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A Mechanical lnvestigation of Osteoarthritic Degeneration of the Hip Associated With lmpingement.

机译:与撞击相关的髋关节骨关节炎变性的机械研究。

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摘要

This thesis presents an investigation into pathomechanisms of hip osteoarthritis (OA) associated with cam-type femoroacetabular impingement (FAI). OA involves degeneration of the articular cartilage layer and subchondral sclerosis, although the pathomechanism is not completely understood.;BMD was higher in subjects with cam deformities, regardless of symptomatic status, by up to 40%. The largest differences were seen in the antero-superior region of the acetabulum where impingement is expected to occur. On the femoral side, subchondral BMD was higher in the deformity compared to the peripheral bearing region of control subjects.;Cartilage from the cam deformity exhibited a non-fibrillar modulus approximately 80% lower than normal cartilage, and permeability was an order of magnitude higher. The non-fibrillar modulus and permeability were explained by the lower proteoglycan content.;Simulated cartilage degeneration resulted in increased cartilage consolidation in an axisymmetric model of the hi p. Lower stiffness of the components was offset by higher strains, resulting in cartilage stresses and fluid pressure similar to the healthy model. Increased subchondral stiffness resulted in higher non-fibrillar compressive stresses, fluid pressure and tangential fibril stress. Increased volumetric compressive strain was found due to cartilage degeneration as well as increased bone stiffness.;Subchondral sclerosis was investigated using three dimensional quantitative computed tomography. Bone density around the acetabulum and at the femoral head-neck junction was measured in subjects with cam-type deformities with and without symptoms, and compared to normal controls. Cartilage degeneration was assessed in osteochondral biopsies of patients undergoing surgical correction of FAI and compared to control specimens. The mechanical properties were determined by optimization of a finite element simulation combined with in vitro indentation stress relaxation data. The cartilage region was modelled as a fibril-reinforced poroelastic (FRPE) material to mimic the macromolecular and water content of the tissue. The effects of degenerative changes in bone and cartilage properties on cartilage stresses and pressure were investigated in an axisymmetric finite element model of the hip.;These results support the hypothesis that subchondral sclerosis plays an important early role in OA degeneration and may be a disease potentiator. OA treatments that target only cartilage may have minimal efficacy and should address sclerotic bone changes.
机译:本文提出了与凸轮型股骨髋臼撞击(FAI)相关的髋骨关节炎(OA)的发病机制的研究。 OA涉及关节软骨层的退化和软骨下硬化,尽管其致病机理尚未完全被理解。;无论有症状状态如何,患有凸轮畸形的受试者的BMD最高可达40%。在预计会发生撞击的髋臼前上区发现最大的差异。在股骨侧,与对照组相比,软骨下BMD的畸变要高。 。非原纤维模量和通透性由较低的蛋白聚糖含量解释。模拟的软骨变性导致在hi p的轴对称模型中增加的软骨固结。部件的较低刚度被较高的应变所抵消,从而导致软骨应力和流体压力与健康模型相似。软骨下硬度的增加导致更高的非原纤维压应力,流体压力和切向原纤维应力。由于软骨退变以及骨骼僵硬增加,导致体积压缩应变增加。;使用三维定量计算机断层扫描技术研究了软骨下硬化。在有和没有症状的凸轮型畸形患者中,测量髋臼周围和股骨头-颈部交界处的骨密度,并与正常对照进行比较。在接受FAI手术矫正的患者的骨软骨活检中评估了软骨变性,并与对照样本进行了比较。通过优化有限元模拟并结合体外压痕应力松弛数据来确定机械性能。将软骨区域建模为纤维增强的多孔弹性(FRPE)材料,以模仿组织的大分子和水含量。在髋关节轴对称有限元模型中研究了骨骼和软骨特性的退化变化对软骨应力和压力的影响。这些结果支持以下假设:软骨下硬化在OA退变中起着重要的早期作用,并且可能是疾病的增强剂。仅针对软骨的OA治疗可能效果不佳,应该解决硬化性骨的变化。

著录项

  • 作者

    Speirs, Andrew D.;

  • 作者单位

    Carleton University (Canada).;

  • 授予单位 Carleton University (Canada).;
  • 学科 Engineering Biomedical.
  • 学位 Ph.D.
  • 年度 2013
  • 页码 235 p.
  • 总页数 235
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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