[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.

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.