Intervertebral disc degeneration (IVDD)‐induced lower back pain (LBP) is a common problem worldwide. The underlying mechanism is partially accredited to ferroptosis, based on sequencing analyses of IVDD patients from the gene expression omnibus (GEO) databases. In this study, it is shown that polydopamine nanoparticles (PDA NPs) inhibit oxidative stress‐induced ferroptosis in nucleus pulposus (NP) cells in vitro. PDA NPs scavenge reactive oxygen species (ROS), chelate Fe²⁺ to mitigate iron overload, and regulate the expression of iron storage proteins such as ferritin heavy chain (FHC), ferritin, and transferrin receptor (TFR). More importantly, PDA NPs co‐localize with glutathione peroxidase 4 (GPX4) around the mitochondria and suppress ubiquitin‐mediated degradation, which in turn exerts a protective function via the transformation and clearance of phospholipid hydroperoxides. PDA NPs further down‐regulate malondialdehyde (MDA) and lipid peroxide (LPO) production; thus, antagonizing ferroptosis in NP cells. Moreover, PDA NPs effectively rescue puncture‐induced degeneration in vivo by targeting ferroptosis and inhibiting GPX4 ubiquitination, resulting in the upregulation of antioxidant pathways. The findings offer a new tool to explore the underlying mechanisms and a novel treatment strategy for IVDD‐induced LBP.

The neuronal engagement of the peripheral nerve system plays a crucial role in regulating fracture healing, but how to modulate the neuronal activity to enhance fracture healing remains unexploited. Here it is shown that electrical stimulation (ES) directly promotes the biosynthesis and release of calcitonin gene‐related peptide (CGRP) by activating Ca²⁺/CaMKII/CREB signaling pathway and action potential, respectively. To accelerate rat femoral osteoporotic fracture healing which presents with decline of CGRP, soft electrodes are engineered and they are implanted at L3 and L4 dorsal root ganglions (DRGs). ES delivered at DRGs for the first two weeks after fracture increases CGRP expression in both DRGs and fracture callus. It is also identified that CGRP is indispensable for type‐H vessel formation, a biological event coupling angiogenesis and osteogenesis, contributing to ES‐enhanced osteoporotic fracture healing. This proof‐of‐concept study shows for the first time that ES at lumbar DRGs can effectively promote femoral fracture healing, offering an innovative strategy using bioelectronic device to enhance bone regeneration.

The aim of this work was to quantify the prevalence and years lived with disability (YLDs) caused by low back pain (LBP) in China from 1990 to 2016. Data from the GBD 2016 (Global Burden of Diseases, Injuries, and Risk Factors Study 2016) were used. We analyzed the age-sex-province-specific prevalence and YLDs for LBP of 33 provinces/regions in China. Comparisons were made with the data retrieved from the 1990 GBD study. We estimated that 5.45 × 10⁷ individuals had LBP in 1990, which rose to 6.73 × 10⁷ in 2016. The age-standardized prevalence of LBP decreased from 5.6% (95% uncertainty interval [95% UI]: 4.9%-6.3%) in 1990 to 4.2% (95% UI: 3.8%-4.8%) in 2016. The YLDs for LBP increased from 6.2 million (95% UI: 4.3-8.3 million) in 1990 to 7.7 million (95% UI: 5.4-10.2) in 2016. Age-standardized YLD rate (per 100,000 person) decreased from 637.5 (95% UI: 449.9-848.8) in 1990 to 481.9 (95% UI: 338.6-637.0) in 2016. A female preponderance was observed for prevalence and YLDs. The prevalence and YLDs rate for LBP slightly decreased from 1990 to 2016 in China; however, the total individuals and YLDs increased. Low back pain still ranks as the second leading cause of YLD burden disease in China. Considerable attention should be paid for LBP, especially in the female population.

Discography often destroys the hypoxic environment in the intervertebral disc and accelerates intervertebral disc degeneration (IVDD). Therefore, it often fails to meet the requirements for application in clinical practice. This technology mainly increases the reactive oxygen species (ROS) in the IVD. As so, it is particularly critical to develop strategies to avoid this degeneration mechanism. Prussian blue nanoparticles (PBNPs) are found to enhance development under magnetic resonance T1 and have antioxidant enzyme activity. The key results of the present study confirm that PBNPs alleviate intracellular oxidative stress and increase the intracellular activities of antioxidant enzymes, such as superoxide dismutase 1 (SOD1). PBNPs can rescue nucleus pulposus cell degeneration by increasing oxidoreductase system‐related mRNA and proteins, especially by stabilizing SOD1 from ubiquitination‐proteasome degradation, thus improving the mitochondrial structure to increase antioxidation ability, and finally rescuing ROS‐induced IVDD in a rat model. Therefore, it is considered that PBNPs can be a potential antioxidation‐protective discography contrast agent.

A peripheral nerve injury (PNI) has severe and profound effects on the life of a patient. The therapeutic approach remains one of the most challenging clinical problems. In recent years, many constructive nerve regeneration schemes are proposed at home and abroad. Nerve tissue engineering plays an important role. It develops an ideal nerve substitute called artificial nerve. Given the complexity of nerve regeneration, this review summarizes the pathophysiology and tissue-engineered repairing strategies of the PNI. Moreover, we discussed the scaffolds and seed cells for neural tissue engineering. Furthermore, we have emphasized the role of 3D printing in tissue engineering.

Distraction osteogenesis (DO) is a well-established surgical technique for treating bone defect and limb lengthening. The major drawback of DO is the long treatment period as the external fixator has to be kept in place until consolidation is completed. Calcitonin gene-related peptide (CGRP) has been reported to promote angiogenesis by affecting endothelial progenitor cells (EPCs) in limb ischemia and wound healing. Thus, the goal of this study was to evaluate the angiogenic effect of exogenous CGRP on bone regeneration in a rat DO model. Exogenous CGRP was directly injected into the bone defect after each cycle of distraction in vivo. Micro-computed tomography, biomechanical test and histological analysis were performed to assess the new bone formation. Angiography and immunofluorescence were performed to assess the formation of blood vessels. CD31+CD144+ EPCs in the bone defect were quantified with flow cytometry. In in vitro study, bone marrow stem cells (BMSCs) were used to investigate the effect of CGRP on EPCs production during endothelial differentiation. Our results showed that CGRP significantly promoted bone regeneration and vessel formation after consolidation. CGRP significantly increased the fraction of CD31+CD144+EPCs and the density of capillary density in the bone defect at the end of distraction phase. CGRP increased EPCs population in the endothelial differentiation of BMSCs in vitro by activating PI3K/AKT signaling pathway. Furthermore, differentiated EPCs rapidly assembled into tube-like structures and promoted osteogenic differentiation of BMSCs. In conclusion, CGRP increased EPCs population and promoted blood vessel formation and bone regeneration at the defect region in a DO model.