压缩载荷下不同应变判定皮质骨断裂准确性分析

目的 寻找适合压缩断裂工况下的应变判据。方法 基于连续损伤力学理论进行皮质骨在压缩载荷下的断裂模拟。分别将等效应变与主应变设置为有限元模型单元损伤与失效判据进行断裂模拟,通过对比两种预测结果与动物实验数据,探究应用两种应变判据进行断裂模拟的准确性。结果 应用等效应变判据模拟的断裂时间晚于应用主应变模拟;相比等效应变,应用主应变进行仿真所得结果与动物实验结果更为接近。结论 压缩载荷下,应用主应变判定皮质骨单元力学状态进行断裂模拟较为准确。通过对比分析找到准确模拟皮质骨在压缩载荷下断裂的数值方法,能够为临床中提高骨折预测精度提供理论基础。     

基于不同应变判定准则模拟皮质骨断裂的准确性

文题释义：基于等效应变断裂模拟：即在大鼠股骨皮质骨断裂模拟过程中，应用皮质骨有限元模型在外部载荷作用下所产生的等效应变数值，与皮质骨组织的失效应变进行对比，当等效应变数值大于皮质骨组织失效应变时，有限元模型内的单元便发生失效，直至失效单元达到一定数量，模型便发生整体失效，此过程为基于等效应变的断裂模拟。 基于主应变断裂模拟：即在大鼠股骨皮质骨断裂模拟过程中，应用皮质骨有限元模型在外部载荷作用下所产生的主应变数值，与皮质骨组织的失效应变进行对比，当主应变数值大于皮质骨组织失效应变时，有限元模型内的单元便发生失效，直至失效单元达到一定数量，模型便发生整体失效，此过程为基于主应变的断裂模拟。 背景：由于意外碰撞等外力因素所产生的皮质骨裂纹是引起骨折的重要原因之一，要防止此类骨折发生，首先需弄清不同载荷作用下皮质骨裂纹的产生与扩展机制。由于实验分析对样本具有破坏性，难以同时了解骨结构在断裂前后的内部力学状态，找到一种能够准确模拟皮质骨从裂纹产生、扩展，直至断裂过程的有限元方法就显得尤为重要。当前模拟方法主要应用主应变或等效应变判定模型单元力学状态，继而进行断裂模拟，却鲜有关于这2种应变进行模拟准确性的探究。 目的：验证应用主应变与等效应变进行皮质骨断裂模拟的准确程度。 方法：结合实验与仿真分析，应用主应变与等效应变进行皮质骨断裂模拟，将仿真与实验结果进行对比，确定应用哪种应变进行模拟更加准确。 结果与结论：①应用主应变模拟的皮质骨断裂时间要明显晚于应用等效应变；②通过与实验对比发现，相比主应变，应用等效应变进行仿真所得结果与实验值更为接近；③因此，应用等效应变进行皮质骨断裂模拟相对更加准确。 ORCID: 0000-0003-0313-1359(王伟军) 中国组织工程研究杂志出版内容重点：人工关节；骨植入物；脊柱；骨折；内固定；数字化骨科；组织工程     

不同失效模式下皮质骨结构临界能量释放率预测

背景:临界能量释放率是结构在破坏过程中可测得的一个全局断裂力学参数,即使针对同一结构,在不同失效模式下其数值也可能存在差异。目的:提出一种方法预测皮质骨结构在不同失效模式下的临界能量释放率。方法:针对大鼠股骨皮质骨结构进行三点弯曲与轴向压缩实验以及相应断裂仿真。通过对有限元模型赋予不同临界能量释放率进行断裂模拟,并将每次模拟所得载荷-位移曲线与实验数据进行比较,当仿真与实验所得断裂参数差异小于5%时,即代表拟合成功,以此反演预测皮质骨结构在不同失效模式下的临界能量释放率。结果与结论:①结果显示大鼠股骨皮质骨结构在三点弯曲载荷下主要发生拉伸破坏,该失效模式下所预测临界能量释放率为0.16N/mm;②在轴向压缩载荷下主要发生剪切破坏,所预测临界能量释放率为0.12N/mm,这说明同一皮质骨结构在不同失效模式下的临界能量释放率存在差异;③此文通过对结构力学性能与损伤机制进行综合分析,揭示了不同失效模式下皮质骨结构临界能量释放率存在差异的原因,为能量释放率测量以及准确的皮质骨断裂模拟提供理论依据。     

