The gradual deterioration following central nervous system (CNS) injuries or neurodegenerative disorders is usually accompanied by infiltration of degenerated and apoptotic neural tissue debris. A rapid and efficient clearance of these deteriorated cell products is of pivotal importance in creating a permissive environment for regeneration of those damaged neurons. Our recent report revealed that the phagocytic activity of olfactory ensheathing cells (OECs) can make a substantial contribution to neuronal growth in such a hostile environment. However, little is known about how to further increase the ability of OECs in phagocytosing deleterious products. Here, we used an in vitro model of primary cells to investigate the effects of lipopolysaccharide (LPS) and curcumin (CCM) co-stimulation on phagocytic activity of OECs and the possible underlying mechanisms. Our results showed that co-stimulation using LPS and CCM can significantly enhance the activation of OECs, displaying a remarkable up-regulation in chemokine (C-X-C motif) ligand 1, chemokine (C-X-C motif) ligand 2, tumor necrosis factor-α, and Toll-like receptor 4, increased OEC proliferative activity, and improved phagocytic capacity compared with normal and LPS- or CCM-treated OECs. More importantly, this potentiated phagocytosis activity greatly facilitated neuronal growth under hostile culture conditions. Moreover, the up-regulation of transglutaminase-2 and phosphatidylserine receptor in OECs activated by LPS and CCM co-stimulation are likely responsible for mechanisms underlying the observed cellular events, because cystamine (a specific inhibitor of transglutaminase-2) and neutrophil elastase (a cleavage enzyme of phosphatidylserine receptor) can effectively abrogate all the positive effects of OECs, including phagocytic capacity and promotive effects on neuronal growth. This study provides an alternative strategy for the repair of traumatic nerve injury and neurologic diseases with the application of OECs in combination with LPS and CCM.

Purpose: To explore the risk factors of bone cement displacement after percutaneous vertebral augmentation (PVA) in patients with osteoporotic vertebral compression fracture (OVCF).Methods: We retrospectively reviewed the records of 1,538 patients with OVCF treated with percutaneous vertebroplasty (PVP) or percutaneous vertebroplasty (PKP) from January 2016 to June 2021. Patients were divided into bone cement displacement group (n = 78) and bone cement non-displacement group (n = 1,460) according to the radiographic images. Possible risk factors for bone cement displacement were noted, including age, gender, body mass index (BMI), bone mineral density (BMD), underlying disease, number of fractured vertebrae, involved vertebral segment, surgical method, surgical approach, vertebral height, Cobb angle, cement leakage, the viscosity of bone cement, bone cement diffuse ratio, degree of bone cement interweaving, sagittal bone cement placement, targeted location of bone cement, the distance between the bone cement and the upper and lower endplates, the time of wearing brace and postoperative osteoporosis treatment. Risk factors were identified with univariate and multivariate logistic regressions and the discrimination ability of the predictive indicators was evaluated using area under the curve (AUC) of the receiver operating characteristic (ROC).Results: In multivariate regression, independent risk factors for bone cement displacement included: high restoration of Cobb angle (OR = 2.019, 95%[CI] 1.545–4.852, P < 0.001), cement leakage (anterior edge) (OR = 1.727, 95%[CI] 1.05–2.20, P < 0.001), small degree of bone cement interweaving (OR = 1.917, 95%[CI] 1.129–2.747, P < 0.001), non-targeted location of bone cement (OR = 2.323, 95%[CI] 1.645–4.134, P < 0.001), short duration of brace wearing (OR = 3.207, 95%[CI] 2.036–4.348, P < 0.001) and postoperative osteoporosis treatment (OR = 0.422, 95% CI = 0.323–0.547, P < 0.001). The AUCs for the high restoration of Cobb angle, cement leakage (anterior edge), small degree of bone cement interweaving, non-targeted location of bone cement, short duration of brace wearing and non-postoperative osteoporosis treatment were 0.784 (95% CI, 0.747–0.821), 0.811 (95% CI 0.764–0.859), 0.917 (95%CI 0.864–0.970), 0.610 (95%CI 0.552–0.669), 0.854 (95%CI 0.816–0.892) and 0.756 (95% CI, 0.712–0.800), respectively.Conclusion: High restoration of Cobb angle, cement leakage (anterior edge), small degree of bone cement interweaving, non-targeted location of bone cement, short duration of brace wearing and non-postoperative osteoporosis treatment were the independent risk factors of bone cement displacement after PVA.

Purpose: Residual back pain (RBP) after percutaneous vertebral augmentation (PVA) still exists considerable, and it even affects daily life due to moderate or severe back pain. A variety of risk factors have been previously identified for developing residual back pain. However, there are conflicting reports regarding the association between sarcopenia and residual back pain. As such, the aim of this study was to investigate whether paraspinal muscle fatty degeneration is a predictor of residual back pain. Methods: We retrospectively reviewed the medical records of patients with single-segment OVCF who underwent PVA from January 2016 to January 2022. Patients were divided into RBP group (86 patients) and control group (790 patients) according to whether the visual analog scale (VAS) score ≥ 4. The clinical and radiological data were analyzed. Paraspinal musculature fatty degeneration was measured using the Goutallier classification system (GCS) at the L4 − 5 intervertebral disc level. Univariate and multivariate logistic regression analyses were performed to identify risk factors. Results: The results of multivariate logistical regression analysis revealed that posterior fascia injury (odds ratio (OR) = 5.23; 95% confidence interval (CI) 3.12–5.50; P < 0.001), as regards paraspinal muscle fatty degeneration, including Goutallier grading (OR = 12.23; 95% CI 7.81–23.41; P < 0.001), fCSA (OR = 3.06; 95% CI 1.63–6.84; P = 0.002), fCSA/CSA (%) (OR = 14.38; 95% CI 8.80–26.29; P < 0.001), and facet joint violation (OR = 8.54; 95% CI 6.35–15.71; P < 0.001) were identified as independent risk factors for RBP. Conclusions: Posterior fascia injury, paraspinal muscle fatty degeneration, and facet joint violation were identified as independent risk factors for RBP, with paraspinal muscle fatty degeneration playing an important role.