It is unclear why ACL rupture increases osteoarthritis risk, regardless of ACL reconstruction. Our aims were: 1) to establish the reliability and accuracy of a direct method of determining tibiofemoral contact in vivo with UO-MRI, 2) to assess differences in knees with ACL rupture treated nonoperatively versus operatively, and 3) to assess differences in knees with ACL rupture versus healthy knees.

We recruited a convenience sample of patients with prior ACL rupture. Inclusion criteria were: 1) adult participants between 18–50 years old; 2) unilateral, isolated ACL rupture within the last five years; 3) if reconstructed, done within one year from injury; 4) intact cartilage; and 5) completed a graduated rehabilitation program culminating in return to sport or recreational activities. Participants were excluded if they had other ligament ruptures, osteoarthritis, an incompletely rehabilitated injury, were prohibited from undergoing MRI, or had a history of ACL re-rupture. Using the UO-MRI, we investigated tibiofemoral contact area, centroid location, and six degrees of freedom alignment under standing, weightbearing conditions with knees extended. We compared patients with ACL rupture treated nonoperatively versus operatively, and ACL ruptured knees versus healthy control knees. We assessed reliability using the intra-class correlation coefficient, and accuracy by comparing UO-MRI contact area with a 7Tesla MRI reference standard. We used linear mixed-effects models to test the effects of ACL rupture and ACL reconstruction on contact area. We used a paired t test for centroid location and alignment differences in ACL ruptured knees versus control knees, and the independent t test for differences between ACL reconstruction and no reconstruction. Analyses were performed using R version 3.5.1. We calculated sample size based on a previous study that showed a contact area standard deviation of 13.6mm2, therefore we needed eight or more knees per group to detect a minimum contact area change of 20mm2with 80% power and an α of 0.05.

We recruited 18 participants with ACL rupture: eight treated conservatively and 10 treated with ACL reconstruction. There were no significant differences between the operative and nonoperative ACL groups in terms of age, gender, BMI, time since injury, or functional knee scores (IKDC and KOOS). The UO-MRI demonstrated excellent inter-rater, test-retest, and intra-rater reliability with ICCs for contact area and centroid location ranging from 0.83–1.00. Contact area measurement was accurate to within 5% measurement error. At a mean 2.7 years after injury, we found that ACL rupture was associated with a 10.4% larger medial and lateral compartment contact areas (P=0.001), with the medial centroid located 5.2% more posterior (P=0.001). The tibiae of ACL ruptured knees were 2.3mm more anterior (P=0.003), and 2.6° less externally rotated (P=0.010) relative to the femur, than contralateral control knees. We found no differences between ACL reconstructed and nonreconstructed knees.

ACL rupture was associated with significant mechanical changes 2.7 years out from injury, which ACL reconstruction did not restore. These findings may partially explain the equivalent risk of post-traumatic osteoarthritis in patients treated operatively and nonoperatively after ACL rupture.

Femoroacetabular impingement (FAI) deformities are a potential precursor to hip osteoarthritis and an important contributor to non-arthritic hip pain. Some hips with FAI deformities develop symptoms of pain in the hip and groin that are primarily position related. The reason for pain generation in these hips is unclear. Understanding potential impingement mechanisms in FAI hips will help us understand pain generation. Impingement between the femoral head-neck contour and acetabular rim has been proposed as a pathomechanism in FAI hips. This proposed pathomechanism has not been quantified with direct measurements in physiological postures. Research question: Is femoroacetabular clearance different in symptomatic FAI hips compared to asymptomatic FAI and control hips in sitting flexion, adduction, and internal rotation (FADIR) and squatting postures?. We recruited 33 participants: 9 with symptomatic FAI, 13 with asymptomatic FAI, and 11 controls from the Investigation of Mobility, Physical Activity, and Knowledge Translation in Hip Pain (IMAKT-HIP) cohort. We scanned each participant's study hip in sitting FADIR and squatting postures using an upright open MRI scanner (MROpen, Paramed, Genoa, Italy). We quantified femoroacetabular clearance in sitting FADIR and squatting using beta angle measurements which have been shown to be a reliable surrogate for acetabular rim pressures. We chose sitting FADIR and squatting because they represent, respectively, passive and active maneuvers that involve high flexion combined with internal/external rotation and adduction/abduction, which are thought to provoke impingement. In the squatting posture, the symptomatic FAI group had a significantly smaller minimum beta angle (−4.6º±15.2º) than the asymptomatic FAI (12.5º ±13.2º) (P= 0.018) and control groups (19.8º ±8.6º) (P=0.001). In the sitting FADIR posture, both symptomatic and asymptomatic FAI groups had significantly smaller beta angles (−9.3º ±14º [P=0.010] and −3.9º ±9.7º [P=0.028], respectively) than the control group (5.7º ±5.7º). Our results show loss of clearance between the femoral head-neck contour and acetabular rim (negative beta angle) occurred in symptomatic FAI hips in sitting FADIR and squatting. We did not observe loss of clearance in the asymptomatic FAI group for squatting, while we did observe loss of clearance for this group in sitting FADIR. These differences may be due to accommodation mechanisms in the active, squatting posture that are not present in the passive, sitting FADIR posture. Our results support the hypothesis that impingement between the femoral head-neck contour and acetabular rim is a pathomechanism in FAI hips leading to pain generation