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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.

Since microglia-associated neuroinflammation plays a critical role in the progression of acute spinal cord injury, modulation of microglial activation has been suggested as a potential therapeutic strategy. Progranulin has been reported to exert neuroprotective effects by attenuating neuroinflammation, but whether these effects are due to the modulation of microglial polarization and the underlying mechanism remain unclear. Here, we investigated the effect of progranulin on microglial polarization and analyzed the crosstalk between microglial autophagy and polarization. We found that progranulin could reduce proinflammatory cytokine production in the lesion site and promote locomotor functional recovery after acute spinal cord injury. In vitro, we found that progranulin could activate microglia to an anti-inflammatory phenotype and express IL-10. Moreover, progranulin-mediated enhancement of anti-inflammatory microglial polarization was attributed to the protection of lysosomal function and the enhancement of autophagic flux. Above all, progranulin exerts anti-inflammatory effects by protecting lysosomal function to enhance microglial autophagy to induce M2 microglial polarization and ultimately improves neurological function after acute spinal cord injury. These results suggest that targeting autophagy-lysosomal pathway to modulate microglial polarization to reduce neuroinflammation is a potential treatment for spinal cord injury.