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Purpose To investigate the isolated and combined effects of medial patellofemoral ligament (MPFL) and medial patellotibial ligament (MPTL) deficiency and reconstruction on patellofemoral kinematics. Methods Sixteen matched-paired female cadaveric knee specimens with a mean age of 53.5 years (range, 26-65) were tested in 5 conditions: (1) intact, (2) MPFL or MPTL cut, (3) MPFL and MPTL combined cut, (4) MPFL or MPTL reconstruction, and (5) MPFL and MPTL combined reconstruction. Dynamic testing allowed continuous analysis of kinematics from 0° to 90° of knee flexion. Knees were also tested statically using a lateral load of 45 N at 0°, 30°, 60°, and 90° of flexion. In both dynamic and static loading tests, a motion capture system detected patellar position for each testing state to distinguish changes in patellar kinematics. Random-intercepts linear mixed-effects models were used to compare patellar kinematics. Results The MPFL is the primary restraint to lateral translation of the patella at all knee flexion angles. MPTL deficiency alone did not create significant patella instability, but further increased instability when the MPFL was deficient. Isolated MPFL and combined reconstruction provided improved stability. Through full range of motion native patella tracking was best recreated with combined ligament reconstruction. Conclusions The MPFL plays the greatest role in medial patellar stability, but the MPTL appears to have an influence on patella tracking. This study provides further understanding to the impact of the MPFL and MPTL on patellofemoral motion with implications for reconstruction to improve stability and optimize patellofemoral tracking. Clinical Relevance This study provides further understanding of the role of the MPFL and MPTL on patellofemoral motion with implications for reconstruction to improve stability and optimize patellofemoral tracking.

Cell-based therapy for augmentation of core decompression (CD) using mesenchymal stromal cells (MSCs) is a promising treatment for early stage osteonecrosis of the femoral head (ONFH). Recently, the therapeutic potential for immunomodulation of osteogenesis using preconditioned (with pro-inflammatory cytokines) MSCs (pMSCs), or by the timely resolution of inflammation using MSCs that over-express anti-inflammatory cytokines has been described. Here, pMSCs exposed to tumor necrosis factor-alpha and lipopolysaccharide for 3 days accelerated osteogenic differentiation in vitro. Furthermore, injection of pMSCs encapsulated with injectable hydrogels into the bone tunnel facilitated angiogenesis and osteogenesis in the femoral head in vivo, using rabbit bone marrow-derived MSCs and a model of corticosteroid-associated ONFH in rabbits. In contrast, in vitro and in vivo studies demonstrated that genetically-modified MSCs that over-express IL4 (IL4-MSCs), established by using a lentiviral vector carrying the rabbit IL4 gene under the cytomegalovirus promoter, accelerated proliferation of MSCs and decreased the percentage of empty lacunae in the femoral head. Therefore, adjunctive cell-based therapy of CD using pMSCs and IL4-MSCs may hold promise to heal osteonecrotic lesions in the early stage ONFH. These interventions must be applied in a temporally sensitive fashion, without interfering with the mandatory acute inflammatory phase of bone healing.