Background: Anterior cruciate ligament (ACL) tears have been implicated in the development of osteoarthritis. Limited data exist on longitudinal follow-up of isolated ACL injury.
Hypotheses: All isolated ACL tears are associated with some degree of cartilage injury that will deteriorate over time. There is a threshold of magnetic resonance imaging (MRI)–detectable cartilage injury that will correlate with adverse change in subjective patient-reported outcome measures.
Study Design: Cohort study, Level of evidence, 2.
Methods: The authors conducted a prospective, observational analysis of 42 knees in 40 patients with acute, isolated ACL injury (14 treated nonoperatively, 28 by reconstruction) with imaging at the time of injury and yearly follow-up for a maximum of 11 years. Morphologic MRI and quantitative T2 mapping was performed with validated outcome measures.
Results: All patients sustained chondral damage at initial injury. The adjusted risk of cartilage loss doubled from year 1 for the lateral compartment and medial femoral condyle (MFC) and tripled for the patella. By years 7 to 11, the risk for the lateral femoral condyle was 50 times baseline, 30 times for the patella, and 19 times for the MFC. There was increased risk of cartilage degeneration over the medial tibial plateau (MTP) (P = .047; odds ratio = 6.23; 95% confidence interval [CI], 1.03-37.90) and patella (P = .032; odds ratio = 4.88; 95% CI, 1.14-20.80) in nonsurgical patients compared with surgically treated patients. Size of the bone-marrow edema pattern was associated with cartilage degeneration from baseline to year 3 (P = .001 to .039). Each increase in the MFC Outerbridge score resulted in a 13-point decrease in the International Knee Documentation Committee subjective knee score (P = .0002). Each increase in the MTP resulted in a 2.4-point decrease in the activity rating scale (P = .002).
Conclusion: All patients with acute, traumatic ACL disruption sustained a chondral injury at the time of initial impact with subsequent longitudinal chondral degradation in compartments unaffected by the initial “bone bruise,” a process that is accelerated at 5 to 7 years’ follow-up.