Poster 259: Compartmental Static Anterior Tibial Translation After ACL Reconstruction: A Quantitative MRI Study

OBJECTIVES: Post-traumatic osteoarthritis (PTOA) develops in 50% of individuals who sustain an anterior cruciate ligament (ACL) injury. The mechanisms responsible for accelerated cartilage deterioration in ACL-injured knees are not well established. Abnormal tibiofemoral spatial relationship, resulting from ACL deficiency, has been purported as a potential contributor to altered cartilage loading and, consequently, accelerated PTOA. On magnetic resonance imaging (MRI), ACL-injured knees have been found to exhibit excess static anterior tibial translation (ATT) relative to control knees of separate, uninjured patients (Figure 1). However, the quantitative extent of ATT restoration following ACL reconstruction (ACLR) is largely unknown. We aimed to determine if ACLR restores static ATT in the lateral and medial compartments in comparison to the contralateral knee. We hypothesized that ACLR would not restore static ATT of the lateral and medial compartments back to the normal position. METHODS: A prospective cohort study consisting of 30 patients with an acute ACL injury, with or without reparable meniscus tears, was designed. All patients underwent ACLR, performed by fellowship-trained orthopaedic surgeons using an anatomic, single bundle technique with accessory anteromedial portal drilling using autografts. MRI scans of both the injured and uninjured knees were performed 1) preoperatively within one month of ACL injury and 2) postoperatively six months after reconstruction. ATT of the lateral tibial plateau (LTP) and medial tibial plateau (MTP) were measured using a previously validated measurement method (Figure 2). This method entails identifying the mid-sagittal T1 MRI slice of the LTP and of the MTP. On each slice, the posterior aspect of the femoral condyle is located by plotting a best-fit ellipse to the condyle. The posterior aspect of the tibial plateau is then also identified. ATT for each compartment is then calculated as the anterior-to-posterior distance between tangential lines coincident with the posterior aspect of the femoral condyle and tibial plateau (Figure 2). Two-way analysis of variance (ANOVA) testing was performed to compare ATT between knees before and six months after ACLR. The two requisite factors for two-way ANOVA testing were limb, i.e. injured vs. uninjured, and time, i.e. preop vs. six months postop. RESULTS: ACL-injured knees exhibited higher LTP ATT than uninjured control knees, regardless of timepoint (Pre-op: Injured = 5.73 ± 2.67mm; Uninjured = 3.35 ± 2.06mm. 6 months post-op: Injured = 4.81 ± 2.38mm; Uninjured = 3.36 ± 1.96mm, p < 0.001). LTP ATT trended towards decreasing in the injured limb after ACLR but this difference did not reach statistical significance (p for limb x time interaction = 0.053, Figure 3). ACL-injured knees also exhibited higher MTP ATT than uninjured control knees, regardless of timepoint (Pre-op: Injured = 1.52 ± 2.58mm; Uninjured = -0.12 ± 2.44mm. 6 months post-op: Injured = 1.46 ± 2.46mm; Uninjured = 0.07 ± 2.46mm, p < 0.001). MTP ATT did not change after ACLR as there was no significant interaction of limb x time (p = 0.486, Figure 4). CONCLUSIONS: ACLR did not restore pathologic ATT of the LTP and MTP back to levels present in uninjured knees. Persistent pathologic tibiofemoral relationships may contribute to abnormal cartilage loading over time and possible accelerated PTOA. Further study of early chondral changes after ACLR is necessary to elucidate if compartment-specific ATT is associated with local cartilage degeneration. Such understanding of the mechanistic factors responsible for PTOA after ACL injury may inform future potential preventative interventions.