Predictive risk factors for recollapse of cemented vertebrae after percutaneous vertebroplasty: A meta-analysis

BACKGROUND As one of the most common complications of osteoporosis,osteoporotic vertebral compression fracture(OVCF)increases the risk of disability and mortality in elderly patients.Percutaneous vertebroplasty(PVP)is considered to be an effective,safe,and minimally invasive treatment for OVCFs.The recollapse of cemented vertebrae is one of the serious complications of PVP.However,the risk factors associated with recollapse after PVP remain controversial.AIM To identify risk factors for the recollapse of cemented vertebrae after PVP in patients with OVCFs.METHODS A systematic search in EMBASE,MEDLINE,the Cochrane Library,and PubMed was conducted for relevant studies from inception until March 2020.Studies investigating risk factors for the recollapse of cemented vertebrae after PVP without additional trauma were selected for analysis.Odds ratios(ORs)or standardized mean differences with 95%confidence interval(CI)were calculated and heterogeneity was assessed by both the chi-squared test and the I-squared test.The methodological quality of the included studies was assessed according to the Newcastle-Ottawa Scale.RESULTS A total of nine case-control studies were included in our meta-analysis comprising 300 cases and 2674 controls.The significant risk factors for the recollapse of cemented vertebrae after PVP in OVCF patients were fractures located at the thoracolumbar junction(OR=2.09;95%CI:1.30 to 3.38;P=0.002),preoperative intravertebral cleft(OR=2.97;95%CI:1.93 to 4.57;P<0.00001),and solid lump distribution pattern of the cement (OR = 3.11;95%CI: 1.91 to 5.07;P < 0.00001).The analysis did not support that age, gender, lumbar bone mineral density,preoperative visual analogue scale score, injected cement volume, intradiscalcement leakage, or vertebral height restoration could increase the risk forcemented vertebra recollapse after PVP in OVCFs.CONCLUSIONThis meta-analysis suggests that thoracolumbar junction fractures, preoperativeintravertebral cleft, and solid lump cement distribution pattern are associatedwith the recollapse of cemented vertebrae after PVP in OVCF patients.

Decoding epigenetic codes: new frontiers in exploring recovery from spinal cord injury

Spinal cord injury that results in severe neurological disability is often incurable.The poor clinical outcome of spinal cord injury is mainly caused by the failure to reconstruct the injured neural circuits.Several intrinsic and extrinsic determinants contribute to this inability to reconnect.Epigenetic regulation acts as the driving force for multiple pathological and physiological processes in the central nervous system by modulating the expression of certain critical genes.Recent studies have demonstrated that post-SCI alteration of epigenetic landmarks is strongly associated with axon regeneration,glial activation and neurogenesis.These findings not only establish a theoretical foundation for further exploration of spinal cord injury,but also provide new avenues for the clinical treatment of spinal cord injury.This review focuses on the epigenetic regulation in axon regeneration and secondary spinal cord injury.Together,these discoveries are a selection of epigenetic-based prognosis biomarkers and attractive therapeutic targets in the treatment of spinal cord injury.

Signaling pathways that regulate axon regeneration

Neurons in the mammalian central nervous system （CNS） cannot regenerate axons after injury. In contrast, neurons in the mammalian peripheral nervous system and in some non-mammalian models, such as C. elegans and Drosophila, are able to regrow axons. Understanding the molecular mechanisms by which these neurons support axon regeneration will help us find ways to enhance mammalian CNS axon regeneration. Here, recent studies in which signaling pathways regulating naturally-occurring axon regeneration that have been identified are reviewed, focusing on how these pathways control gene expression and growth-cone function during axon regeneration.