Biomechanical factors affecting metatarsal fatigue and bone stress injury risk

项目摘要 近50%的骨应力损伤（BSI）诊断发生在20岁以下的个体中， 青少年BSI在过去十年中增加了两倍。BSI是骨骼反复超负荷的结果， 超过了骨重建，导致微损伤的积累。足部解剖、生物力学、肌肉 功能和外部因素决定了在行走或跑步期间传递到跖骨上的力。反过来， 所产生的力产生机械应变，该机械应变根据跖骨结构和局部骨密度而变化。在这里， 我们提出了一种新的力学测试，计算建模和定量图像的组合， 分析以表征足部肌肉力、跖骨结构和跖骨之间的相互作用 损伤累积我们假设，支持足弓的肌肉减少了背侧弯曲， 压缩跖骨（目标1）。我们相信这可能会减少疲劳过程中的损伤积累 载荷，由于骨的各向异性材料特性（目标2）。我们还认为受损的肌肉 功能和骨结构将通过增加骨应变的机制与BSI（目的3）相关。 这些假设是基于足部肌肉无力，足部解剖结构的变化， 在BSI跑步者中观察到低骨密度。为了更好地理解 跖骨损伤和肌肉激活在运行过程中，我们提出了三个目标。目标1：确定如何 肌肉激活可以影响跑步过程中跖骨的负荷，通过模拟分析， 内在和外在足部肌肉的生物力学贡献。目的2：比较弯曲与 使用实验测试对整个跖骨疲劳失效/损伤累积施加轴向载荷。目标3： 比较近期（4岁以内）女子跑步运动员足部肌肉力量和跖骨结构 测试周）与无跖骨BSI的比较。 如果我们的假设得到支持，这表明跖骨BSI的风险可以通过加强 以及通过改变跖骨负荷方向和减少应变的机制激活足部肌肉。 这可以直接告知临床干预，例如步态再训练、足部强化或 鞋袜.这项研究将为跖骨疲劳失效的机制提供证据， 跖骨BSI风险个体的识别。我们的研究团队包括骨科专家 生物力学（特洛伊），跑步损伤生物力学（戴维斯），骨骼健康和运动损伤（滕福德）， 使我们有独特的资格来从事这个多学科的项目。此外，我们的计划表明， 通过整合本科生和研究生，持续致力于学生培训 参与项目的各个方面。

Project Summary Nearly 50% of all bone stress injury (BSI) diagnoses occur in individuals under age 20 and the prevalence of adolescent BSI has tripled over the past decade. A BSI is the result of repetitive overload of the skeleton that exceeds bone remodeling, resulting in accumulation of microdamage. Foot anatomy, biomechanics, muscle function, and external factors dictate forces transmitted onto the metatarsals during walking or running. In turn, resulting forces create mechanical strain that varies by metatarsal structure and regional bone density. Here, we propose a novel combination of mechanical testing, computational modeling, and quantitative image analysis to characterize the interactions between foot muscle forces, metatarsal bone structure, and metatarsal damage accumulation. We hypothesize that muscles supporting the arch reduce dorsal bending and increase compression of the metatarsals (Aim 1). We believe this may reduce damage accumulation during fatigue loading, due to the anistropic material properties of bone (Aim 2). We also expect that impaired muscle function and bone structure will be associated with BSI (Aim 3) through mechanisms of increased bone strain. These hypotheses are based on clinical reports of foot muscle weakness, variations in foot anatomy, and observations of low bone density in runners with a BSI. To better understand the interactions between metatarsal damage and muscle activation during running, we propose three aims. Aim 1: Determine how muscle activation can influence metatarsal loading during running, by using simulation to analyze the biomechanical contribution of intrinsic and extrinsic foot muscles. Aim 2: Compare the effect of bending vs. axial loading on whole metatarsal fatigue failure/damage accumulation using experimental testing. Aim 3: Compare foot muscle strength and metatarsal bone structure between female runners with recent (within 4 weeks of testing) versus no metatarsal BSI. If our hypotheses are supported, it suggests that the risk of metatarsal BSI may be reduced via strengthening and activation of foot muscles, through mechanisms of altered metatarsal loading direction and reduced strain. This may directly inform clinical interventions such as gait retraining, foot strengthening, or changes in footwear. This research will provide evidence for the mechanisms contributing to metatarsal fatigue failure and the identification of individuals at risk for metatarsal BSI. Our research team includes experts in orthopaedic biomechanics (Troy), running injury biomechanics (Davis), and bone health and sports injury (Tenforde), making us uniquely qualified to pursue this multidisciplinary project. Additionally, our plan demonstrates our ongoing commitment to student training through integration of both undergraduate and graduate student involvement in all aspects of the project.