The cause of subchondral bone cysts in osteoarthrosis: a finite element analysis

BACKGROUND: The etiology of subchondral bone cysts in arthrotic joints is unclear. MATERIALS AND METHODS: We used two-dimensional finite element analysis to evaluate the hypothesis that subchondral bone cysts in the osteoarthrotic hip joint may be the result of microfractures caused by localized cartilage defects or a thinned layer of cartilage. We evaluated the equivalent bone stress (von Mises (VM) stress) in the cancellous bone as an indicator of potential microfractures and further development of cystic lesions. RESULTS: Cartilage defects induced stress peaks in the subchondral bone. This peak stress distribution corresponded to the clinical observation of development of acetabular and femoral subchondral cysts in a "kissing" position. A femoral subchondral bone cyst induced a stress peak at the corresponding acetabular site, whereas subchondral acetabular cysts did not increase stress in the femoral head. Acetabular cysts showed an increased level of stress at the lateral and medial border of the lesion which was much higher than the stress levels in the femoral head, indicating a tendency to faster growth. INTERPRETATION: Our study supports the theory that stress-induced bone resorption may cause development of subchondral bone cysts in osteoarthrosis.     

Macrophage-osteoclast differentiation and bone resorption in osteoarthrotic subchondral acetabular cysts

A macrophage infiltrate is commonly found in enlarging subchondral cysts in osteoarthrosis (OA) and the surrounding bone. To determine whether osteoclast differentiation by these cells contributes to the increase in the number of osteoclasts and bone resorption that accompanies OA cyst enlargement, we isolated macrophages from the wall of OA cysts and co-cultured them with osteoblast-like UMR106 cells in the presence or absence of 1,25(OH) 2 D 3 and M-CSF. After 14 days of incubation, co-cultures of UMR106 cells and cyst-derived macrophages showed evidence of osteoclast differentiation by expression of TRAP, VNR and formation of numerous lacunar pits. We found that, unlike osteoclast precursors in monocyte and other tissue macrophage populations, the addition of M-CSF to medium is not required for osteoclast differentiation. Our findings suggest that macrophage-osteoclast differentiation is one means whereby the osteolysis associated with the enlargement of OA cysts could be effected.     

Macrophage-osteoclast differentiation and bone resorption in osteoarthrotic subchondral acetabular cysts

A macrophage infiltrate is commonly found in enlarging subchondral cysts in osteoarthrosis (OA) and the surrounding bone. To determine whether osteoclast differentiation by these cells contributes to the increase in the number of osteoclasts and bone resorption that accompanies OA cyst enlargement, we isolated macrophages from the wall of OA cysts and co-cultured them with osteoblast-like UMR106 cells in the presence or absence of 1,25(OH)2D3 and M-CSE After 14 days of incubation, co-cultures of UMR106 cells and cyst-derived macrophages showed evidence of osteoclast differentiation by expression of TRAP, VNR and formation of numerous lacunar pits. We found that, unlike osteoclast precursors in monocyte and other tissue macrophage populations, the addition of M-CSF to medium is not required for osteoclast differentiation. Our findings suggest that macrophage-osteoclast differentiation is one means whereby the osteolysis associated with the enlargement of OA cysts could be effected.     

Macrophage-osteoclast differentiation and bone resorption in osteoarthrotic subchondral acetabular cysts

A macrophage infiltrate is commonly found in enlarging subchondral cysts in osteoarthrosis (OA) and the surrounding bone. To determine whether osteoclast differentiation by these cells contributes to the increase in the number of osteoclasts and bone resorption that accompanies OA cyst enlargement, we isolated macrophages from the wall of OA cysts and co-cultured them with osteoblast-like UMR106 cells in the presence or absence of 1,25(OH) 2 D 3 and M-CSF. After 14 days of incubation, co-cultures of UMR106 cells and cyst-derived macrophages showed evidence of osteoclast differentiation by expression of TRAP, VNR and formation of numerous lacunar pits. We found that, unlike osteoclast precursors in monocyte and other tissue macrophage populations, the addition of M-CSF to medium is not required for osteoclast differentiation. Our findings suggest that macrophage-osteoclast differentiation is one means whereby the osteolysis associated with the enlargement of OA cysts could be effected.     

