PurposeTo investigate the usefulness of three-dimensional (3D) printing in complex spinal surgery.MethodsThe study was conducted from October 2014 to March 2015 in Shenzhen Second Peoples' Hospital and 4 cases of complex severe spinal disorders were selected from our department. Among them one patient combined with congenital scoliosis, one with atlas neoplasm, one with atlantoaxial dislocation, and the rest one with atlantoaxial fracture-dislocation. The data of the diseased region was collected from computerized tomography scans for 3D digital reconstruction and rapid prototyping to prepare photosensitive resin models, which were applied in the treatment of these cases.ResultsThe use of 3D models reduced operating time and intraoperative blood loss as well as the risk of postoperative complications. Furthermore, no pedicle penetrations or screw misplacement occurred according to the postoperative planar radiographic images.ConclusionThe tactile models from 3D printing allow direct observation and measurement, helping the orthopedists to have accurate morphometric information to provide personalized surgical planning and better communication with the patient and coworkers. Moreover, the photosensitive resin models can also guide the actual surgery with the drilling of pedicle screws and safe resection of tumor.

MicroRNAs (miRNAs) have been corroborated to engage in the process of cellular activities in osteoporosis. However, few researches have been conducted to expose the integrated role of miR-497, leucine-rich alpha-2-glycoprotein-1 (LRG1) and transforming growth factor beta 1 (TGF-β1)/Smads signalling pathway in osteoporosis. Thereafter, the study is set out to delve into miR-497/LRG1/TGF-β1/Smads signalling pathway axis in osteoporosis. Osteoporosis bone tissues and normal bone tissues were collected. Rat osteoporosis models were constructed via ovariectomy. Model rats were injected with restored miR-497 or depleted LRG1 to explore their roles in osteoporosis. Rat osteoblasts were extracted from osteoporosis rats and transfected with restored miR-497 or depleted LRG1 for further verification. MiR-497 and LRG1 expression in femoral head tissues and osteoblasts of osteoporosis rats were detected. TGF-β1/Smads signalling pathway-related factors were detected. MiR-497 was poorly expressed while LRG1 was highly expressed and TGF-β1/Smads signalling pathway activation was inhibited in osteoporosis. MiR-497 up-regulation or LRG1 down-regulation activated TGF-β1/Smads signalling pathway, promoted collagen type 1 synthesis and suppressed oxidative stress in femoral head tissues in osteoporosis. MiR-497 restoration or LRG1 knockdown activated TGF-β1/Smads signalling pathway, promoted viability and suppressed apoptosis of osteoblasts in osteoporosis. Our study suggests that miR-497 up-regulation or LRG1 down-regulation

High-mobility group box 1 (HMGB1) is a nuclear protein that involves the binding with DNA and influences chromatin regulation and transcription. HMGB1 activates monocytes and neutrophils, which are involved in inflammation during wounding. In this study, we investigated the promotion of HMGB1 under hypoxia and determined the regulatory role of HMGB1 on the fibrosis of mouse osteoblast-like MC3T3-E1 cells or of human osteoblast MG-63 cells. Results demonstrated that HMGB1 expression was significantly upregulated in MC3T3-E1 or MG-63 cells under hypoxia. We also found that treatment with 10 and 100 ng/mL of HMGB1 significantly promoted the fibrosis-associated markers such as Collagen I, α-SMA, whereas downregulated the E-cadherin, indicating the differentiation of MC3T3-E1 or MG-63 cells into fibroblast cells. Further investigation indicated that the HMGB1 treatment markedly activated the mitogen-activated protein kinases (MAPKs), including extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38) phosphorylation, as well as nuclear factor (NF)-κB nuclear translocation. On the other side, using specific inhibitors and shRNAs of protein kinases, we observed that repression of ERK, JNK, p38, and NF-κB all inhibited HMGB1-induced cellular differentiation and migration of MC3T3-E1 cells. In addition, knocking down of advanced glycation end products (RAGE) but not Toll-like receptor (TLR)2 and TLR4 by shRNAs attenuated HMGB1-induced myofibroblast differentiation and migration. In conclusion, our study demonstrated that HMGB1 induced the fibrosis of osteoblasts in vitro via activating the RAGE-MAPK and NF-κB interaction signaling pathways.

The healing process of fractured bone is affected by the multiple factors regulating the growth and differentiation of osteoblasts and bone mesenchymal stem cells (MSCs), however, such markers and molecular events need to be orchestrated in details. This study investigated the effect of polyphenol(-)-epigallocatechin-3-gallate (EGCG) on the hypoxia-induced apoptosis and osteogenic differentiation of human bone marrow-derived MSCs, examined the miR-210 induction by EGCG, explored the target inhibition of the expression of receptor tyrosine kinase ligand ephrin-A3 (EFNA3) by miR-210, and then determined the association of the miR-210 promotion with the hypoxia-induced apoptosis and osteogenic differentiation. Results demonstrated that EGCG treatment significantly inhibited the hypoxia-induced apoptosis in MSCs and promoted the level of alkaline phosphatase (ALP), bone morphogenetic protein 2 (BMP-2), propeptide of type I procollagen I (PINP) and runt-related transcription factor 2 (RUNX2) in MSCs under either normoxia or hypoxia. Moreover, the EGCG treatment upregulated the miR-210 expression, in an association with EFNA3 downregulation; and the miR-210 upregulation significantly downregulated the expression of EFNA3 via the specific binding to the 3' UTR of EFNA3. In addition, the manipulated miR-210 upregulation exerted amelioration on the hypoxia-induced apoptosis and on the hypoxia-reduced expression of ALP, BMP-2, PINP and RUNX2 in MSCs. In summary, our study indicated the protective role of EGCG in response to hypoxia and promontory role to osteogenic differentiation in MSCs via upregulating miR-210 and downregulating the expression of miR-210-targeted EFNA3. Our study implies the protective role of EGCG in the hypoxia-induced impairment in MSCs.

ObjectiveTo assess the early curative effect of epidural or intravenous administration of steroids during a percutaneous endoscopic lumbar discectomy (PELD).Methods28 consecutive patients who underwent PELD due to large lumbar disc herniation between November 2014 and January 2016 were followed up for 6 months. These patients were divided into two groups according to the treatment they received after PELD. 14 patients (Group A) were treated by PELD and epidural steroids, while the other 14 patients (Group B) were treated by PELD and intravenous steroids. We evaluated the effectiveness by the preoperative and postoperative visual analogue scale (VAS) scores for back and leg pain, and the postoperative Oswestry disability index (ODI) at 3 weeks after surgery via the clinical charts and telephone interview. Postoperative hospital stay and time return to work were investigated as well.ResultsThere is a significant decrease in VAS (back, leg), ODI, and time return to work (p < 0.05). For VAS (back), Group A showed a significant decrease compared with Group B at 1 day and 1 week after surgery (p = 0.011, p = 0.017). As for VAS (leg), Group A showed a significant decrease compared with Group B at 1 day, 1 week, 3 weeks, and 3 months follow-up examinations (p = 0.002, p = 0.006, p < 0.001, p < 0.001). For ODI, Group A showed a notable decrease compared with Group B (p < 0.001). The postoperative hospital stay in two groups was not statistically different (p = 0.636). But the time return to work in Group A was significantly shorter than that in Group B (p = 0.023).ConclusionPatients who underwent PELD with epidural steroid administration for large lumbar disc herniation showed favorable curative effect compared with those who underwent PELD with intravenous steroid administration.