基于表观压缩实验与有限元分析相结合的骨微观力学性能参数预测方法的研究

骨表观力学性能参数常被用来评定骨质量,而微观力学性能参数由于难以测得尚未被广泛应用。为从微观水平评判骨质量,本研究提出一种骨微观力学性能参数的预测方法。该方法以大鼠股骨皮质骨为研究对象,预测其在微观水平的失效应变。首先依据扫描影像建立大鼠股骨皮质骨有限元模型,然后以表观压缩实验为研究依据,模仿实验条件,模拟皮质骨有限元模型在压缩载荷作用下的断裂过程,并通过与实验所测表观应力-应变曲线进行对比、反演,预测出大鼠股骨皮质骨在微观水平的失效应变。分析结果显示四只7月龄大鼠股骨皮质骨的微观失效应变数值处于4.53%~4.75%之间。经验证,本方法能够准确预测出骨结构在微观水平的力学性能参数。     

下颌第一磨牙不同冠根比种植修复体的三维有限元分析

背景：为了尽量避免种植义齿修复时出现种植体周围骨组织应力集中。以往有研究应用增大种植体与骨界面的结合面积、增加直径、增加长度等方法以期使种植体骨界面应力分布更趋均匀,以提供更大的支持力,但观察时间较短,且临床报告并不一致。 目的：设计不同冠根比种植修复体,采用三维有限元法,对轴向加载和颊舌向加载下的不同冠根比种植修复体周围骨组织应力分布进行分析,以求找到适合临床种植修复的冠根比范围。 方法：应用CT断层扫描技术得到下颌骨和下颌牙列的大致轮廓,通过交互式的医学影像控制系统对图形特征进行整体图像拟合,再以计算机软件生成云图,根据云图的数据进行三维重建,从而得到包括下颌骨和下颌牙列的三维有限元模型;运用几何模型方法建立不同冠根比种植修复下颌第一磨牙的三维模型。运用Hyperwork 8.0及Ansys 11.0大型有限元分析软件,建立下颌不同冠根比的种植修复体模型,并完成牙冠的修复。在模拟牙合向载荷的基础上,比较不同冠根比种植修复体周围骨组织应力分布状况。 结果与结论：获得了下颌骨及下颌牙列的三维有限元模型,以及下颌不同冠根比种植修复体的有限元模型。通过对不同冠根比种植体施加轴向100 N及颊舌向50 N的力,种植体周围骨组织产生的应力分布状况比较发现,颊舌向受力下种植体颈部及周围骨皮质为应力集中区;轴向施力时种植体颈部、根尖部周围的骨组织为应力集中区。     

椎弓根螺钉长度变化对螺钉-骨复合体模型 应力影响的三维有限元分析研究

目的 利用三维有限元模型研究椎弓根螺钉长度变化对生理载荷下螺钉骨复合体模型的应用影响。方法 建立椎弓根螺钉和L1椎体的三维模型,并对其进行网格划分,设置椎弓根钉长度尺寸的变化范围。模拟生理载荷条件下,对不同长度尺寸的椎弓根钉有限元模型进行应力分析。结果椎弓根螺钉长度在30～50 mm范围内变化时,随着螺钉长度的增大,螺钉骨复合体模型的骨质部分承担的应力均减小,而螺钉承担的应力则增加。螺钉最大平均主应变出现在螺钉的尾端,皮质骨发生的最大平均主应力位置出现在螺钉与皮质骨接触面两侧,松质骨发生的最大平均主应力位置出现在螺钉头部与松质骨接触面两侧。当螺钉长度达到50 mm时,载荷力传递到皮质骨和松质骨分别减小了43.1%和42.3%,而螺钉上出现的则增加了38%。当椎弓根螺钉长度大于45 mm时,螺钉骨复合体模型各部分应力变化不明显。结论 椎弓根螺钉长度在30～50 mm范围变化时,在生理载荷下,椎弓根螺钉长度的增大有利于改善螺钉、皮质骨及松质骨上轴向应力的力学分布;只要骨量允许,临床选择椎弓根螺钉的长度应不小于45 mm。     

