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Objective Although many risk factors for cage retropulsion (CR) after lumbar interbody fusion (LIF) have been described in the literature, they still remain controversial. The purpose of this study is to investigate the risk factors for CR after LIF. Methods The literature was searched in PubMed, Cochrane library, and Embase from October 2000 to October 2018. The key words and combinations used in the search included LIF, cage, retropulsion, posterior migration, and risk factors. Only studies with sufficient data to calculate odds ratio for CR were included. Odds ratio and 95% confidence interval were calculated for outcomes via RevMan5.3 and SPSS 22.0. Results A total of 10 studies were included in this study. Twelve risk factors were assessed by analyzing 4467 patients. The pooled results indicated that a pear-shaped disk and straight cage were significant risk factors for CR. However, factors that had no significant relation with CR were preoperative diagnosis (disk herniation, spinal stenosis, and spondylolisthesis); gender; surgical segments (from L2 to S1); multilevel fusion; and unilateral pedicle screws fixation. Conclusions According to current evidence, a pear-shaped disk and straight cage are significant risk factors for CR. However, preoperative diagnosis, gender, multilevel fusion, surgical segments, and unilateral pedicle screws fixation are not the risk factors associated with CR. A revision surgery is needed when neurologic symptoms happen after CR. The conclusion should be consulted cautiously due to the limited number of included studies. Therefore larger-scale studies are still needed to investigate the risk factors for CR.

Iron is known to be a crucial regulator of glucose, and several studies have demonstrated that iron overload is one of the risk factors for insulin resistance and diabetes; however, the mechanism has not yet been clarified. To investigate the effect of iron overload on glucose metabolism and the underlying mechanism, Irp2 knockout (Irp2-/-) mice (endogenous iron overload model) were used. We found that Irp2-/- mice exhibited hyperglycemia and iron overload in the liver and skeletal muscle. Increased MDA, decreased SOD levels, and increased cell apoptosis were also found in the liver and muscle of Irp2-/- mice. Glucose concentrations were significantly higher in Irp2-/- mice in insulin tolerance tests. However, early-phase insulin secretion was not altered in Irp2-/- mice. The expression of hepatic IRS2 and muscle GLUT4 was declined in Irp2-/- mice at both mRNA and protein levels when compared with those of wild-type control. In conclusions, Irp2-/- mice showed hyperglycemia, which might due to insulin resistance rather than due to impaired insulin secretion.

Background Osteoporosis is frequently accompanied by iron disorders. Calcitonin (CT) was approved as a clinical drug to treat osteoporosis. Hepcidin is a peptide hormone that is secreted by the liver and controls body iron homeostasis. Hepcidin deficiency leads to iron overload diseases. This study was aimed at investigating the effect of CT on hepatic hepcidin and the mechanism by which CT modulates hepatic hepcidin pathways and iron metabolism. Method RT-PCR, Western blot, ELISA and siRNA were used to detect the effect of CT on iron metabolism in vivo and in vitro. In addition, the regulatory signal molecules of hepcidin were measured to explore the molecular mechanism of its regulation. Results The results showed that CT strongly increased hepcidin expression and altered iron homeostasis, after mice were intraperitoneal injection of CT. In response to CT administration, BMP6 level in kidney and the serum BMP6 was increased significantly. The phosphorylation of Smad1/5/8 proteins in liver was increased at 3 h and 6 h. Moreover, the Bmp inhibitor LDN-193,189 pretreatment significantly attenuated the CT-mediated increases in phosphorylated Smad1/5/8 and Hamp1 mRNA levels. Calcitonin receptor (CTR) siRNA transfection significant suppressed the role of CT on BMP6 expression in Caki-1 cells. Conclusion Our results suggest that CT strongly induces hepcidin expression and affected iron metabolism. It will provide a new strategy for the treatment of calcium iron related diseases.

Recent findings have shown a trend toward recommending against the routine use of drains in spinal surgery because it carries the risk for potential complications. However, most surgeons still use closed suction drainage to prevent hematoma formation. This study is to compare the clinical outcomes between natural pressure drainage and negative pressure drainage after posterior lumbar interbody fusion.Consecutive 132 patients who underwent spinal fusion in the Third Hospital of Hebei Medical University and met the inclusion criteria were reviewed from January 2018 to January 2019 and divided into negative pressure drainage group and natural pressure drainage group according to different pressure drainage. There were 64 patients who had a negative pressure drainage placed and 68 patients who had a natural pressure drainage placed. Demographics, intraoperative blood loss, operative room time, drainage volume at the 1st postoperative day, total volume of postoperative drainage, the total drainage days, postoperative temperature, and postoperative complications (wound infection, symptomatic hematoma) were compared between the 2 groups.The median drainage volume at the 1st postoperative day in negative pressure group was 204.89 ± 95.19 mL, while in natural pressure group, it was 141.00 ± 52.19 mL (P = .000). The median total volume of postoperative drainage in negative pressure group was 378.06 ± 117.98 mL, while in natural pressure group, it was 249.32 ± 70.74 mL (P = .000). The median total drainage days between natural pressure group and negative pressure group were obviously different (2.93 ± 0.55 vs 3.51 ± 0.71 days, P = .000). There was no difference in patient characteristics, operative data, postoperative temperature, and complications.Natural pressure drainage significantly reduced postoperative drainage volume and indwelling time, but did not increase postoperative complications. Therefore, it may offer an alternative to negative pressure drainage and is as safe and effective as negative pressure drainage.

