Lee DY, et al. Clin Orthop Surg. 2018 Dec;10(4):448-454. https://doi.org/10.4055/cios.2018.10.4.448

Antioxidant enzymes are decreased in osteoarthritis (OA) patients, implying the role of oxidative stress in osteoarthritis pathogenesis. The aim of this study was to evaluate the cytoprotective effects of delphinidin, a potent antioxidant, in human chondrocytes and the underlying mechanisms. The cytoprotective mechanism induced by delphinidin against oxidative stress (H₂O₂) in human chondrocytes was investigated. Cell viability and death were evaluated using proapoptotic and antiapoptotic markers such as cleaved caspase-3 (c-caspase-3), cleaved poly(ADP-ribose) polymerase N-acetylcysteine (c-PARP), Bcl-X_L, and transcription factors associated with redox and inflammation regulation, including nuclear factor kappa B (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Induction of autophagy was assessed by formation of LC3-II and autophagosome-(LC3 punctate, monodansylcadaverine (MDC) and acridine orange staining) in the presence or absence of an autophagy inhibitor. Treatment with delphinidin itself at concentration below 50 µM for 24 h did not affect viability of chondrocytes. Delphinidin inhibited reactive oxygen species (ROS)-induced apoptosis by significantly decreasing apoptosis markers such as c-caspase-3 and c-PARP while increasing antiapoptotic marker Bcl-X_L and antioxidant response NF-κB and Nrf2 pathways. Delphinidin also activated cytoprotective autophagy to protect chondrocytes during oxidative stresses. Activation of autophagy with autophagy inducer rapamycin also inhibited ROS-induced cell death and decreased proapoptotic proteins but increased antiapoptotic protein Bcl-X_L, NF-κB, and Nrf2. Delphinidin can protect chondrocytes against H₂O₂-induced apoptosis via activation of Nrf2 and NF-κB and protective autophagy. Thus, it can inhibit OA with protection of chondrocytes. Delphinidin can protect chondrocytes against H₂O₂-induced ROS with maintenance of homeostasis and redox. These results suggest that delphinidin could be used to protect chondrocytes against age-related oxidative stress and other oxidative stresses in the treatment of OA. Thus, delphinidin may play a critical role in preventing the development and progression of OA.

This study used the finite element method(FEM) to investigate how pressure on the lumbar spine changes during dynamic movements in different postures: standing, erect sitting on a chair, slumped sitting on a chair, and sitting on the floor. Three load modes (flexion, lateral bending, and axial rotation) were applied to the FEM, simulating movements of the lumbar spine. Results showed no significant difference in pressure distribution on the annulus fiber and nucleus pulposus, representing intradiscal pressure, as well as on the cortical bone during movements between standing and erect sitting postures. However, both slumped sitting on a chair and sitting on the floor postures significantly increased pressure on the nucleus pulposus, annulus fibrosus, and cortical bone in all three movements when compared to standing or erect sitting on a chair. Notably, sitting on the floor resulted in even higher pressure on the nucleus pulposus and annulus fibers compared to slumped sitting on a chair. The decreased lumbar lordosis while sitting on the floor led to the highest increase in pressure on the annulus fiber and nucleus pulposus in the lumbar spine. In conclusion, maintaining an erect sitting position with increased lumbar lordosis during seated activities can effectively reduce intradiscal pressure and cortical bone stress associated with degenerative disc diseases and spinal deformities.

