Biomechanical Markers of PTOA after ACL Reconstruction and Meniscal Resection

项目摘要 据估计，每年有12万例前十字韧带(ACL)撕裂通过手术修复。 美国。手术修复可以稳定前交叉韧带缺陷的膝盖，但越来越多的证据表明 手术不能改变进展为早发性骨关节炎，即创伤后骨关节炎。 (PTOA)。接受前十字韧带重建术(ACLR)的患者更有可能患PTOA， 尤其是那些在前交叉韧带撕裂的同时遭受半月板损伤的人。半月板切除和半月板切除 摘除可能会对患者长期的膝关节健康造成灾难性的后果。大约21%-48% 在ACLR期间全部或部分切除半月板的患者中，继续发展为PTOA。有效 半月板切除后停止PTOA的治疗方法还没有构思，因为为什么 疾病的发展还没有得到很好的了解。理论化的机制推测，尽管整体恢复 稳定性、前交叉韧带手术重建和半月板切除改变了膝关节的生物力学 关节：改变软骨对负荷的反应方式，移动胫骨和股骨之间的接触点 软骨，增加胫骨和股骨在物理过程中彼此移动的速度 活动，并减少骨骼之间的距离。反过来，软骨的切片体验 不习惯的负载，以及不可逆的损害结果。这一理论的核心是这样一个概念，即骨骼 与非手术膝关节相比，膝关节的发音不同。虽然这一论点在概念上是有道理的，但它 在体力活动中，骨骼的关节结构可能不同，但关节软骨的关节结构不同 受伤时的损伤会引发一系列分解代谢事件，最终导致关节间隙宽度的丧失 骨性关节炎的标志性结局。研究团队成员拥有必要的技能、专业知识和 通过直接测量来支持或驳斥上述假设框架的设备 生物力学因素。具体地说，高速双荧光透视，一种X射线技术，将测量骨骼 具有亚毫米和亚度偏差和精度的运动；定量磁共振成像(QMRI) 将评估软骨成分；传统MRI将量化三维软骨结构。在 目前的提议是，PTOA疾病发生和发展的生物力学标志物将被一次测量 手术后两年。这项纵向研究将解决以下两个目标。目标1：改进 活体膝关节对比分析对PTOA发病机制的认识 ACLR+M术后一年患者的力学(胫股软骨劳损和关节运动学)。目标2： 通过对纵向变化进行基于图像的分析，提高对PTOA发病机制的理解 在ACLR+M之后的软骨方面，完成本提案中的目标将产生新的和有影响力的见解 通过提高我们对初始事件的理解，ACLR+M患者PTOA的加速时间线 与PTOA的发病和早期进展有关。

Project Summary An estimated 120,000 anterior cruciate ligament (ACL) tears are repaired surgically on an annual basis in the United States. Surgical repair stabilizes the ACL-deficient knee, but a growing body of evidence suggests that surgery does not alter the progression to early-onset osteoarthritis, known as post-traumatic osteoarthritis (PTOA). Patients who undergo anterior cruciate ligament reconstruction (ACLR) are more likely to get PTOA, especially those who sustained a meniscal injury at the same time as their ACL tear. Meniscal resection and removal can have disastrous consequences for patients’ long-term knee joint health. Approximately 21%-48% of patients who had all or part of their meniscus removed during ACLR go on to develop PTOA. Effective treatments for stopping PTOA after meniscal resection have not been conceived because the reasons why the disease develops are not well understood. The theorized mechanism speculates that, despite restoring overall stability, surgical reconstruction of the ACL and resection of the meniscus alter the biomechanics of the knee joint: changing the way cartilage responds to load, shifting the point of contact between tibial and femoral cartilage, increasing the speed at which the tibia and femur bones move past one another during physical activities, and decreasing in the distance between the bones. In turn, sections of cartilage experience unaccustomed loads, and irreversible damage results. Central to this theory is the notion that the bones articulate differently compared to non-surgical knees. While this argument makes sense conceptually, it’s possible that the bones do not articulate differently during physical activity, but instead articular cartilage damage at the time of injury starts a sequence of catabolic events culminating in loss of joint space width—the hallmark outcome of osteoarthritis. The study team members possess the necessary skills, expertise and equipment to support or refute the aforementioned hypothetical framework through direct measurements of biomechanical factors. Specifically, high-speed dual fluoroscopy, an X-ray technique, will measure bone motion with submillimeter and subdegree bias and precision; quantitative magnetic resonance imaging (qMRI) will assess cartilage composition; traditional MRI will quantify three-dimensional cartilage structure. In the current proposal, biomechanical markers for PTOA disease onset and progression will be measured at one and two years after surgery. This longitudinal study will address the following two aims. Aim 1: To improve understanding of PTOA pathogenesis by performing a side-to-side comparative analysis of in-vivo knee mechanics (tibiofemoral cartilage strain and arthrokinematics) in patients one year after ACLR+M. Aim 2: To improve understanding of PTOA pathogenesis by performing an image-based analysis of longitudinal changes in cartilage after ACLR+M. Completion of the aims in this proposal will generate new and impactful insights into PTOA’s accelerated timeline in ACLR+M patients by improving our understanding of the initial events associated with the onset and early progression to PTOA.