膝关节单髁置换胫骨优化截骨设计的生物力学研究

目的 比较膝关节单髁置换术(unicompartmental knee arthroplasty, UKA)常规截骨、保留圆角截骨及全新扩大圆角截骨方法对术后胫骨近端生物力学特性的影响。方法 基于Sawbones胫骨的CT数据,构建完整胫骨模型及不同截骨方式下UKA术后胫骨模型,采用轴向压缩工况对模型进行有限元分析,比较不同模型间胫骨近端应变情况及骨水泥应力差异。结果 在轴向压缩工况下,扩大圆角组其截骨区皮质骨von Mises应变峰值较常规截骨组与保留圆角组有所增加,而松质骨von Mises应变峰值则分别减少24.3%～42.9%、26.0%～48.7%。对比截骨区松质骨与皮质骨von Mises应变峰值差Δε_peak,发现扩大圆角组其Δε_peak远远小于其余两组。UKA后不同模型间胫骨前内侧皮质骨最小主应变无明显差异,但较完整胫骨模型增加23.3%～34.5%。扩大圆角组骨水泥单元平均von Mises应力随着圆角半径增大呈现下降趋势,且整体均小于常规截骨组与保留圆角组。结论 全新扩大圆角截骨方法可使健康骨质条件下胫骨近端应力传递更均匀...     

下颌后牙单端桥基牙骨支持组织应力的动力学分析

目的: 建立下颌后牙单端固定桥及其支持组织的三维有限元模型,采用瞬态动力学分析,比较单端桥修复前后基牙骨支持组织的应力分布规律。方法: 用ANSYS 10.0软件对模型施以不同部位和方向的冲击载荷,分析单端桥基牙骨支持组织的应力大小、分布及变化规律。结果: 斜向载荷下,基牙骨支持组织存在明显应力集中;单端桥修复后,应力峰值77.676 MPa位于近缺隙侧基牙的皮质骨颈部;一个咀嚼周期末存在应力残余,其值不显著。结论: 单端桥近缺隙侧基牙承受主要应力,载荷方向影响应力大小及分布,应力峰值小于下颌骨应变极限强度。     

侧向冲击载荷作用下髋护具对股骨-骨盆复合体生物力学响应的影响

目的利用三维有限元法研究髋部护具对人体股骨-骨盆复合体在侧向冲击载荷作用下生物力学响应的影响。方法基于中国力学虚拟人模型库建立股骨-骨盆-软组织复合体的三维有限元模型,包括皮质骨、松质骨和软组织,并在此基础上建立髋部护具和股骨-骨盆-软组织复合体系统的三维有限元模型;同时,在两个模型中构建刚体平面仿真地面。约束地面刚体,对两个模型均施加侧向2 m/s的速度载荷,整个仿真分析时间设定为20 ms。通过三维有限元分析计算获得两模型受侧向冲击载荷过程中应力、应变变化特性,对比分析髋部护具对股骨-骨盆复合体生物力学响应的影响。结果髋部护具使股骨-骨盆复合体在侧向冲击载荷作用下的应力峰值出现时间提前4 ms以上,且应力应变水平出现大幅度降低;皮质骨上的应力峰值降低67.88%以上,松质骨上的峰值应力下降69.34%以上,松质骨上的压缩主应变峰值降低可达63%。结论在侧向冲击载荷作用下,髋部护具对股骨-骨盆复合体具有良好的保护作用,能够有效预防骨折的发生或降低骨折风险。     

肱骨远端三维有限元模型的建立及生物力学分析

背景：采用有限元分析法进行骨与关节的生物力学分析得到了广泛应用,但是关于肱骨远端的有限元分析较少,且所建模型粗糙,方法繁琐。 目的：建立肱骨远端的三维有限元模型,并模拟不同受力状态下的应力分布及应变特征。 方法：通过对正常成年男性肘关节的多排螺旋CT扫描,获得连续断层图片,导入Mimics医学建模软件生成实体模型后,应用大型通用有限元分析软件ANSYS 10.0,进行网格划分、材料属性赋值生成有限元模型。约束边界条件,模拟肱骨远端轴向受力,得出肱骨远端有限元模型上的应力分布与应变结果。 结果与结论：建立的肱骨远端有限元模型总单元数为6 292,总节点数为10 232。肱骨远端在轴向载荷状态下的应力集中主要位于内、外侧柱区域。提示建立的有限元模型精确度高,符合肱骨远端的临床特点,较好地模拟了肱骨远端的生物力学特性。     