The first metatarsal bone under loading conditions: a finite element analysis

An individual-based, three-dimensional finite element model of the first metatarsal (MT I) bone was created with fine CT. The three-dimensional model of the bone was fixed proximally at the metatarsocuneiform joint and load was applied on the metatarsal head. Loading conditions were simulated, including muscular forces as described for a normal metatarsophalangeal (MTP) joint during three typical phases of gait as the combination of the load in the contact areas of the sesamoid bones and the base of the proximal phalanx. The resultant strain and stress distributions within the loaded MT I were calculated and visualized with the MTP in different positions.     

软骨下骨在骨关节炎发病中作用的研究进展

骨关节炎是最常见的骨科疾患,通常被认为与关节软骨的退变有关,骨软骨损伤的修复仍是巨大的挑战。近年来,越来越多的研究者们开始重视软骨下骨在骨关节炎发病机制中的重要作用。在骨关节炎的出现及进展过程中,软骨下骨在生物力学、生物化学等方面的改变均能够影响其表面紧密连接的关节软骨,并导致关节软骨的损害,软骨的退变以及软骨下骨的结构变化都是影响骨关节炎的重要因素。软骨与软骨下骨紧密结合,应整体化对待"软骨-软骨下骨"。随着对软骨下骨认识的提高,对骨关节炎的治疗也就不仅仅局限于治疗软骨损伤,可以选择针对"软骨及软骨下骨"一体来治疗。本文综述了软骨下骨在骨关节炎发病中重要作用的研究进展情况。     

腰椎间盘膨隆的有限元分析

目的：了解椎间盘膨隆的力学机制。方法：建立腰椎三维有限元要模型,模拟腰椎推退行性改变的压损伤椎间盘盘位移情况。结果：在压力状态下,椎间盘膨出半径增大,椎间盘高度下降。结论：腰椎间盘膨隆是腰椎退行性改变的一利表现,与椎间盘突出症发生机制不同。     

四维有限元骨承载力分析技术在判断长管骨愈合程度中的应用

目的利用四维有限元骨承载力分析的方法，对于长管骨骨折术后患者采用双腿平行CT扫描、双腿几何建模、有限元分析的方法，通过与健侧肢体相同部位的对比分析，根据时间轴上的变化趋势，判断目标骨段骨愈合的程度，辅助诊断长管骨的骨愈合、骨延迟愈合和骨不连。 方法选择2014年到2017年间，临床诊断骨延迟愈合的26例病例进行了系统随访。在骨愈合不同阶段的CT数据进行三维建模，材料赋值，建立下肢长管骨的三维有限元模型，模拟仿真计算目标骨段承载受力状况，通过有限元分析软件，进行单轴压缩实验的仿真，分析双腿目标骨段的受载荷情况。结合米塞斯应力最大值及载力-位移曲线下总面积进行比值分析，作为观察骨愈合程度的指标，对于临床诊断进行二次修正，并观察最终临床愈合结果。 结果所有病例均获得2~4年的随访，平均随访时间3.4年。临床诊断骨延迟愈合完整病例26例，对26例病例采用有限元骨承载力分析法共分析54次，修正诊断为：6例（23.1%）病例判定骨愈合；16例（61.5%）病例判定骨愈合不良；4例（15.4%）病例判定骨不连。利用米塞斯应力最大值及载力-位移曲线下总面积进行比值分析，并进行卡方检验，差异无统计学意义。通过Fisher精确概率检验法得到P=0.170，具有统计学意义，两种方法存在非随机相关性。 结论采用有限元骨承载力分析的技术，可以三维定量分析骨折端的骨愈合程度，结合时间轴上变化规律的描述，可以给骨不连和骨延迟愈合的临床诊断提供一个相对客观的诊断依据。该方法也较好的观察到，高能量损伤的骨愈合过程难以按照经典骨愈合理论的进程演变，通常其骨愈合所需的时间更长，但能显示出其缓慢的愈合趋势，应用前景广阔。     

