Background: The senescence of nucleus pulposus cells (NPCs) at the heart of the pathogenesis of intervertebral disc degeneration (IVDD), which causes low back pain. Abnormal mechanical stress causes intracellular Ca ²⁺ overload by activating the Piezo‐type mechanosensitive ion channel component 1 (PIEZO1) channel. Aims: This creates a positive feedback loop of oxidative‐inflammatory damage by inducing endoplasmic reticulum stress and mitochondrial reactive oxygen species (ROS) bursts, as well as directly activating the NLRP3 inflammasome/NF‐кB axis to promote the release of pro‐inflammatory factors like IL‐1β. Results: Energy metabolism collapsed as a result of mechanistic cause that caused excessive activation of mitophagy via the ROS‐PINK1/Parkin pathway, and SIRT1 functional suppression further compromised mitochondrial quality control. The inflammatory nucleus pulposus (NP) brought on by mechanical stimulation caused macrophages to polarize toward the M1 type, and the p38MAPK pathway was activated by the TNF‐α/IL‐1β released, which in turn increased senescence markers like p16/p21. Notably, ROS both triggers mitophagy and activates the p53 pathway. On the one hand, oxidative damage‐induced ATM/ATR kinase activation leads to p53 phosphorylation, which triggers p21‐mediated cell‐cycle block. On the other hand, p53 exacerbates mitochondrial dysfunction by inhibiting SIRT1 expression, creating a triangular amplification loop of p53‐ROS‐mitophagy. Furthermore, p53 stimulates apoptosis by altering the Bax/Bcl‐2 balance and works in concert with inflammatory substances secreted by M1‐type macrophages to cause the development of senescence‐associated secretory phenotype (SASP). Conclusion: This interaction network reveals the dynamic coupling of mechano‐immune‐metabolic pathways in the course of IVDD, providing a theoretical basis for the development of multi‐targeted intervention strategies, such as PIEZO1 inhibitors combined with M2‐type macrophage polarization modulation, which are expected to delay disease progression by blocking key nodes.

The aims of this study were to determine (1) the agreement in Epworth Sleepiness Scale (ESS) evaluated by patients and their close relatives (CRs), and (2) the correlation of objective sleepiness as measured by multiple sleep latency test (MSLT) with self-evaluated and close relative-evaluated ESS. A total of 85 consecutive patients with obstructive sleep apnea (OSA) (70 males, age 46.7 ± 12.9 years old) with an apnea-hypopnea index (AHI) > 5 events per hour (mean 38.9 ± 26.8/h) were recruited into this study. All participants underwent an overnight polysomnographic assessment (PSG), MSLT, and ESS rated by both patients and their CRs. Mean sleep latency < 8 min on MSLT was considered objective daytime sleepiness. Self-evaluated global ESS score (ESSG) was closely correlated with evaluation by CRs (r = 0.79, p < 0.001); the mean ESSG score evaluated by patients did not significantly differ from that evaluated by CRs (p > 0.05). However, Bland- Altman plot showed individual differences between self-evaluated and CR-evaluated ESS scores, with a 95%CI of -9.3 to 7.0. The mean sleep latency on MSLT was significantly associated with CR-evaluated ESSG (r = -0.23, p < 0.05); significance of association with self-evaluated ESSG was marginal (r = -0.21, p = 0.05). CR-evaluated ESS has a good correlation but also significant individual disagreement with self-evaluated ESS in Chinese patients with OSA. CR-evaluated ESS performs as well as, if not better than, self-evaluated ESS in this population when referring to MSLT.

The reparative process following spinal cord injury (SCI) is extremely complicated. Cells in the microenvironment express multiple inhibitory factors that affect axonal regeneration over a prolonged period of time. The axon growth inhibitory factor glycogen synthase kinase-3 (GSK-3) is an important factor during these processes. TDZD-8 (4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione) is the most effective and specific non-ATP-competitive inhibitor of GSK-3. Here, we show that administering TDZD-8 after SCI was associated with significantly inhibited neuronal apoptosis, upregulated GAP-43 expression, increased density of cortical spinal tract fibers around areas of injury, and increased Basso, Beattie, and Bresnahan (BBB) scores in the lower limbs. These findings support the notion that GSK-3 inhibitors promote neuronal cell regeneration and lower limb functional recovery.