骨组织疲劳损伤的生物力学研究概述

骨组织是人体重要的承重器官,具有力学适应性,在疲劳载荷作用下会出现疲劳损伤,常见于运动员长跑、新兵训练以及老年人的日常活动,主要表现为骨组织显微裂纹的萌生、扩展,力学性能下降甚至是应力性骨折,危害很大。骨组织的疲劳损伤存在于包括超显微结构、显微结构和组织宏观的各个层面,皮质骨中的抗疲劳结构(骨单元)及内部的细胞成分(主要为骨细胞)对抵抗疲劳损伤、识别显微裂纹以及诱导后续定向骨重建过程具有重要作用。总结相关研究结果与结论有助于系统了解骨组织疲劳损伤行为及相应识别修复过程,同时也为后续骨组织疲劳损伤预防及治疗等临床研究工作的开展提供参考和方向。     

Microelectrode study of stress-generated potentials obtained from uniform and nonuniform compression of human bone.

By use of a previously developed microelectrode technique, the effect of nonuniform stresses on the stress-generated potentials (SGP) in bone were studied to a resolution of 5 micrometers. Comparison was made between uniformly and nonuniformly applied compression of human cortical bone. It was found that the radial electric fields for osteons in a specimen under uniform compression were equivalent, and such specimens possessed no macroscopic SGP; for nonuniform compression, the electric fields of osteons differed, and a macroscopic SGP was measured. The magnitude of the macroscopic SGP thus appears to be dependent upon local stress differences and, hence, on the SGP of local regions.     

Spatial distribution of osteocyte lacunae in equine radii and third metacarpals: considerations for cellular communication, microdamage detection and metabolism

Osteocytes, which are embedded in bone matrix, are the most abundant cells in bone. Despite the ideal location of osteocytes to sense the local environment and influence bone remodeling, their functions, and the relative importance of these functions, remain controversial. In this study, we tested several hypotheses that address the possibilities that population densities of osteocyte lacunae (Ot.Lc.N/B.Ar) correlate with strain-, remodeling- or metabolism-related aspects of the local biomechanical environments of mid-third diaphyseal equine radii and third metacarpals from skeletally mature animals. Ot.Lc.N/B.Ar data, quantified in multiple cortical locations, were analyzed for possible correlations with (1) structural and material characteristics (e.g., cortical thickness, percent ash, secondary osteon population density, mean osteon cross-sectional area, and predominant collagen fiber orientation), (2) strain characteristics, including prevalent/predominant strain magnitude and mode (tension, compression, shear), (3) hypothesized strain-mode-related microdamage characteristics, which might be perceived by osteocyte 'operational' networks, and (4) variations in remodeling dynamics and/or metabolism (i.e. presumably higher in endocortical regions than in other transcortical locations). Results showed relatively uniform Ot.Lc.N/B.Ar between regions with highly non-uniform strain and strain-related environments and markedly heterogeneous structural and material organization. These results suggest that population densities of these cells are poorly correlated with mechanobiological characteristics, including local variations in metabolic rate and strain magnitude/mode. Although osteocytes hypothetically evolved both as strain sensors and fatigue damage sensors able to direct the removal of damage as needed, the mechanisms that govern the distribution of these cells remain unclear. The results of this study provide little or no evidence that the number of osteocyte lacunae has a functional role in mechanotransduction pathways that are typically considered in bone adaptation.     