It has been found that iron disorder may lead to osteoporosis. However, the mechanism has been little explored. In the present study, we try to investigate the effects of iron disorder on bone metabolism using Irp2 knockout (Irp2-/-) mice. Female Irp2-/- mice were used in this study. Bone mineral density (BMD) was measured by Micro-CT. Serum markers for bone turnover were measured by enzyme-linked immunosorbent assay. Content of iron was measured in bone and liver tissue, and Vitamin D 25-hydroxylase (CYP2R1) content was measured in liver tissue. Relative gene expression involved in iron export and uptake, and some genes involved in activities of osteoblast and osteoclast were all measured by real-time PCR and western blot. Compared to wild-type mice, Irp2-/- mice exhibited reduced BMD, bone iron deficiency, and hepatic iron overload. Serum levels of 25(OH)D3 and markers for bone formation such as bone alkaline phosphatase (Balp), bone-gla-protein (BGP), and type I collagen alpha1 chain (Col I α1) were decreased, while markers for bone resorption including cathepsin K (Ctsk) and tartrate-resistant acid phosphatase (Trap) were all significantly increased. Hepatic CYP2R1 level was decreased in Irp2-/- mice compared with wild-type control mice. Compared to wild-type C57BL6 control mice, the expression of genes involved in osteoblast activity such as Balp, BGP, and Col I α1 were all significantly decreased in bone tissue, while genes for osteoclast activity such as Ctsk and Trap were all markedly increased in Irp2-/- mice at mRNA level. Genes involved in iron storage, uptake, and exporting were also measured in bone tissue. Posttranscriptionally decreased ferritin (FTL), ferroportin 1 (FPN1), and increased transferrin receptor 1 (TfR1) gene expressions have been unexpectedly found in bone tissue of Irp2-/- mice. Irp2-/- mice exhibit reduced bone iron content and osteoporosis. Decreased circulating 25(OH)D3 levels promoted activity of osteoclast, while impaired activity of osteoblast may contribute to pathogenesis of osteoporosis. And, reduced bone iron content may not be totally caused by TfR1-dependent pathways.

Lumbar spinal canal stenosis (LSCS) associated with degenerative scoliosis has being increasingly aware by the public and studied by many researchers. Degenerative changes leading to spinal stenosis can precede a spinal deformity which will develop into the de novo scoliosis. There are few studies focusing on the risk factors contributing to the degenerative lumbar scoliosis (DLS) in lumbar spinal stenosis patients. From September, 2017 to December, 2017, 181 patients who were diagnosed with LSCS in the outpatient department of our hospital were enrolled in this retrospective investigation. The patients were divided into 2 groups: DLS group (Cobb angle >10°) and LSCS group. Sex, age, smoking status (yes or no), occupation (heavy or light labor), body mass index (BMI), bone mineral density (BMD) and radiographic parameters including the lumbar lordosis (LL), pelvic incidence (PI), pelvic tilt (PT), sacral slope (SS), thoracic kyphosis (TK), coronal vertical axis, and sagittal vertical axis (SVA) are all evaluated as potential risk factors. Multivariate logistic regression analysis and receiver-operating characteristic curves were used to identify potential risk factors. Forty-five of 181 patients were diagnosed with DLS and involved in the DLS group. There were significant differences between the 2 groups in BMI (P 25.57 kg/m2 (AOR 1.270, 95% CI 1.040–1.551, P = .019), and SVA >3.98 cm (AOR 3.651, 95% CI 2.226–5.990, P 25.57 kg/m2, and SVA >3.98 cm were the potential risk factors for the formation of degenerative lumbar scoliosis based on degenerative lumbar spinal stenosis.

Background:The application of tubular microscopes discectomy (TMD) was supposed to have similar or better results than conventional microdiscectomy (CMD). However, this conclusion had not been verified by sufficient evidence. Therefore, the focus of this meta-analysis was to assess the effic