Hip Biomechanics and Tissue Damage Mechanisms in Femoroacetabular Impingement

股骨髋臼撞击中的髋关节生物力学和组织损伤机制

• 批准号: 9232897
• 负责人: Niccolo M Fiorentino
• 金额: $ 2.54万
• 依托单位: UNIVERSITY OF UTAH
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-04-01 至 2017-08-20
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9232897
• 关键词: Anatomy; Animal Model; Area; Articular Range of Motion; Articulation; Biomechanics; Bone Growth; Cartilage; Clinical; Computer Simulation; Conflict (Psychology); Data; Degenerative polyarthritis; Diagnosis; Disease; Elements; Encapsulated; Etiology; Exhibits; Fellowship; Femur; Finite Element Analysis; Fluoroscopy; Funding; Future; Geometry; Goals; Hip Joint; Hip Osteoarthritis; Hip region structure; Image; Image-Guided Surgery; Injury; Investigation; Joints; Lead; Life; Link; Location; Lower Extremity; Measures; Mechanics; Methodology; Modeling; Motion; Motivation; Movement; Muscle; Musculoskeletal; Operative Surgical Procedures; Orthopedics; Outcome; Pain; Patients; Pattern; Postdoctoral Fellow; Reaction; Research; Research Personnel; Rest; Risk; Source; Speed; Stress; Surgeon; System; Technology; Testing; Tissues; Torque; Training Programs; Universities; Utah; Walking; Work; X-Ray Computed Tomography; acetabulum; base; bone; career; experience; hip bone; human subject; in vivo; insight; instrument; kinematics; osteochondral tissue; premature; prevent; public health relevance; shear stress; simulation; treadmill

 DESCRIPTION (provided by applicant): Femoroacetabular impingement (FAI) is characterized by abnormal bone growth on the femur and/or acetabulum in the hip and may be the principle etiology of hip osteoarthritis (OA). Patients diagnosed with FAI exhibit restricted hp joint motion and damaged cartilage and labral (i.e., chondrolabral) tissue, suggesting that FAI restricts range of motion and elevates chondrolabral stresses. Biomechanical factors are considered the key initiator of OA. Thus, to establish the link between FAI and OA, it is imperative to confirm that FAI patients indeed have deleterious hip biomechanics. Unfortunately, hip impingement has yet to be observed in-vivo. Furthermore, it is not understood whether muscle activations/forces and chondrolabral mechanics are disrupted in the hip with FAI. The goals of this fellowship are therefore to measure hip kinematics, muscle forces/activations, and chondrolabral stresses in live human subjects with and without FAI. For Aim 1, dual fluoroscopy and model-based markerless tracking will capture the motion of hip bones while subjects walk, squat and pivot, and reflective marker-based motion capture will track kinematics for those joints outside of the dual fluoroscopy field of view. Muscle models developed as part of Aim 1 will then predict muscle activations and forces required to produce the observed movements and will estimate the net hip joint reaction force (JRF). The hypothesis of Aim 1 is that, relative to controls, during walking, squatting and pivoting motions, patients with FAI will have reduced hip range of motion, different locations of minimum bone- to-bone distance/impingement, and altered muscle activation/force levels. For Aim 2, finite element (FE) models will predict tissue mechanics during the activities from Aim 1. FE models will include patient-specific bone and chondrolabral tissue anatomy and will be loaded using the hip JRF quantified from Aim 1. Using the FE-predicted chondrolabral tissue biomechanics, a validated stress-threshold-criterion will evaluate the risk of OA in hips with FAI. It is expected that FAI patients will experience increased maximum shear stress near the osteochondral and chondrolabral borders, and that areas of maximum stress will correspond to locations of damage observed intra-operatively for the same patients. The long-term goal of this work is to establish an empirical link between FAI and OA. Aim 1 will clarify if FAI patients move differently than size-matched controls (via joint kinematics), use their muscles differently (muscle activations/forces) and experience potentially damaging higher joint reaction forces. Aim 2 will show how differences in kinematics, forces and anatomy result in dissimilar (and deleterious) chondrolabral mechanics that may lead to OA later in life. Together, Aims 1 and 2 will result in the most comprehensive biomechanical study of FAI and help provide direction for future investigations of FAI and OA. The fellowship training program will encapsulate all aspects of experimental and computational biomechanics and will prepare the applicant for a successful career in musculoskeletal research.

 描述（由适用提供）：股骨映射撞击（FAI）的特征是髋关节骨骼和/或髋臼的异常骨骼生长，并且可能是髋关节骨关节炎（OA）的原理病因。被诊断为FAI暴露限制的HP关节运动，软骨和Labral（即软骨支出）组织的患者表明，FAI限制了运动范围并提高了软骨固定应力。生物力学因子被认为是OA的关键引发剂。为了建立FAI和OA之间的联系，必须确认FAI患者确实已经删除了髋关节生物力学。不幸的是，髋关节撞击尚未在体内观察到。此外，尚不理解肌肉激活/力和软骨力学是否在髋关节中被FAI中断。因此，该团契的目标是衡量有或没有FAI的活人受试者中的髋部运动学，肌肉力量/激活和软骨的压力。对于AIM 1，双重透视镜和基于模型的无标记跟踪将捕获髋骨的运动，而受试者步行，下蹲和枢轴以及基于反射标记的运动捕获将跟踪在双透视视野外部的这些关节的运动学。作为AIM 1的一部分而开发的肌肉模型将预测产生观察到的运动所需的肌肉活化和力量，并将估计净髋关节反应力（JRF）。 AIM 1的假设是，相对于对照组，在步行，蹲和旋转运动过程中，FAI患者的髋关节运动范围会降低，最小骨至骨距离/撞击的不同位置以及肌肉激活/力量的改变。对于AIM 2，有限元（FE）模型将在AIM 1的活动中预测组织力学。Fe模型将包括患者特异性的骨骼和软骨组织解剖结构，并将使用AIM 1量化的HIP JRF进行加载。使用FE预测的软骨Babrabral组织生物力学，验证的压力 - 培训将与FAIS threshold-Certirip一起评估FAI的风险。预计FAI患者将在骨软骨和软骨边界附近会增加最大的剪切应力，并且最大压力的区域将对应于同一患者术中观察到的损害的位置。这项工作的长期目标是建立FAI和OA之间的经验联系。 AIM 1将阐明FAI患者的运动是否不同于尺寸匹配的对照（通过关节运动学），使用不同的肌肉（肌肉激活/力），并且经历了可能损害更高的关节反作用力的肌肉。 AIM 2将显示运动学，力和解剖学的差异如何导致不同（和有害的）软骨力学，这可能会导致生命以后的OA。共同，目标1和2将导致FAI最全面的生物力学研究，并为FAI和OA的未来研究提供指导。奖学金培训计划将囊括实验和计算生物力学的各个方面，并将为申请人做好准备，以成功地从事肌肉骨骼研究。