Fluoride-coated high-purity magnesium cage promotes bone fusion in goat models.

Background: Cervical fusion devices made by polyether ether ketone (PEEK) cause concomitant effects which decompress the spinal cord and nerve roots. Magnesium has good biocompatibility and bioactivity as a biodegradable orthopedic implant material; however, its fusion rate is low. In this paper, we aimed to improve interbody fusion rate of high-purity magnesium (HP-Mg) by coating it with fluoride. Methods: Fluoride-coated HP-Mg (F-HP-Mg) cages were prepared, and HP-Mg cages served as controls. We tested hydrogen release in phosphate-buffered saline (PBS) and weight loss in chromic acid. Anterior cervical discectomy and bone graft fusion (ACDF) was performed at the C2-C3 segment on goats with F-HP-Mg and HP-Mg cages to evaluate fusion score. Results: Hydrogen release of F-HP-Mg cages was significantly lower than that of HP-Mg cages. Weight was significantly decreased in both types of cages after rinsing with chromic acid, while F-HP-Mg cages were more resistant to corrosion compared to HP-Mg cages. There were no significant differences in disc space height (DSH) and remaining cage volume between the two groups in computed tomography (CT) images of goat cervical spine, while cavities were found at postoperative 12 weeks and confirmed by histological staining. No complications were found, while serum aspartate aminotransaminase (AST) level was significantly higher in the HP-Mg group compared to the F-HP-Mg group. Fusion rate at 24 weeks after ACDF was significantly higher with F-HP-Mg cages. Conclusions: The use of F-HP-Mg improved histological fusion in the cervical intervertebral space of goats compared to HP-Mg and showed good biosafety.

Genetically modified mesenchymal stem cells promote spinal fusion through polarized macrophages.

Spinal fusion is an effective treatment for low back pain and typically applied with prosthetic fixation devices. Spinal fusion can be improved by transplantation of mesenchymal stem cells (MSCs) into the paraspinal muscle. However, in contrast to the direct contribution of MSCs to spinal fusion, the indirect effects of MSCs on spinal infusion have not been studied and were thus addressed here. The correlation between the outcome of spinal fusion and the local macrophage number, polarization and the levels of placental growth factor (PlGF) in patients was analyzed. MSCs were genetically modified to overexpress PlGF, and its effects on macrophage proliferation and polarization were analyzed in vitro in a transwell co-culture system, as well as in vivo in a mouse model for spinal fusion, for which the cells were bilaterally injected into paravertebral muscles of the mouse lumbar spine. The effects on spinal fusion were assessed by microcomputed tomography and a custom four-point bending apparatus for structural bending stiffness. Local macrophages were analyzed by flow cytometry. We found that posterior spinal fusion could be improved by PlGF-expressing MSCs, compared to the control MSCs, evident by significant improvement of bone bridging of the targeted vertebrae. Mechanistically, PlGF-expressing MSCs appeared to attract macrophages and induce their M2 polarization, which in turn promotes the bone formation. Together, our data suggest that PlGF-expressing MSCs may improve spinal fusion through macrophage recruitment and polarization.

RNA binding protein Lin28A promotes osteocarcinoma cells progression by associating with the long noncoding RNA MALAT1.

OBJECTIVES: To explore the effects of Lin28A on progression of osteocarcinoma (OS) cells. RESULTS: Lin28A mRNA and protein expressions were significantly increased in OS tissues compared with that in normal adjacent tissues. Expressions of Lin28A and long noncoding RNA MALAT1 were positively correlated. Patients with higher Lin28A expression had shorter overall survival. Moreover, Lin28A knockdown inhibited OS cells proliferation, migration, invasion and promoted cell apoptosis; Lin28A was found to harbor binding sites on MALAT1 sequences and associated with MALAT1, and increased MALAT1 stability and expression. Notably, the inhibition of Lin28A knockdown was attenuated or even reversed by MALAT1 overexpression. CONCLUSIONS: RNA binding protein Lin28A could facilitate OS cells progression by associating with the long noncoding RNA MALAT1.