Quantifying the Pathophysiology of Femoroacetabular Impingement Syndrome

项目总结 据估计，髋臼撞击综合征(FAIS)占髋关节骨关节炎的82% (OA)病例。FAIS患者表现为股骨头球形丧失，股骨颈缩小 偏移量和/或过度突出的髋臼壁。患者报告的疼痛与位置或运动有关。 通常情况下，软骨从骨骼中剥离，唇骨撕裂。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量化的了解。研究 对FAIS患者的髋关节解剖和生物力学进行了研究，得出了相互矛盾的数据，可能是由于 不准确测量技术的应用。FAI形态的发病率也很高 在无症状人群中(即阳性对照)，这阻碍了理解为什么 FAI形态会造成损害。在这里，我们提高了我们对FAIS病理生理学的理解。我们建议 一项横断面设计，包括三个队列：FAIS患者、阴性对照和阳性对照。 目标1将对FAIS的病理形态进行量化。更具体地说，我们将可视化并比较3D HIP 使用统计形状建模的解剖学。我们假设形状建模将检测3D中的差异 有症状和无症状髋关节之间的骨盆和股骨近端的形状；我们假设这种差异 无论对照是一起分析，还是作为单独的积极/消极组进行分析，都会发生。完成目标1 将提高我们对这种疾病的临床认识，并为更好的放射学检查的发展提供信息 评估髋关节解剖的影像技术。 目标2将量化FAIS的病理机制。更具体地说，我们将量化体内髋关节运动学 使用双重透视和软骨唇力学，使用患者特定的有限元模型。我们 假设髋关节运动学改变，转移到唇部的负荷增加，软骨剪应力增加。 在FAIS患者中，骨软骨和软骨唇连接处的应变增加。我们推论 阳性对照组的个体通过改变髋关节运动来应对FAI的形态，这 用于将软骨唇力学保持在标准范围内(即有限元预测没有差异 阳性对照和阴性对照之间的差异)。目标2将通过使我们能够提高对FAIS的临床理解 在动态加载过程中“看到”疾病的过程。AIM 2的数据也将指导新疗法的开发 通过更好地了解发生在这三个群体的补偿机制，提供各种选择。 目标3将提高我们对髋关节FAIS的OA发病机制的理解 解剖学、软骨力学和软骨超微结构之间的关系。这里，定量的磁力 磁共振成像将估计髋关节软骨中蛋白多糖的含量和胶原组织。这些 数据还可能为诊断、分期和监测疾病的新方法提供依据。

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 improve our understanding of FAIS pathophysiology. We propose a cross-sectional design with three cohorts: FAIS patients, negative controls, and positive controls. Aim 1 will quantify the pathomorphology of FAIS. More specifically, we will visualize and compare 3D hip anatomy using statistical shape modeling. We hypothesize shape modeling will detect differences in the 3D shape of the pelvis and proximal femur between symptomatic and asymptomatic hips; we posit this difference will occur whether controls are analyzed together or as separate positive/negative groups. Completion of Aim 1 will improve our clinical understanding of this disease and inform the development of better radiographic imaging techniques to evaluate hip anatomy. Aim 2 will quantify the pathomechanics of FAIS. More specifically, we will quantify in-vivo hip kinematics using dual fluoroscopy and chondrolabral mechanics using patient-specific finite element models. We hypothesize hip kinematics are altered, load transfer to the labrum is increased, and cartilage shear stresses and strains at the osteochondral and chondrolabral junctions are elevated in FAIS patients. We theorize individuals in the positive control group cope with FAI morphology through alterations in hip joint motion, which serve to keep chondrolabral mechanics within the normative range (i.e. no difference in FE predictions between positive and negative controls). Aim 2 will improve our clinical understanding of FAIS by enabling us to ‘see’ the disease process during dynamic loading. Aim 2 data will also guide development of new treatment options through a better understanding of compensation mechanisms that occur across the three groups. Aim 3 will improve our understanding of the pathogenesis of OA in hips with FAIS by identifying relationships between anatomy, chondral mechanics, and cartilage ultrastructure. Here, quantitative magnetic resonance imaging will estimate proteoglycan content and collagen organization within hip cartilage. These data may also inform new methods to diagnose, stage, and monitor the disease.