Morphological and Biomechanical Insights into the Pathophysiology of Femoroacetabular Impingement Syndrome

项目摘要 据估计，股骨髋臼撞击综合征（FAIS）占髋关节骨关节炎的82 (OA)例FAIS患者表现为股骨头球形度丧失，股骨颈偏心距减少， 和/或过度突出的髋臼壁。患者报告疼痛与体位或运动相关。很多时候， 软骨从骨上剥离，并且唇被撕裂。FAIS病理生理学的理论是， 病理解剖学导致病理力学。然而，我们对这种疾病缺乏定量的了解。研究 在FAIS患者中检查髋关节解剖结构和生物力学的研究产生了相互矛盾的数据，可能是由于 使用不准确的测量技术。FAI形态学的患病率也很高 在无症状人群中（即，阳性对照），这阻碍了理解FAI为什么 形态学导致损伤。在此，我们应用实验和计算技术， 了解FAIS的病理生理学。我们将检查三个队列：FAIS患者，阴性对照， 阳性对照。目标1将在倾斜行走、旋转和下蹲期间测量体内髋关节关节 三个队列使用双透视。我们假设FAIS患者会表现出运动学改变; 然而，根据我们初步数据，我们认为患者的活动范围不会减少。我们还 假设与阴性对照相比，阳性对照将具有改变的运动学。在子目标中 1，我们将可视化髋关节的形状和其运动学位置之间的相互作用， 使用所述双重荧光透视数据的统计形状建模进行加载。完成目标1改善临床 通过使我们能够可视化动态负荷过程中病理形状的影响，从而了解FAIS。目的 2将通过计算机模拟分析软骨盂唇力学，以提高对FAIS病理生理学的理解。具体地说， 我们将使用经过验证的管道生成骨、软骨和盂唇的有限元模型。我们将比较 载荷转移到盂唇，骨软骨和软骨盂唇连接处的剪切应力和应变 倾斜行走、旋转和下蹲。我们假设向盂唇的负荷转移增加， 在FAIS中，骨软骨和软骨盂唇连接处的软骨剪切应力和应变升高 患者阳性对照组经历的代偿运动可保持软骨盂唇应力， 正常范围内的应变。因此，我们假设， 两个对照组。子目标2将量化髋关节形状的局部测量值与 软骨唇力学目标2的完成将提高对OA患者发病机制的理解， FAIS。确定阳性对照如何科普他们的畸形可以为新的治疗策略提供信息。

PROJECT SUMMARY By some estimates, femoroacetabular impingement syndrome (FAIS) accounts for 82% of hip osteoarthritis (OA) cases. FAIS patients present with a loss of sphericity of the femoral head, reduction in femoral-neck offset, and/or an excessively prominent acetabular wall. Patients report pain that is position- or motion-related. Often, cartilage is delaminated from bone and the labrum is torn. The theory of FAIS pathophysiology is that pathoanatomy causes pathomechanics. However, we lack a quantitative understanding of the disease. Studies that have examined hip anatomy and biomechanics in FAIS patients have yielded conflicting data, likely due to the application of inaccurate measurement techniques. There is also a high prevalence of FAI morphology among the asymptomatic population (i.e., positive controls), which has hindered progress to understand why FAI morphology causes damage. Herein, we apply experimental and computational techniques to advance understanding of FAIS pathophysiology. We will examine three cohorts: FAIS patients, negative controls, and positive controls. Aim 1 will measure in-vivo hip articulation during inclined walking, pivoting, and squatting in the three cohorts using dual fluoroscopy. We hypothesize that patients with FAIS will exhibit altered kinematics; however, given our preliminary data, we posit that range of motion will not be reduced in patients. Further, we hypothesize that positive controls will have altered kinematics when compared to negative controls. In Sub-Aim 1, we will visualize the interaction between the shape of the hip joint and its kinematic position during dynamic loading using statistical shape modeling of the dual fluoroscopy data. Completion of Aim 1 improve clinical understanding of FAIS by enabling us to visualize the effects of pathologic shape during dynamic loading. Aim 2 will analyze chondrolabral mechanics in-silico to improve understanding of FAIS pathophysiology. Specifically, we will generate finite element models of bone, cartilage, and labrum using a validated pipeline. We will compare load transfer to the labrum and shear stresses and strains at the osteochondral and chondrolabral junction during inclined walking, pivoting, and squatting. We hypothesize that load transfer to the labrum is increased, and cartilage shear stresses and strains at the osteochondral and chondrolabral junctions are elevated in FAIS patients. Compensatory motion experienced by the positive control group may keep chondrolabral stresses and strains within normal. Thus, we hypothesize that there will be no significant differences in FE results between the two control groups. Sub-Aim 2 will quantify relationships between local measures of hip shape and chondrolabral mechanics. Completion of Aim 2 will enhance understanding of OA pathogenesis in patients with FAIS. Identifying how positive controls cope with their deformities could inform new treatment strategies.