Purpose. The occurrence of new vertebral compression fractures (VCFs) is a common complication after percutaneous kyphoplasty (PKP). Secondary VCFs after PKP occur predominantly in the thoracolumbar segment (T11 to L2). Prophylactic injections of cement into vertebral bodies in order to reduce new VCFs have rarely been reported. The main purpose of this study was to investigate whether prophylactically injecting cement into a nonfractured vertebral body at the thoracolumbar level (T11‐L2) could reduce the occurrence of new VCFs. Methods. From July 2011 to July 2018, PKP was performed in 86 consecutive patients with osteoporotic vertebral compression fractures (OVCFs) in the thoracolumbar region (T11‐L2). All patients selected underwent PKP because of existing OVCFs (nonprophylactic group). Additionally, 78 consecutive patients with fractured vertebrae in the thoracolumbar region (T11‐L2) with OVCFs underwent PKP and received prophylactic injections of cement into their nonfractured vertebrae in the thoracolumbar region (T11‐L2) (prophylactic group). The visual analog scale (VAS) scores and incidence of new VCFs after PKP were compared between the two groups. Results. The mean VAS scores improved from 8.00 ± 0.79 preoperatively to 1.62 ± 0.56 at the last follow‐up in the nonprophylactic group and improved from 8.17 ± 0.84 to 1.76 ± 0.34 in the prophylactic group (P > 0.05). In the nonprophylactic group, 21 of 86 patients (24.4%) developed new VCFs within one year after PKP, of whom 15 patients (71.4%) developed VCFs within 3 months. In the prophylactic group, 8 of 78 patients (10.3%) developed new VCFs within one year, and 6 of these 8 patients (75%) developed new VCFs within 3 months. The incidence of new VCFs was significantly higher in the nonprophylactic group than that in the prophylactic group at one year (P = 0.018), but there were no statistically significant differences at three months (P = 0.847). Conclusions. Prophylactic injections of cement into nonfractured (T11‐L2) vertebral bodies reduced the incidence of secondary VCFs after PKP in patients with OVCFs, but there was no significant difference in local back pain (VAS) scores between the two groups.

Surgical treatment of suppurative spondylitis requires focus debridement, spinal stability, and deformity correction. Different approaches face challenges like complex anatomical structures and greater trauma. The aim is to evaluate the clinical efficacy of One-stage debridement approach combined with autogenous bone grafting and internal fixation for the treatment of adult thoracic or lumbar suppurative spondylitis via the multifidus and longissimus interspaces. From July 2018 to July 2021, 91 patients (65 male, 26 female) with single - level thoracic or lumbar suppurative spondylitis underwent the one-stage posterior procedure. Operative details and hospital stay were recorded. ESR, CRP, and PCT levels were analyzed at specific times. Pain was rated by VAS, Using ODI score to evaluate the improvement of lumbar activity, and neurological function was assessed by ASIA scale. Cobb angles were measured for deformity evaluation. Bony fusion was evaluated by radiography and computed tomography. The mean operative duration was 195.6 ± 15.4 min, blood loss was 575.9 ± 90.1 ml, and hospital stay was 19.9 ± 2.2 days. ESR, CRP, and PCT levels significantly decreased before discharge (ESR: 80.2 ± 14.6 mm/h vs. 30.2 ± 8.9 mm/h, CRP: 58.5 ± 13.6 mg/L vs. 15.1 ± 7.4 mg/L, PCT: 0.8 ± 0.2 ng/ml vs. 0.1 ± 0.1 ng/ml, P < 0.05). All patients had pain relief. VAS scores improved (preoperative 7.7 ± 1.1, before discharge 2.8 ± 0.6, final follow-up 1.3 ± 0.6). The lumbar activity of all patients was significantly improved compared with preoperative(preoperative 41.36 ± 3.20, final follow-up 6.18 ± 1.33). Neurologically impaired patients improved in ASIA grade. The mean preoperative Cobb angle was 19.6 ± 1.6°, reduced to 6.2 ± 1.5° before discharge and 9.4 ± 1.0° at final follow-up. The mean angle correction was 13.4 ± 0.6°, correction rate 68.7% ± 5.4% (P < 0.05), with a final loss angle of 3.2 ± 0.7° and loss rate 24.1% ± 4.8%. All grafts achieved complete fusion. This one-stage posterior approach is effective and feasible for adult single - level thoracic or lumbar suppurative spondylitis, protecting paravertebral muscles and posterior ligament complexes. However, further studies with larger samples and longer follow-up are needed.