ex vivo loading device inducing micromotions on human bone samples.
机译：在未发光和粘合的植入物中经常观察到总关节假体的骨和植入物界面处的无辐射区。这种代表纤维组织的辐射区是骨周围植入物的逐渐恶化的结果。纤维组织影响植入物固定，增加无菌松动的风险。如今，无菌松动是关节塑料修订的最常见原因。植入物周围的骨吸收在纤维组织的形成之前，因此需要了解其活化途径。有不同的假设来解释植入物周围的骨吸收。安装证据表明，植入磨损后的碎片，诱导骨植入界面处的炎症反应。在对外碎片的积累后，将一系列细胞事件触发在导致骨质刺激骨解的组织内，纤维组织形成和植入物松开[1,2]。观察到植入物周围的骨吸收与界面的高峰应力相关联，立即op-op [3]。数值模型已被用于评估骨植入界面处的微调幅度。已经计算出在正常的步态界面的骨植入界面处，在髋部植入物的正常步态界面处发生5至150μm的微调。 Jasty等人，发现微调低于40μm的有利骨形成，而微调高于100μm导致Peri植入物骨溶解和纤维组织的产生[4]。这些数据被收集在动物模型上，并据我们所知，没有人类数据可以确认这些结果。我们假设骨植入界面处的微调可以通过朝向人骨中的骨髓细胞向植入物传导的植入物周围引起骨髓溶解的直接激活，并用诱导人骨样上的emvivo装载装置测试我们的假设。

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