Differential Diagnosis Strategy between Lower Extremity Arterial Occlusive Disease and Lumbar Disc Herniation

Considering the increasingly incidence rate of lower extremity arterial occlusive disease and difficult to distinguish from lumbar disc herniation, it is very necessary to exclude lower extremity arterial occlusive disease resulting in lower limb symptoms from lumbar disc herniation. More importantly, who have a higher risk of combining with lower extremity arterial occlusive disease and misdiagnosed as lumbar disc herniation? Why those patients are easy to be misdiagnosed as lumbar disc herniation? It is worth analyzing and discussing. The risk factors including age, gender, the medical history of high blood pressure, diabetes, smoking and coronary, pulse pressure, lumbar disc herniation segment and type, ankle-brachial index, and straight leg raising test were observed. The Oswestry disability index and the Japanese Orthopedic Association score were collected preoperative, six months after posterior lumbar interbody fusion and six months after vascular interventional treatment to evaluate the symptoms relief and surgical efficacy. There was a statistically significant difference (P<0.01) in pulse pressure, ankle-brachial index, central disc herniation, and straight leg raising test between two groups. There was a high risk to missed diagnosis of lower extremity arterial occlusive disease and misdiagnosed as lumbar disc herniation when patients are with a mild central lumbar disc herniation, higher pulse pressure, lower ankle-brachial index, and straight leg raising test negative. Therefore, sufficient history-taking and cautious physical examinations contributed to find risk factors and attach importance to such patients and, further, to exclude lower extremity arterial occlusive disease from lumbar disc herniation using lower extremity vascular ultrasound examination

Calcium Phosphate Cement Causes Nucleus Pulposus Cell Degeneration Through the ERK Signaling Pathway

While calcium phosphate cement (CPC) is recognized as one of the most likely substitutes for the conventional Polymethylmethacrylate (PMMA), there are very few studies about its intradiscal leakage consequences. Herein, the goal of our study was to examine the effect of CPC particles on the ERK (extracellular regulatory kinase) pathway in human nucleus pulposus cell (HNPC) degeneration. Different concentrations of CPC particles (0.00‰, 0.01‰, 0.05‰, 0.1‰ v/v) were added to human nucleus pulposus cell cultures. After 10 days of treatment, HNPC biological behaviors and degeneration degree were analyzed by CCK-8 assay, crystal violet staining, flow cytometer and western blot. The effect of CPC on the ERK pathway was also analyzed by western blot. After activating the ERK path by overexpressing Ras, HNPCs’ biological behaviors and degeneration degree were analyzed again. We found that CPC particles had a negative effect on human nucleus pulposus cells (HNPCs), which are mainly reflected in cell growth and the cell cycle. After activation of the ERK signaling pathway, the negative effects of CPC on cell growth and the cell cycle were significantly reduced and the degeneration degree of HNPCs was reversed. CPC particles can probably block the activation of the ERK pathway, thus causing the HNPCs’ degeneration

Tea Polyphenol Attenuates Oxidative Stress-Induced Degeneration of Intervertebral Discs by Regulating the Keap1/Nrf2/ARE Pathway

Objective. Intervertebral disc degeneration (IDD) and low back pain caused by IDD have attracted public attention owing to their extremely high incidence and disability rate. Oxidative stress is a major cause of IDD. Tea polyphenols (TP) are natural-derived antioxidants extracted from tea leaves. This study explored the protective role of TP on the nucleus pulposus cells (NPCs) of intervertebral discs and their underlying mechanism. Methods. An in vitro model of H2O2-induced degeneration of NPCs was established. RT-qPCR and western blotting were used to detect the mRNA and protein expression of the targets. An in vivo model of IDD was established via acupuncture of the intervertebral disc. Radiological imaging and histological staining were performed to evaluate the protective role of TP. Results. H2O2 contributed to NPC degeneration by inducing high levels of oxidative stress. TP treatment effectively increased the expression of nucleus pulposus matrix-associated genes and reduced the expression of degeneration factors. Further mechanistic studies showed that TP delayed H2O2-mediated NPC degeneration by activating the Keap1/Nrf2/ARE pathway. In vivo experiments showed that TP delayed the degeneration of NPCs in rats through the Keap1/Nrf2/ARE pathway. Conclusion. Our study confirmed that TP activates the Keap1/Nrf2/ARE pathway to exert an antioxidative stress role, ultimately delaying the degeneration of intervertebral discs