Study DesignA retrospective clinical case series.PurposeTo determine the strength of association between cage retropulsion and its related factors.Overview of LiteratureLumbar interbody fusion with cage can obtain a firm union and can restore the disc height with normal sagittal and coronal alignment. Although lumbar interbody fusion procedures have satisfactory clinical outcomes, peri- and postoperative complications regarding the cage remain challenging.MethodsFrom January 2006 to June 2016, 1,047 patients with lumbar degenerative disc disease who underwent posterior lumbar interbody fusion or transforaminal interbody fusion at Gyeongsang National University Hospital were enrolled. Medical records and pre- and postoperative radiographs were reviewed to identify significant cage retropulsion-related factors. The associations between cage retropulsion with various risk factors were evaluated by calculating odds ratios (ORs) and 95% confidence intervals (CIs) using multiple logistic regression analysis.ResultsOf 1,229 disc levels, 16 cases (1.3%, 10 men and 6 women) had cage retropulsion. Univariate analysis revealed no significant differences between the cage retropulsion group and the no cage retropulsion group with regard to demographic data such as age, sex, weight, height, body mass index (BMI), smoking habits, presence of osteoporosis, and duration of follow-up. Multivariate analysis revealed that low BMI (OR, 0.875; 95% CI, 0.771–0.994; p=0.040), presence of screw loosening (OR, 27.400; 95% CI, 7.818–96.033; p<0.001), and pear-shaped disc (OR, 9.158; 95% CI, 2.455–34.160; p=0.001) were significantly associated with cage retropulsion.ConclusionsThis study demonstrated that low BMI, loosening of posterior instrumentation, and pear-shaped disc were associated with cage retropulsion after lumbar interbody fusion. Therefore, when performing lumbar interbody fusion with a cage, surgeons should have skillful surgical techniques for firm fixation to prevent cage retropulsion, particularly in non-obese patients.

Introduction The aim of this study is to evaluate whether early (<8 h) surgical decompression is better in improving neurologic outcomes than late (?8 h) surgical decompression for traumatic spinal cord injury (tSCI). Methods The various electronic databases were used to detect relevant articles published up until May 2016 that compared the outcomes of early versus late surgery for tSCI. Data searching, extraction, analysis, and quality assessment were performed according to Cochrane Collaboration guidelines. The results are presented as relative ratio (RR) for binary outcomes and mean difference (MD) for continuous outcomes with 95% confidence intervals (CIs). Results Seven studies were finally included in this meta-analysis. There were significant differences between the 2 groups in neurologic improvement (MD = 0.54, 95% CI = -18.52 to -7.02, P < 0.0001) and length of hospital stay (MD = -12.77, 95% CI = 0.34–0.74, P < 0.00001). However, no significant differences were found between the 2 groups in perioperative complications (OR = 0.95, 95% CI = 0.35–2.61, P = 0.92). Conclusions Early surgical decompression within 8 h after tSCI was beneficial in terms of neurologic improvement compared with late surgery. Early surgical decompression (within 8 h) is recommended for patients with tSCI. Level of evidence Level III, therapeutic study. ER - Keywords Spinal cord injuries Decompression Timing of surgery Meta-analysis

Introduction The aim of this study was to evaluate whether delphinidin is cytoprotective or cytotoxic in osteosarcoma cell lines, and to elucidate the underlying mechanisms. Materials and methods The present study investigated whether apoptosis or autophagy is induced by delphinidin in human osteosarcoma cell lines. Delphinidin was used as the antioxidant, along with two autophagy inhibitors: 3-methyladenine and bafilomycin A1. Cell viability and known autophagic markers, such as LC3-II expression, were evaluated. Reactive oxygen species (ROS) formation and cell cycle analysis were also investigated. Results Delphinidin showed concentration-dependent cytotoxicity to osteosarcoma cell. Delphinidin is closely associated with apoptotic cell death mechanisms and pathways related to ROS accumulation. In addition, we observed delphinidin-induced autophagosome formation and increasing levels of LC3-II conversion. However, in spite of delphinidin induced autophagy, the cytotoxic effects induced in the osteosarcoma cells may not be operating via autophagic cell death mechanisms. Conclusions Delphinidin compromises the cellular protective mechanisms by inhibiting autophagy, permitting ROS to accumulate and finally enhance apoptotic cell death. Our results indicate that delphinidin may play a critical role as a chemotherapeutic agent by preventing the development and progression of osteosarcoma cells. ER - Keywords Delphinidin Cytotoxicity Autophagy Apoptosis Osteosarcoma