半月板有限元分析的研究进展

对半月板生物力学研究一直是医学科研热点之一。有限元分析法(FEA)提供了一种新的思路和方法。通过建立半月板有限元模型,利用软件分析可获得正常半月板的应力应变分布特点,也可模拟半月板撕裂、半月板切除、以及膝关节各组织损伤,研究半月板力学特性的改变,为临床疾病的预防治疗以及康复提供理论力学依据。但目前的有限元分析法存在其局限性,未来建立高质量的有限元模型,使模型更真实反应半月板的解剖特点,以及将有限元分析法运用到更多的膝关节损伤中应是研究的方向。     

骨密度对距下关节融合初稳性影响的三维有限元分析

目的 通过有限元分析的方法研究骨密度对于距下关节融合初稳性的影响. 方法 选取1名男性健康志愿者,25岁,体质量为70kg.基于志愿者右足的三维CT扫描数据利用Mimics 13.0、Geomagic 10.0等软件重建距下关节融合的三维有限元双顶模型:即距骨颈联合距骨顶前外、后外、前内、后内侧4种双钉模型,同时通过降低骨的弹性模量模拟不同程度的疏松骨质,最后将模型导入Abaqus 6.9软件进行赋值、划分网格,对每个模型施加4N·m的内旋、外旋作用力,通过计算分析模型应力后距下关节面间的相对位移来评估骨密度对距下关节融合初稳性的影响. 结果 随着骨密度的降低,4种融合模型应力后关节面间的相对位移峰值均增大;距骨颈联合距骨前外侧顶的双钉模型在正常骨密度和骨质疏松存在的情况下,其应力后关节面间相对位移峰值均较其他模型低,是距下关节融合最优的选择;而距骨颈联合距骨后内侧顶的双钉模型,应力后关节面间相对位置峰值最大,关节融合时应避免使用此种配置. 结论 骨密度越低融合后稳定性越差;距骨颈联合前外侧顶双钉模型对于正常或疏松骨质的距下关节融合都具有最好的稳定性,是距下关节融合最优的选择.     

软骨下骨骨重塑与骨关节炎的关系

骨关节炎本质上可能是一种生物学的改建过程,是多种生物因素与机械损伤因素相互作用所致生物力学紊乱而引起的病理改变.骨关节炎中软骨下骨的改变是否早于关节软骨的退变尚未得到证实,但软骨下骨改变是骨关节炎进程中必经的病理变化.近年有研究发现软骨下骨改变在骨关节炎发病过程中起积极作用.在外部异常因素作用下,软骨下骨代谢加强、骨重塑加快导致的软骨下骨增厚和密度增高是引起软骨退变的重要因素之一.有效控制软骨下骨的代谢速度和骨重塑速度,改变软骨下骨的硬度,可能为骨关节炎的防治开辟一个新领域.     

膝关节三维有限元分析

有限元分析是在工程科学技术领域广泛应用的数学物理方法,是解决复杂工程学问题的必备工具之一.将有限元分析应用于人体生物力学研究,已显示出极大的优越性.通常的力学试验手段基本上不直接应用于人体,其试验结果并不十分准确;有限元分析则可通过对实验条件的控制,更准确地模拟体内的力学情况.对人体力学行为进行有限元数值模拟已成为深化对人体认识的一种有效手段.该文对膝关节三维有限元分析的近期研究进展进行综述,讨论在临床应用中的实际意义,并总结目前有限元分析在膝关节生物力学研究中存在的不足.     

