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胫骨平台微观结构控制体内高周疲劳骨折。

Tibial Baseplate Microstructure Governs High Cycle Fatigue Fracture In Vivo.

机构信息

Implant Research Core, School of Biomedical Engineering, Science, and Health Systems, Drexel University, Philadelphia, Pennsylvania, USA.

Department of Bioengineering, Clemson University, Clemson, South Carolina, USA.

出版信息

J Biomed Mater Res B Appl Biomater. 2024 Dec;112(12):e35507. doi: 10.1002/jbm.b.35507.

Abstract

Previous studies report rare occurrences of tibial baseplate fractures following primary total knee arthroplasty (TKA). However, at a microstructural scale, it remains unclear how fatigue models developed in vitro apply to fractures in vivo. In this study, we asked: (1) do any clinical factors differentiate fracture patients from a broader revision sample; and (2) in vivo, how does microstructure influence fatigue crack propagation? We identified three fractured tibial baseplates from an institutional review board exempt implant retrieval program. Then, for comparison, we collated clinical data from the same database for n = 2120 revision TKA patients with tibial trays. To identify mechanisms, we characterized fracture features using scanning electron and digital optical microscopy. Additionally, we performed cross sectional analysis using focused ion beam milling. The fracture cohort consisted of moderately to very active patients with increased implantation time (15.6 years) compared to the larger revision patient sample (5.1 years, p = 0.009). We did not find a significant difference in patient weight between the two groups (p = 0.98). Macroscopic fracture features aligned well with both previous retrieval analysis and in vitro baseplate fatigue tests. On a micron scale, we identified striations on each baseplate, demonstrating fatigue as the fracture mechanism. In vivo fatigue fracture processes depended on both the alloy (Ti-6Al-4V vs. CoCrMo) and the microstructure of the alloy formed during manufacturing. For Ti-6Al-4V, the presence of equiaxed or acicular microstructure influenced the fatigue crack propagation, the latter arising from large prior β grains and a Widmanstatten microstructure, degrading fatigue strength. CoCrMo alloy fatigue cracks propagated linearly, crystallographically influenced by planar slip. However, we did not document any features of overload or fast fracture, suggesting a high cycle, low stress fatigue regime. Ultimately, the crack profiles we present here may provide insight into fatigue fractures of modern tibial baseplates.

摘要

先前的研究报告指出,初次全膝关节置换(TKA)后胫骨基板骨折的发生率较低。然而,在微观结构层面上,尚不清楚体外开发的疲劳模型如何适用于体内骨折。在这项研究中,我们提出了以下两个问题:(1)是否存在任何临床因素可以区分骨折患者和更广泛的翻修样本;(2)在体内,微结构如何影响疲劳裂纹扩展?我们从机构审查委员会豁免的植入物检索计划中确定了三个骨折的胫骨基板。然后,为了进行比较,我们从相同的数据库中收集了 n=2120 例胫骨托翻修 TKA 患者的临床数据。为了确定机制,我们使用扫描电子显微镜和数字光学显微镜对骨折特征进行了表征。此外,我们还使用聚焦离子束铣削进行了横截面分析。骨折组由植入时间较长(15.6 年)的中度至非常活跃的患者组成,与更大的翻修患者样本(5.1 年,p=0.009)相比。两组患者的体重无显著差异(p=0.98)。宏观骨折特征与之前的检索分析和体外基板疲劳测试结果一致。在微米尺度上,我们在每个基板上都发现了条纹,表明疲劳是骨折的机制。在体内,疲劳断裂过程取决于合金(Ti-6Al-4V 与 CoCrMo)及其制造过程中形成的合金微观结构。对于 Ti-6Al-4V,等轴晶或针状微观结构的存在会影响疲劳裂纹扩展,后者是由大的原始β晶粒和魏氏组织微观结构引起的,从而降低了疲劳强度。CoCrMo 合金的疲劳裂纹呈线性扩展,受到平面滑移的晶向影响。然而,我们没有记录任何过载或快速断裂的特征,这表明是一种高周低应力的疲劳状态。最终,我们提出的裂纹形态可能为现代胫骨基板的疲劳断裂提供一些见解。

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