No abstract

For all 102 cases of ankle joint fracture involving the posterior malleolus, the treatment effect was satisfactory. Restoration of an even articular surface, especially when fragment size ≥ 25 %, should be attempted during treatment.

At present, repair methods for peripheral nerve injury often fail to get satisfactory result. Although various strategies have been adopted to investigate the microenvironment after peripheral nerve injury, the underlying molecular mechanisms of neurite outgrowth remain unclear. In this study, we evaluate the effects of exosomes from gingival mesenchymal stem cells (GMSCs) combined with biodegradable chitin conduits on peripheral nerve regeneration. GMSCs were isolated from human gingival tissue and characterized by surface antigen analysis and in vitro multipotent differentiation. The cell supernatant was collected to isolate the exosomes. The exosomes were characterized by transmission electron microscopy, Western blot, and size distribution analysis. The effects of exosomes on peripheral nerve regeneration in vitro were evaluated by coculture with Schwann cells and DRGs. The chitin conduit was prepared and combined with the exosomes to repair rat sciatic nerve defect. Histology, electrophysiology, and gait analysis were used to test the effects of exosomes on sciatic nerve function recovery in vivo. We have successfully cultured GMSCs and isolated exosomes. The exosomes from GMSCs could significantly promote Schwann cell proliferation and DRG axon growth. The in vivo studies showed that chitin conduit combined with exosomes from GMSCs could significantly increase the number and diameter of nerve fibers and promote myelin formation. In addition, muscle function, nerve conduction function, and motor function were also obviously recovered. In summary, this study suggests that GMSC-derived exosomes combined with biodegradable chitin conduits are a useful and novel therapeutic intervention in peripheral nerve repair.

Osteoporosis, characterized by bone mass reduction and increased fractures, has become a global health problem that seriously affects the health of people, especially postmenopausal women; however, the current pathogenesis of postmenopausal osteoporosis (PMOP) has not been thoroughly elucidated to date. In this study, bilateral ovariectomy was performed to establish an OVX mouse model of osteoporosis. UPLC-Q-TOF-MS-based lipidomics in combination with metabolomics were used to analyze the femur tissue of osteoporosis mice. We found that 11 polar metabolites and 93 lipid metabolites were significantly changed and were involved in amino acid metabolism, nucleotide metabolism and lipid metabolism. Among the lipids, fatty acyls, glycerolipids, glycerophospholipids, sphingolipids and sterols showed robust changes. These results revealed that several metabolic disorders caused by changes in the hormone levels in OVX, especially disordered lipid metabolism, are closely related to the imbalance between bone resorption and formation and may underlie the development of PMOP. The data generated via lipidomics and metabolomics presented in this study shows good applicability and wide coverage in the construction of the metabolic profile of bone tissue. Therefore, this approach may provide the pathway focusing and data support at the metabolite level for the in-depth mechanism of PMOP.

In humeri with normal alignment, calcar screws can provide additional stability even when a medial deficiency exists. The use of calcar screws in humeri with varus deformity showed no biomechanical superiority.

Background Vertebral augmentation is the first-line treatment for the osteoporosis vertebral compression fractures. Bone cement leakage is the most common complication of this surgery. This study aims to assess the risk factors for different types of cement leakage and provides a nomogram for predicting the cement intradiscal leakage. Methods We retrospectively reviewed 268 patients who underwent vertebral augmentation procedure between January 2015 and March 2019. The cement leakage risk factors were evaluated by univariate analysis. Different types of cement leakage risk factors were identified by the stepwise logistic analysis. We provided a nomogram for predicting the cement intradiscal leakage and used the concordance index to assess the prediction ability. Results A total of 295 levels of vertebrae were included, with a leakage rate of 32.5%. Univariate analysis showed delayed surgery and lower vertebral compression ratio were the independent risk factors of cement leakage. The stepwise logistic analysis revealed percutaneous vertebroplasty was a risk factor in vein cement leakage; delayed surgery, preoperative compression ratio, and upper endplate disruption were in intradiscal cement leakage; age, preoperative fracture severity, and intravertebral vacuum cleft were in perivertebral soft tissue cement leakage; no factor was in spinal canal cement leakage. The nomogram for intradiscal cement leakage had a precise prediction ability with an original concordance index of 0.75. Conclusions Delayed surgery and more vertebral compression increase the risk of cement leakage. Different types of cement leakage have different risk factors. We provided a nomogram for precise predicting the intradiscal cement leakage.

