An understanding of a hierarchy of prosthetic design and implantation factors may be important to maximize impingement-free abduction motion as well as to avoid inferior impingement.

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Mesenchymal stem cells (MSCs) represent an attractive source for stem cell-based regenerative therapy, but they are vulnerable to oxidative stress-induced premature senescence in pathological conditions. We previously reported antioxidant and antiarthritic effects of melatonin on MSCs against proinflammatory cytokines. In this study, we hypothesized that melatonin could protect MSCs from premature senescence induced by hydrogen peroxide (H2O2) via the silent information regulator type 1 (SIRT1)-dependent pathway. In response to H2O2 at a sublethal concentration of 200 μM, human bone marrow-derived MSCs (BM-MSCs) underwent growth arrest and cellular senescence. Treatment with melatonin before H2O2 exposure cannot significantly prevent premature senescence; however, treatment with melatonin subsequent to H2O2 exposure successfully reversed the senescent phenotypes of BM-MSCs in a dose-dependent manner. This result was made evident by improved cell proliferation, decreased senescence-associated β-galactosidase activity, and the improved entry of proliferating cells into the S phase. In addition, treatment with 100 μM melatonin restored the osteogenic differentiation potential of BM-MSCs that was inhibited by H2O2-induced premature senescence. We also found that melatonin attenuated H2O2-stimulated phosphorylation of p38 mitogen-activated protein kinase, decreased expression of the senescence-associated protein p16INK4α, and increased SIRT1. Further molecular experiments revealed that luzindole, a nonselective antagonist of melatonin receptors, blocked melatonin-mediated anti-senescence effects. Inhibition of SIRT1 by sirtinol counteracted the protective effects of melatonin, suggesting that melatonin reversed senescence in cells through the SIRT1-dependent pathway. Together, these findings lay new ground for understanding oxidative stress-induced premature senescence and open perspectives for therapeutic applications of melatonin in stem cell-based regenerative medicine.

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Reverse shoulder arthroplasty is being used more frequently to treat irreparable rotator cuff tears in the presence of glenohumeral arthritis and instability. To date, however, design features and functions of reverse shoulder arthroplasty, which may be associated with subluxation and dislocation of these implants, have been poorly understood. We asked: (1) what is the hierarchy of importance of joint compressive force, prosthetic socket depth, and glenosphere size in relation to stability, and (2) is this hierarchy defined by underlying and theoretically predictable joint contact characteristics? We examined the intrinsic stability in terms of the force required to dislocate the humerosocket from the glenosphere of eight commercially available reverse shoulder arthroplasty devices. The hierarchy of factors was led by compressive force followed by socket depth; glenosphere size played a much lesser role in stability of the reverse shoulder arthroplasty device. Similar results were predicted by a mathematical model, suggesting the stability was determined primarily by compressive forces generated by muscles.

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The influence of lateral release of retinaculum on patellofemoral kinematics and contact characteristics after total knee arthroplasty was investigated in vitro. Lateral release altered the patellar tracking in patellar flexion, rotation, tilting, and translation. The contact force was decreased at high flexion angles. The contact area was slightly decreased and the contact region shifted laterally on the patellar button and medially on the femoral component at most of the flexion angles. The results suggest that the lateral release in total knee arthroplasty can change some patellar tracking and patellofemoral joint contact characteristics.