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（由申请人提供）：股骨髋臼撞击（FAI）的特征是髋关节中股骨和/或髋臼上的异常骨生长，可能是髋关节骨关节炎（OA）的主要病因。诊断为FAI的患者表现出受限的髋关节运动和受损的软骨和盂唇（即，软骨唇）组织，表明FAI限制了活动范围并提高了软骨唇应力。生物力学因素被认为是骨关节炎的主要诱因。因此，为了建立FAI和OA之间的联系，必须确认FAI患者确实具有有害的髋关节生物力学。不幸的是，髋关节撞击尚未在体内观察到。此外，尚不清楚FAI是否会破坏髋关节的肌肉激活/力和软骨盂唇力学。因此，本研究的目标是测量髋关节运动学，肌肉力量/激活，和软骨盂唇应力在活的人类受试者与FAI。 对于目标1，双重荧光透视和基于模型的无标记跟踪将在受试者行走、下蹲和旋转时捕获髋骨的运动，基于反射标记的运动捕获将跟踪双重荧光透视视野之外的关节的运动学。作为目标1的一部分开发的肌肉模型将预测肌肉激活和产生所观察到的运动所需的力，并估计净髋关节反作用力（JRF）。目标1的假设是，相对于对照组，在行走、下蹲和旋转运动期间，FAI患者的髋关节活动范围将减少，最小骨间距离/撞击的位置不同，肌肉激活/力水平改变。对于目标2，有限元（FE）模型将预测目标1活动期间的组织力学。FE模型将包括患者特定的骨和软骨盂唇组织解剖结构，并将使用目标1量化的髋关节JRF加载。使用FE预测的软骨盂唇组织生物力学，经验证的应力阈值标准将评估FAI髋关节OA的风险。预计FAI患者在骨软骨和软骨盂唇边界附近的最大剪切应力将增加，最大应力区域将对应于相同患者术中观察到的损伤位置。 这项工作的长期目标是建立固定资产投资和OA之间的经验联系。目标1将阐明FAI患者的运动方式是否与尺寸匹配的对照组不同（通过关节运动学），使用肌肉的方式是否不同（肌肉激活/力量），以及是否经历了潜在的破坏性关节反作用力。目标2将显示运动学、力和解剖结构的差异如何导致不同（和有害）的软骨盂唇力学，这些力学可能导致以后的OA。目标1和2将共同导致FAI最全面的生物力学研究，并有助于为FAI和OA的未来研究提供方向。奖学金培训计划将涵盖实验和计算生物力学的各个方面，并将为申请人在肌肉骨骼研究中的成功职业生涯做好准备。