Bone marrow stromal cells (MSCs) have been shown to differentiate into various lineage cells including neural cells in vitro and in vivo. We therefore examined whether MSCs can differentiate into Schwann cells in injured peripheral nerves, After cultured in vitro, PKH-67-labeled MSCs were injected into the mechanically injured rat sciatic nerves. Three weeks after injection, immunofluorescent examinations were carried out. MSCs had been incorporated around the injured nerves and differentiated into Schwann cells. MSCs had accumulated mainly in the epineurium around the injured nerve. The incorporated cells partially expressed GFAP, S-100, and P75. These results confirmed the possibility that MSCs have the ability to differentiate into Schwann cells, and that injection of MSCs into the injured peripheral nerve would help repair damaged nerve.

To investigate the changes of calcitonin gene-related peptide (CGRP) in rat's blood plasma, spinal anterior motorneuron, and dorsal root ganglion (DRG) after fractures combined with central or peripheral nerve injuries and its influence on fracture healing, 72 healthy adult SD rats (male or female) were divided into 4 groups (18 rats in each group): group A, simple(left) tibial fracture; group B, left tibial fracture combined with left sciatic nerve injury; group C, left tibial fracture combined with T9-11 spinal cord transection injury; group D, left tibial fracture combined with right cerebral cortex injury. Group A was the control group. The concentration of serum CGRP was measured immediately, 1w, 2w, and 4w after injury using radio immunoassay. X-ray photograph was taken at 1w, 2w, and 4w after injury to assess fracture healing. The concentration of serum CGRP in spinal anterior motorneuron and dorsal root ganglion was measured 1w, 2w, and 4w after injury. Bony callus at 2w after injury using H.E.staining was observed. 1w and 2w after injury, the fracture line was still clear on the X-ray of all groups, but 4w after injury the fracture line disappeared with complete healing except the peripheral nerve injury group. By H.E. staining, we found lesser bony callus contents in the peripheral nerve injury group than the simple fracture group at 2w after injury; irregular bone trabecula and healing defect were found in the former group. While the spinal injury group and cerebral cortex injury group represented more bony callus than the simple fracture group, increased bone trabecula and regularity, medullary cavity occluded and finally solid bony connections were found. CGRP concentration in blood plasma and spinal anterior motorneuron represented no apparent differences among all groups during each observation period. For the dorsal root ganglion group, 1w after fracture, there was no apparent difference of CGRP concentration in the peripheral nerve injury group and cerebral cortex group compared with the control group (P > 0.05), but the spinal injury group showed more CGRP than the control group (P < 0.01). 2w after injury, the peripheral nerve injury group and cerebral cortex group also showed no difference compared with the control group, but the cerebral cortex group had more CGRP contents than the peripheral nerve injury group (P < 0.05), and the spinal injury group showed more CGRP than the control group (P < 0.01). 4w after injury, the peripheral nerve group, spinal injury group, and cerebral cortex injury group all showed higher concentration of CGRP than the control group. Among the 3 groups, the spinal injury group is the highest (P < 0.01). When fracture combined with peripheral nerve injury, the healing process can be slowed down. In contrast, fracture combined with spinal injury and cerebral cortex injury will accelerate the healing process. The CGRP in dorsal root ganglion in spinal injury group and cerebral cortex injury group increased, which may have positive effects on fracture healing.