Microdamage in bone: implications for fracture, repair, remodeling, and adaptation

Fatigue microdamage accumulates in bone as a result of physiological loading. The damage is often manifested as microcracks, which are typically 50-100 mum long. These types of cracks develop in the interstitial bone and frequently abut osteon cement lines. In vitro experimentation has shown that an accumulation of fatigue damage reduces the material properties of bone (e.g., elastic modulus). An accumulation of fatigue damage has been implicated in the etiology of stress fractures and fragility fractures. However, bone has a remarkable ability to detect and repair fatigue microdamage. This article reviews the experimental techniques for identifying and quantifying different types of microdamage in bone, the density of in vivo microcracks at different skeletal locations, the effect of microdamage on bone material properties, the role of microdamage in bone fracture, and the biological mechanisms for the detection and repair of fatigue microdamage.     

An equivalent strain/Coffin-Manson approach to multiaxial fatigue and life prediction in superelastic Nitinol medical devices

Medical devices, particularly endovascular stents, manufactured from superelastic Nitinol, a near-equiatomic alloy of Ni and Ti, are subjected to complex mixed-mode loading conditions in vivo, including axial tension and compression, radial compression, pulsatile, bending and torsion. Fatigue lifetime prediction methodologies for Nitinol, however, are invariably based on uniaxial loading and thus fall short of accurately predicting the safe lifetime of stents under the complex multiaxial loading conditions experienced physiologically. While there is a considerable body of research documented on the cyclic fatigue of Nitinol in uniaxial tension or bending, there remains an almost total lack of comprehensive fatigue lifetime data for other loading conditions, such as torsion and tension/torsion. In this work, thin-walled Nitinol tubes were cycled in torsion at various mean and alternating strains to investigate the fatigue life behavior of Nitinol and results compared to equivalent fatigue data collected under uniaxial tensile/bending loads. Using these strain-life results for various loading modes and an equivalent referential (Lagrangian) strain approach, a strategy for normalizing these data is presented. Based on this strategy, a fatigue lifetime prediction model for the multiaxial loading of Nitinol is presented utilizing a modified Coffin-Manson approach where the number of cycles to failure is related to the equivalent alternating transformation strain.     

Osteonal crack barriers in ovine compact bone

Bone is an anisotropic structure which can be compared to a composite material. Discontinuities within its microstructure may provide stress concentration sites for crack initiation, but act as a barrier to its propagation. This study looks specifically at the relationship between crack length and propagation in compact bone. Beam-shaped bone samples from sheep radii were prepared and stained with fluorochrome dyes and tested in cyclic fatigue under four-point bending in an INSTRON 1341 servo-hydraulic fatigue-testing machine. Samples were tested at a frequency of 30 Hz and stress range of 100 MPa under load control. Specimens were sectioned transversely using a diamond saw, slides prepared and examined using epifluorescence microscopy. Cracks in transverse sections were classified in terms of their location relative to cement lines surrounding secondary osteons. Mean crack length, crack numerical density and crack surface density were examined. Short microcracks (100 microm or less) were stopped at the cement lines surrounding osteons, microcracks of intermediate length (100-300 microm) were deflected as they hit the cement line, and microcracks that were able to penetrate through cement lines were longer (> 400 microm). These data show that bone microstructure allows the initiation of microcracks but acts as a barrier to crack propagation.     

Does bone perfusion/reperfusion initiate bone remodeling and the stress fracture syndrome?

Stress fractures have been proposed to arise from repetitive activity of training inducing an accumulation of microfractures in locations of peak strain. However, stress fractures most often occur long before accumulation of material damage could occur; they occur in cortical locations of low, not high, strain; and intracortical osteopenia precedes any evidence of micro-cracks. We propose that this lesion arises from a focal remodeling response to site-specific changes in bone perfusion during redundant axial loading of appendicular bones. Intramedullary pressures significantly exceeding peak arterial pressure are generated by strenuous exercise and, if the exercise is maintained, the bone tissue can suffer from ischemia caused by reduced blood flow into the medullary canal and hence to the inner two-thirds of the cortex. Site specificity is caused by the lack, in certain regions of the cortex, of compensating matrix-consolidation-driven fluid flow which brings nutrients from the periosteal surface to portions of the cortex. Upon cessation of the exercise, re-flow of fresh blood into the vasculature leads to reperfusion injury, causing an extended no-flow or reduced flow to that portion of the bone most strongly denied perfusion during the exercise. This leads to a cell-stress-initiated remodeling which ultimately weakens the bone, predisposing it to fracture.