Comparison of computer-assisted navigated technology and conventional technology in high tibial osteotomy (HTO): a meta-analysis.

BACKGROUND: Though some studies have reported navigated high tibial osteotomy (HTO) is a useful procedure to correct knee deformity. There is still great controversy whether navigated HTO can achieve better accuracy of limb alignment and greater clinical outcomes. Current meta-analysis was conducted to investigate whether better radiographic outcomes and clinical outcomes could be acquired in navigated HTO compared with the conventional procedure. METHOD: We conducted a literature search in the electronic databases, including Medline, Embase, the Cochrane Library, and Web of Science. We identified studies published before August 2020. We also checked the references of the related articles for any relevant studies. We strictly followed the Preferred Reporting Items for Systematics reviews and Meta-Analysis (PRISMA) guidelines in this review. This research was performed using Review Manager 5.4 software. RESULTS: Fourteen articles were included, involving 1399 knees. Our meta-analysis indicated that patients undergoing navigated HTO had significantly better outcomes in outliers of aimed limb alignment (RD=-0.24, 95% CI: =-0.34 to -0.13, p < 0.01), outliers of aimed tibial posterior slope (TPS) (RD=-0.41, 95% CI: -0.51 to -0.30, p < 0.01), Range of Motion (ROM) (MD = 6.37, 95%CI: 0.83-11.91, p = 0.02), and American knee society knee score (AKS knee score) (MD = 3.88, 95%CI: 1.37-6.39, p = 0.002). No significant differences were found in Lysholm score (MD = 1.30, 95%CI: -0.31 to 2.90, p = 0.11), American knee society function score (AKS function score) (RD = 1.42, 95%CI: -0.15 to 2.99, p = 0.08), complications (RD=-0.01, 95% CI: = -0.05 to 0.04, p = 0.77), delayed union (RD=-0.01, 95% CI: = -0.02 to 0.03, p = 0.59), and reoperation (RD = 0, 95% CI: -0.09 to 0.10, p = 0.98) between the two groups. The operation time in the navigated group was 15.46 min longer than in the conventional group. CONCLUSION: Navigated HTO provided more accurate and reproducible radiographic outcomes in the correction of the malalignment than conventional techniques, and there is no difference in the risk of complications compared with conventional HTO. However, it is unclear whether navigation HTO can achieve better clinical results. More randomized controlled trials (RCTs) with high quality, large sample size, and sufficient follow-up period are required.

MicroRNA-196a overexpression promotes cell proliferation and inhibits cell apoptosis through PTEN/Akt/FOXO1 pathway.

MicroRNAs (miRNAs) are endogenous, non-coding, small RNAs, which play a critical role in regulating varieties of the biological and pathologic processes. MiR-196a has been reported to take part in tumorigenic progression of osteosarcoma (OS). However, the effects of miR-196a on OS are still unclear. The objective of this study is to investigate the molecular mechanism of miR-196a in osteosarcoma cells. In the present study, the expression of miR-196a in OS cell lines was detected by real-time PCR. We found that the expression level of miR-196a was markedly up-regulated in osteosarcoma cell lines compared with normal osteoblastic cells. Then, the miR-196a mimic was transiently transfected into MG63 and U2OS cells using Lipofectamine™ 2000 reagent. Subsequently, the MTT and Brdu-ELISA results showed that up-regulation of miR-196a promoted the cell viability and proliferation. Our results also showed that miR-196a mimic accelerated cell cycle progression of MG63 and U2OS cells by down regulation of p21 and p27, and upregulation of cyclin D1. In addition, overexpression of miR-196a suppressed apoptosis of MG63 and U2OS cells due to increasing BCL2L2 and MCL-1 expressions, and then inactivating caspase-3. Eventually, the effect of miR-196a mimic on the PTEN/phosphoinositide 3-kinase (PI3K)/Akt signaling pathway was explored by Western blot. From our results, transfection of miR-196a decreased the expression of PTEN and increased the phosphorylation of PI3K and Akt. Taken together, miR-196a should be an oncogene in osteosarcoma. The possible mechanism was that overexpression of miR-196a promoted proliferation of MG63 and U2OS cells by modulating the PTEN/PI3K/Akt signaling pathway.