The Effects of Lateral Meniscus Posterior Root Tear and its Repair on Knee Stability of Internal Rotation and Forward Shift: A Biomechanical Kinematics Cadaver Study.

Objective: Lateral meniscal posterior root (LMPR) is an important stabilizer for knee joint, providing the stability during tibia forward shifting and internal rotating. It is still controversial that whether the LMPR tear (LMPRT) should be repaired together with ACL reconstruction. This study aims to investigate the effects of LMPR on knee stability with intact ACL. Methods: Eight cadaver knees were used and performed the biomechanical kinematics tests in orders of: Group A: the LMPR was intact; Group B: the LMPR was cut off from its tibial end; Group C: the LMPRT has been repaired. 1) An internal rotation moment (5 Nm) was given to the tibia, then the internal rotation angle of the tibia was measured; 2) An forward shifting force (134 N) was given to the tibia, then the anterior displacement of the tibia was measured; 3) An internal rotation moment (5 Nm) and a valgus moment (10 Nm) were given to the tibia, then the internal rotation angle and the anterior displacement was measured. The stability was inferred from smaller rotation angle and displacement, and all of the angles and displacements were measured at knee flexion of 0°, 30°, 60° and 90°, respectively. Results: Comparing to Group A, the internal rotation angle in Group B was increased significantly at knee flexion of 30° (p = 0.025), 60° (p = 0.041), 90° (p = 0.002); the anterior tibia displacement in Group B was increased significantly at knee flexion of 30° (p = 0.015), 60° (p = 0.024); at knee valgus, the internal rotation angle was also increased significantly at knee flexion of 60° (p = 0.011), 90° (p = 0.037). Comparing to Group B, the internal rotation angle in Group C was decreased significantly at knee flexion of 30° (p = 0.030), 60° (p = 0.019), 90° (p = 0.021); the anterior displacement in Group C was decreased significantly at knee flexion of 30° (p = 0.042), 60° (p = 0.037); at valgus, the internal rotation angle was also decreased significantly at knee flexion of 60° (p = 0.013), 90° (p = 0.045). Comparing to Group A, only the internal rotation angle (p = 0.047) and anterior displacement (p = 0.033) in Group C were increased at knee flexion of 30°. Conclusion: In simulated knee with intact ACL, LMPRT can still lead to the notable internal rotational instability at knee flexion from 30° to 90°, as well as the anterior shift instability at knee flexion from 30° to 60°. LMPRT repair help to improve the internal rotation stability at 30° and restore it at 60° to 90°, and improve the anterior shift stability at 30° and restore it at 60°.

Peroxisome Proliferator-Activated Receptor-γ Coactivator-1α Inhibits Vascular Calcification Through Sirtuin 3-Mediated Reduction of Mitochondrial Oxidative Stress.

Aims: Vascular calcification is associated with cardiovascular death in patients with chronic kidney disease (CKD). Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) plays an important role in various cardiovascular diseases. However, its role in vascular calcification remains unknown. Results: Adenine-induced rat CKD model was used to induce arterial medial calcification. The level of PGC-1α decreased in abdominal aorta of CKD rats. Overexpression of PGC-1α significantly ameliorated calcium deposition in rat abdominal aorta, isolated carotid rings, and cultured vascular smooth muscle cells (VSMCs). Mitochondrial reactive oxygen species (mtROS) increased in calcifying aorta and VSMCs. Upregulation of PGC-1α inhibited, whereas PGC-1α depletion promoted ß-glycerophosphate-induced mtROS production and calcium deposition. Moreover, PGC-1α increased superoxide dismutase 1 (SOD1) and SOD2 contents in vivo and in vitro, whereas SOD2 deletion eliminated PGC-1α-mediated mtROS change and promoted calcium deposition. Mechanistically, sirtuin 3 (SIRT3) expression declined in calcifying aorta and VSMCs, while PGC-1α overexpression restored SIRT3 expression. Inhibition of SIRT3 by 3-TYP or siRNA (small interfering RNA) reduced PGC-1α-induced upregulation of SOD1 and SOD2, and abolished the protective effect of PGC-1α on calcification of VSMCs. Importantly, PGC-1α was reduced in calcified femoral arteries in CKD patients. In phosphate-induced human umbilical arterial calcification, upregulation of PGC-1α attenuated calcium nodule formation, while this protective effect was abolished by SIRT3 inhibitor. Innovation: We showed for the first time that PGC-1α is an important endogenous regulator against vascular calcification. Induction of PGC-1α could be a potential strategy to treat vascular calcification in CKD patients. Conclusions: PGC-1α protected against vascular calcification by SIRT3-mediated mtROS reduction.