Association between dietary copper, iron, zinc, selenium intake and osteopenia or osteoporosis in elderly hypertensive patients: a retrospective cohort study.

Aim: The study aimed to investigate the link between dietary copper, iron, zinc, selenium intake with osteopenia and osteoporosis in elderly hypertensive patients. Methods: The data of hypertensive patients were extracted from the National Health and Nutrition Examination Survey 2005-2010, 2013-2014, and 2017-2018. Data of dietary iron, zinc, copper and selenium intakes were obtained according to 24-h diet recall interviews. Osteopenia and osteoporosis were determined based on the bone mineral density. Weighted liner regression and weighted logistic regression were employed to assess the association between iron, zinc, copper, and selenium intakes with osteopenia and osteoporosis. All results were presented as ß, odds ratios (ORs), and 95% confidence intervals (CIs). Results: In total, 5,286 elderly hypertensive patients were included. Among them, 2,961 (56.02%) patients have osteopenia, and 566 (10.71%) have osteoporosis. After adjusting all covariates, dietary copper intake ≥the recommended daily allowance was positively correlated with bone mineral density on total femur (ß = 0.086, 95% CI: 0.021-0.152) and femoral neck (ß = 0.097, 95% CI: 0.016-0.178). Dietary zinc intake ≥the recommended daily allowance was also positively correlated with bone mineral density on total femur (ß = 0.092, 95% CI: 0.030-0.153) and femoral neck (ß = 0.122, 95% CI: 0.050-0.193). Dietary copper (O = 0.581, 95% CI: 0.394-0.858) and zinc (OR = 0.595, 95% CI: 0.429-0.827) intake ≥the recommended daily allowance levels were related to increased odds of osteoporosis in elderly with hypertension. Conclusion: Higher dietary copper and zinc intake was associated with lower odds of osteoporosis in the elderly hypertensive patients. Higher dietary intake included copper and zinc may be beneficial for the bone health in the elderly hypertensive patients.

[Analysis of the clinical effect of percutaneous pedicle screw fixation combined with transpedicular bone grafting in the treatment of thoracolumbar fracture].

OBJECTIVE: To investigate the clinical efficacy of percutaneous screw fixation combined with minimally invasive transpedicular bone grafting and non-bone grafting in the treatment of thoracolumbar fractures. METHODS: From Janury 2021 to June 2022, 40 patients with thoracolumbar fracture were divided into the experimental group and the control group. There were 26 patients in the experimental group, including 21 males and 5 females with an aberage age of (47.3±12.3) years old, who underwent percutaneous pedicle screw fixation combined with transpedicular autogenous bone grafting. In the control group, 14 patients received percutaneous pedicle screw fixation only. including 7 makes and 7 females with an average age of (50.2±11.2) years old. The operative time, intraoperative blood loss, anterior height ratio of injured vertebrae, Cobb angle, visual analogue score (VAS), MacNab scores, loosening or broken of the implants. were compared and analyzed. RESULTS: There was no significant difference in operation time, intraoperative blood loss, VAS and anterior height ratio of injured vertebrae between the two groups. Compared with the preoperative results, VAS and anterior height ratio of injured vertebrae were improved statistically(P<0.05). For Cobb angle of injured vertebra, there was no significant difference between the two groups before surgery (P=0.766). While at 1 week, 3 months and 12 months after surgery, there were statistically differences between the two groups (P values were 0.042, 0.007 and 0.039, respectively). The Cobb angle of injured vertebrae one year after operation was statistically decreased in both groups compared with that before surgery (P<0.001). One year after surgery, the excellent and good rate of Macnab scores was 96.15% in the experimental group and 92.86% in the control group, and there was no statistical differences between the two groups (P=0.648). There was one patient in the control group suffering superficial wound infection on the third day, which was cured by dressing change and anti-infection treatment. There were no postoperative screw loosening and broken in both groups. CONCLUSION: The two surgical methods have the advantages of less trauma, less pain and quicker recovery, which can restore the height of the injured vertebra, reconstruct the spinal sequence and reduce the fracture of the vertebral body. Transpedicular autogenous bone grafting can increase the stability of the fractured vertebra and maintain the height of the vertebra better after surgery, thus reducing the possibility of complications such as kyphosis, screw loosening and broken.

miR-877-3p inhibits tumor growth and angiogenesis of osteosarcoma through fibroblast growth factor 2 signaling.

Osteosarcoma (OS) is the most common high-grade malignant bone tumor in teenagers. MicroRNAs can function as posttranscriptional regulators of gene expression, playing critical roles in cancer dev-877-3p in OS. Quantitative real-time RT-PCR was carried out for detecting miR-877-3p expression in OS. The effects of miR-877-3p on proliferation was analyzed via MTT, colony formation, and flow cytometry assays. Angiogenesis of endothelial cells were investigated by wound healing and tube formation assay. Gene profiling based on PCR array and luciferase reporter assay were conducted to determine target genes of miR-877-3p. In-vivo study was used to determine the effects of miR-877-3p on the tumor growth. The expression of miR-877-3p was markedly downregulated in OS tissues and cell lines. Low expression of miR-877-3p predicts poor prognosis of OS patients. miR-877-3p overexpression was found to inhibit the proliferation of OS cell lines. The angiogenesis assays showed that miR-877-3p attenuated the angiogenesis. Further mechanism studies showed that miR-877-3p can reduce (Fibroblast Growth Factor 2) FGF2 expression in OS cells by binding to the 3'UTR end of FGF2. Moreover, increased expression of miR-877-3p was responsible for the inhibition of tumor growth and angiogenesis. Taken together, our findings indicated that miR-877-3p might exhibit tumor suppressive role by targeting FGF2 signaling, which may serve as potential target for OS.

