Biomechanical Markers of PTOA after ACL Reconstruction and Meniscal Resection

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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.