There were multiple risk factors for cage retropulsion after lumbar interbody fusion surgery, including patient factors, radiological characteristics, surgical techniques and postoperative reasons. In case of retropulsion, revision surgery was essential for the patients who presented neurological deficits and conservative treatment was recommended for asymptomatic patients.

BackgroundDiabetes mellitus (DM) and low back pain which is mainly caused by degeneration of the intervertebral discs (IVDs) both are major public health problem worldwide. The present study was designed to investigate the association between type 2 diabetes mellitus (T2D) and severity of lumbar disc degeneration (LDD).MethodsWe retrospectively reviewed patients with low back pain visiting our spine clinic in 2014. Low back pain patients all have the lumbar MRI imaging and no previous treatment. One hundred fifty patients without T2D (group A) and 622 patients with T2D meeting the criteria were included. Sex, age, body mass index (BMI), high blood pressure (HBP), history of smoking, alcohol use, and duration of T2D were recorded. Patients with T2D were assigned to a well-controlled group (group B, n = 380) and a bad-controlled group (group C, n = 242). In group B, T2D duration of 148 patients was ≤ 10 years (group B1) and 232 patients > 10 years (group B2). In group C, T2D duration of 100 patients was ≤ 10 years (group C1) and 142 patients > 10 years (group C2). The severity of LDD was evaluated using the five-level Pfirrmann grading system. Data were analyzed using SPSS 19.0.ResultsDemographic data except age showed no difference among groups (P > 0.5). Compared to patients without T2D, patients with T2D showed more severe disc degeneration after removal of age effects (P < 0.05). From L1/2 to L5/S1, the average Pfirrmann scores between groups A and B1 showed no difference(P > 0.05); groups B2, C1, and C2 showed higher average Pfirrmann scores than group A (P < 0.05). Groups B2 and C2 showed higher average Pfirrmann scores than groups B1 and C1 (P < 0.05). Groups C1 and C2 showed higher average Pfirrmann scores than groups B1 and B2 (P < 0.05). From L1/2 to L5/S1, the severity of LDD was highly positively related to T2D duration both in groups B and C (P < 0.05).ConclusionsT2D duration > 10 years and a bad control of T2D were risk factors for LDD. The longer T2D duration was, the more severe disc degeneration would be.

Compared to other fusion techniques, TLIF shows fewer complications, ALIF shows better sagittal alignment, and circumferential fusion showed better fusion rates. It was difficult to make recommendations about the optimal approach because of the methodological variance in the publications.

The results of the meta-analysis showed that home-based rehabilitation has considerable positive effects on physical functioning after hip fracture. Home-based rehabilitation is therefore recommended for hip fracture.

Background: The leptin receptor-deficient knockout (db/db) mouse is a well-established model for studying type II diabetes mellitus (T2DM). T2DM is an important risk factor of intervertebral disc degeneration (IVDD). Although the relationship between type I diabetes and IVDD has been reported by many studies, few studies have reported the effects of T2DM on IVDD in db/db mice model. Methods: Mice were separated into 3 groups: wild-type (WT), db/db, and IGF-1 groups (leptin receptor-deficient mice were treated with insulin-like growth factor-1 (IGF-1). To observe the effects of T2DM and glucose-lowering treatment on IVDD, IGF-1 injection was used. The IVD phenotype was detected by H&E and safranin O fast green staining among db/db, WT and IGF-1 mice. The levels of blood glucose and weight in mice were also recorded. The changes in the mass of the trabecular bone in the fifth lumbar vertebra were documented by micro-computed tomography (micro-CT). Tunnel assays were used to detect cell apoptosis in each group. Results: The weight of the mice were 27.68 ± 1.6 g in WT group, which was less than 57.56 ± 4.8 g in db/db group, and 52.17 ± 3.7 g in IGF-1 injected group (P < 0.05). The blood glucose levels were also significantly higher in the db/db mice group. T2DM caused by leptin receptor knockout showed an association with significantly decreased vertebral bone mass and increased IVDD when compared to WT mice. The db/db mice induced by leptin deletion showed a higher percentage of MMP3 expression as well as cell apoptosis in IVDD mice than WT mice (P < 0.05), while IGF-1 treatment reversed this situation (P < 0.05). Conclusions: T2DM induced by leptin receptor knockout led to IVDD by increasing the levels of MMP3 and promoting cell apoptosis. IGF-1 treatment partially rescue the phenotype of IVDD induced by leptin receptor knockout.

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This study was aimed to figure out whether long noncoding RNA MEG3/miR‐361‐5p/FoxM1 signaling would contribute to improved proliferation and metastasis of osteosarcoma cells. We altogether collected 204 pairs of osteosarcoma tissues and adjacent normal tissues, and obtained four human osteosarcoma cell lines. Then pcDNA3.1‐MEG3, si‐MEG3, miR‐361‐5p mimic, miR‐361‐5p inhibitor, pcDNA3.1‐FoxM1, si‐FoxM1, and negative control (NC) were, respectively, transfected into the osteosarcoma cells. Furthermore, real time polymerase chain reaction was utilized to determine the mRNA expressions of maternally expressed gene 3 (MEG3) and miR‐361‐5p, and western blot analysis was applied for determining the FoxM1 expression. Besides, dual luciferase reporter gene assay was adopted to verify if MEG3 can be directly targeted by miR‐361‐5p. Finally, 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide, colony formation assay, flow cytometry, wound healing assay, and transwell assay were conducted to investigate the influence of MEG3, miR‐361‐5p, and FoxM1 expressions on the viability, proliferation, apoptosis, migration, and invasion of osteosarcoma cells. MEG3 and miR‐361‐5p were observed to be significantly downregulated within both osteosarcoma tissues and cell lines, whereas FoxM1 was upregulated in osteosarcoma tissues and cell lines (p < 0.05). MEG3 directly bound to miR‐361‐5p, and significantly upgraded its expression (p < 0.05). The upregulated MEG3 and miR‐361‐5p or the downregulated FoxM1 appeared to substantially inhibit proliferation, migration, and invasion of osteosarcoma cells (p < 0.05). Finally, the proliferation, migration, invasion, and motility of osteosarcoma cells within the miR‐NC + pcDNA3.1‐FoxM1 group and pcDNA + pcDNA‐FoxM1 group were markedly promoted when compared with the miR‐361‐5p mimic group and pcDNA3.1‐MEG3 group (p < 0.05). The MEG3/miR‐361‐5p/FoxM1 axis could potentially serve as therapeutic targets or diagnostic biomarkers for osteosarcoma.