股骨上段有限元几何模型的建立与分析

目的建立股骨骨结构三维有限元模型并对其进行分析以指导临床工作。方法在Mimics10.1中直接读取符合Dicom 3.0标准的股骨原始CT数据,经阈值设定、区域增长及形态学操作等生成股骨初始3D模型,后期结合有限元软件ANSYS12.1生成最终的三维有限元网格模型,然后在ANSYS12.1中分别对应用Mimics得到的模型进行分析。结果应用Mimics10.1和Ansys12.1软件建立股骨有限元模型,外形逼真、计算精确。结论 Mimics10.1软件能直接与Ansys12.1软件进行对接,并能根据CT值直接赋值使股骨上段三维有限元模型的建立更加快捷、精确。     

骨水泥不同弥散方式对椎体成形术后生物力学影响的有限元分析

目的:探讨术中骨水泥不同弥散方式在治疗骨质疏松性椎体压缩骨折中的生物力学影响.方法:选取老年骨质疏松性压缩骨折志愿者1例,男性,68岁,身高172 cm,体重60 kg.既往身体健康,行X线片及胸腰部CT检查,诊断为L1椎体压缩性骨折.从T10-L5之间使用CT扫描,采用Mimics软件提取CT数据,使用Geomagi...     

The role of pressurized fluid in subchondral bone cyst growth

Pressurized fluid has been proposed to play an important role in subchondral bone cyst development. However, the exact mechanism remains speculative. We used an established computational mechanoregulated bone adaptation model to investigate two hypotheses: 1) pressurized fluid causes cyst growth through altered bone tissue loading conditions, 2) pressurized fluid causes cyst growth through osteocyte death. In a 2D finite element model of bone microarchitecture, a marrow cavity was filled with fluid to resemble a cyst. Subsequently, the fluid was pressurized, or osteocyte death was simulated, or both. Rather than increasing the load, which was the prevailing hypothesis, pressurized fluid decreased the load on the surrounding bone, thereby leading to net bone resorption and growth of the cavity. In this scenario an irregularly shaped cavity developed which became rounded and obtained a rim of sclerotic bone after removal of the pressurized fluid. This indicates that cyst development may occur in a step-wise manner. In the simulations of osteocyte death, cavity growth also occurred, and the cavity immediately obtained a rounded shape and a sclerotic rim. Combining both mechanisms increased the growth rate of the cavity. In conclusion, both stress-shielding by pressurized fluid, and osteocyte death may cause cyst growth. In vivo observations of pressurized cyst fluid, dead osteocytes, and different appearances of cysts similar to our simulation results support the idea that both mechanisms can simultaneously play a role in the development and growth of subchondral bone cysts.     

髓腔改变对股骨近端假体-骨界面应力的影响

目的 建立股骨近端假体-骨界面应力有限元分析模型.并对中国成年人股骨近端正常受力、翻修过程中扩髓条件下进行静态有限元分析.方法 运用逆向工程与有限元的理论.对CT图像采用了滤波、边界提取、二值化等方法进行处理,所得数据用CAD软件经过曲线重构、曲面重构、实体重构,加工出股骨应力模型.将不同载荷施加与假体-骨界面,改变股骨骨皮质的厚度、假体长度等参数,进行静态模拟应力分析.结果 建立起以国人股骨为基础的有效的假体-骨界面应力分布规律三维有限元模型.股骨的受力主要集中在小转子和大转子之间的股骨距分布区域,并且随着载荷的增加而递增;假体增粗至原来的120%时,股骨最大应力已经接近极限应力值.结论 构建的解剖型股骨假体-骨界面三维有限元模型,几何相似性好.模拟应力分析结果提示接受关节置换的患者应该尽量避免登山等接近加载量极限的活动;对于髓腔骨缺损严重的翻修患者提倡应用骨移植材料.谨慎采用增粗假体固定.