Percutaneous cerclage wiring for type 34-C patella fracture in geriatric patients.

PURPOSE: This study was to retrospectively evaluate clinical outcomes of geriatric patients with patella fracture treated by percutaneous cerclage wiring and to introduce the surgical technique. METHODS: From January 2009 to December 2015, fifty-seven consecutive geriatric patients of type 34-C patellar fracture underwent closed reduction and percutaneous cerclage wiring fixation in our hospital. Visual Analog Scale (VAS) score, Levack score system, WOMAC test form of pain, stiffness and function, and knee joint range of motion (ROM) were applied for functional evaluation. RESULTS: Fifty-three patients were followed up for a mean period of 36 months (12 to 82 months). All fractures were unioned, no wound infection, second displacement of fracture fragment or wire migration was found. Wire breakage happened in one case at six months post-operation. Thirteen patients had hardware removed, nine cases for implant irritation at the knot and four cases for no specific reason. No patient developed postoperative knee stiffness, and range of motion was 128.6° (110-140). The average VAS score of emotional knee function was 87.5 (65-99) preinjury and 78.1 (53-95) at the last follow-up. 86.8% (46/53) patients considered that they regained more than 80% of their knee function. The average Levack score was 10.0 (6-12), which included thirty-five evaluations of "excellent" and eighteen of "good". The average WOMAC score was 21.3 (13-37). CONCLUSIONS: Percutaneous cerclage wiring fixation is a viable option for type 34-C patella fracture in geriatric patients.

Recombinant Human Endostatin Suppresses Mouse Osteoclast Formation by Inhibiting the NF-κB and MAPKs Signaling Pathways.

Rheumatoid arthritis is an autoimmune disease characterized by synovial hyperplasia and progressive joint destruction. As reported previously, recombinant human endostatin (rhEndostatin) is associated with inhibition of joint bone destruction present in rat adjuvant-induced arthritis; however, the effect of rhEndostatin on bone destruction is not known. This study was designed to assess the inhibitory effect and mechanisms of rhEndostatin on formation and function of osteoclasts in vitro, and to gain insight into the mechanism underlying the inhibitory effect of bone destruction. Bone marrow-derived macrophages isolated from BALB/c mice were stimulated with receptor activator of NF-κB ligand (RANKL) and macrophage colony-stimulating factor to establish osteoclast formation. Osteoclast formation was determined by TRAP staining. Cell viability of BMMs affected by rhEndostatin was determined using a MTT assay. Bone resorption was examined with a bone resorption pits assay. The expression of osteoclast-specific markers was analyzed using quantitative real-time PCR. The related signaling pathways were examined using a Luciferase reporter assay and western blot analysis. Indeed, rhEndostatin showed a significant reduction in the number of osteoclast-like cells and early-stage bone resorption. Moreover, molecular analysis demonstrated that rhEndostatin attenuated RANKL-induced NF-κB signaling by inhibiting the phosphorylation of IκBα and NF-κB p65 nuclear translocation. Furthermore, rhEndostatin significantly inhibited the activation of RANKL-dependent mitogen-activated protein kinases, such as ERK1/2, JNK, and p38. Hence, we demonstrated for the first time that preventing the formation and function of osteoclasts is an important anti-bone destruction mechanism of rhEndostatin, which might be useful in the prevention and treatment of bone destruction in RA.

Signal transducer and activator of transcription 3 regulates CCAAT-enhancer-binding homologous protein expression in osteoblasts through upregulation of microRNA-205.

The transcription factor, CCAAT-enhancer-binding protein homologous protein (CHOP), is induced by endoplasmic reticulum-stress and mediates programmed cell death. In osteoblasts, CHOP overexpression increases the rate of apoptosis, leading to osteoblastic dysfunction. However, the regulatory mechanisms underlying CHOP expression remain unclear. In the present study, western blot analysis was used to demonstrate that the activation of signal transducer and activator of transcription 3 (STAT3) inhibited the levels of the CHOP protein, whereas small interfering RNA-mediated the knockdown of STAT3 upregulated CHOP expression. Furthermore, STAT3 was shown to increase the expression level of microRNA (miR)-205. A luciferase reporter assay revealed that miR-205 was able to directly target the 3'-untranslated region of the CHOP gene to inhibit its protein expression. The miR-205 antisense largely abolished the inhibitory effect of STAT3 activation on the levels of CHOP protein. Therefore, the results demonstrated a previously unknown STAT3/miR-205/CHOP signaling pathway in osteoblasts, which may aid the understanding of the pathogenic mechanisms of associated diseases, including osteoporosis.