A case report and literature review. To present a case of dynamic detection of a large pulmonary cement embolus as it formed and migrated during percutaneous vertebroplasty, which was successfully managed by percutaneous endovascular retrieval. Pulmonary embolism resulting from cement leakage after percutaneous vertebroplasty to treat osteoporotic vertebral compression fracture has been described rarely; however, the frequency of this complication may increase secondary to the expanding use of percutaneous vertebral augmentation techniques. The formation of a large embolus of acrylic cement and its migration into the pulmonary artery was observed in real time in a 55-year-old female with osteoporotic vertebral compression fracture of L4 during percutaneous vertebroplasty. Pulmonary arteriography confirmed the presence of the cement embolism in the right pulmonary artery during the operation. Percutaneous endovascular retrieval of the cement fragments was performed successfully via an interventional catheter procedure and subsequent incision of the femoral vein. The patient made an uneventful recovery. As illustrated by our case, large cement emboli may be primarily associated with technical aspects of the surgery. When considering the appropriate treatment strategy, percutaneous endovascular retrieval may be considered first. However, risks and benefits should be carefully evaluated on a case-by-case basis. N/A.

Background: Vertebral augmentation (VA) techniques are used to treat acute osteoporotic vertebral compression fractures (OVCFs). However, the incidence of recurrent vertebral fractures after VA is controversial. Various factors have been discussed in the literature, but no convincing study on the quality of paraspinal muscles has been reported. The purposes of this study were to evaluate the changes in paraspinal muscles and discuss the relationship between paraspinal muscle degeneration and vertebral refractures after percutaneous kyphoplasty (PKP). Methods: This retrospective study was conducted in patients who underwent PKP for an initial OVCF between July 2017 and August 2018. Patients were followed up and categorized in the refractured or non-refractured group. A final magnetic resonance imaging (MRI) scan and a preoperative MRI scan were used to determine the measurements. The paraspinal muscles at the mid-height level of the initial fractured vertebral body were measured using regions of interest (ROIs), including the cross-sectional area (CSA) and signal intensity (SI). The changes in the observed data were compared between the groups using rank-sum tests. Results: Overall, 92 patients were enrolled in the study; 33 of them sustained vertebral refractures during the follow-up and the other 59 patients did not. There were no significant differences in terms of sex, age, preoperative bone mineral density, and body mass index between the groups (all, P > 0.05). The refractured group had a significantly higher decrease in the ROI-CSA and CSA/SI, and a higher increase in ROI-SI, compared with the preoperative data (all, P < 0.05). Conclusions: The quality of paraspinal muscles significantly decreased in patients with new OVCFs after PKP. This brings a new perspective to the study of postoperative recurrent fractures; patients and physicians need to pay more attention to the efficacy of bed rest and bracing.

This study delved into the molecular mechanisms underlying mechanical stress-induced intervertebral disc degeneration (msi-IDD) through single-cell and high-throughput transcriptome sequencing in mouse models and patient samples. Results exhibited an upsurge in macrophage presence in msi-IDD intervertebral disc (IVD) tissues, with secreted phosphoprotein 1 (SPP1) identified as a pivotal driver exacerbating degeneration via the protein kinase RNA-like endoplasmic reticulum kinase/ activating transcription factor 4/ interleukin-10 (PERK/ATF4/IL-10) signaling axis. Inhibition of SPP1 demonstrated promising outcomes in mitigating msi-IDD progression in both in vitro and in vivo models. These findings underscore the therapeutic promise associated with the modulation of the PERK signaling pathway in IDD, shedding light on the pathogenesis of msi-IDD and proposing a promising avenue for intervention strategies. Graphical abstract 1) Macrophage Regulation in IDD: SPP1 activates the PERK/ATF4/IL-10 signaling axis in macrophages, increasing IL-10 production, essential for inhibiting msi-IDD progression. 2) Effective Intervention: Inhibition of SPP1 in macrophages shows potential for therapeutic intervention, significantly mitigating msi-IDD progression in mouse models. 3) Mechanical Stress Insights: Highlights the critical role of mechanical stress in intervertebral disc degeneration, establishing a link between macrophage activity and IDD pathogenesis through advanced molecular profiling.