Background: Ac Lumbo-sacral transitional vertebra (LSTV) represents a common congenital anomaly at the lumbo-sacral junction, often associated with altered biomechanics, early degeneration and chronic low back pain (CLBP). Despite its clinical significance, regional data from South Kashmir remain limited. Objective: To determine the prevalence and types of LSTV among chronic low back pain patients in South Kashmir, using radiological evaluation (X-ray and MRI), and to assess associated degenerative changes and radiculopathy. Methods: This hospital-based cross-sectional study included patients aged 16–80 years presenting with chronic low back pain at MMABM Hospital, GMC Anantnag in South Kashmir, from June 2024 to May 2025. All subjects underwent lumbo-sacral spine imaging—either X-ray, MRI, or both. LSTV was identified and classified according to Castellvi’s classification1. Degenerative changes, adjacent segment disc pathology, and nerve root involvement were assessed. Data were analyzed for prevalence, laterality, and radiological correlations. Results: Of 208 patients evaluated, 35% (n=73) demonstrated LSTV on radiology. The most frequent subtype was Castellvi Type II (40%), followed by Type I (30%). Unilateral LSTV cases exhibited more severe degenerative changes and earlier disc space narrowing than bilateral types. Adjacent segment disc degeneration was observed in a majority of LSTV patients (70%), particularly at the L4–L5 level. Radiculopathy was present in a substantial proportion of cases with LSTV, frequently corresponding to foraminal stenosis or nerve root compression above the transitional level. Conclusion: LSTV is a frequent finding among chronic low back pain patients in South Kashmir, with a prevalence of approximately 35%. Unilateral variants are associated with more pronounced degeneration and radicular symptoms. Recognition of this variant on X-ray and MRI is vital for accurate diagnosis, classification, and management of low back pain

Abstract Spontaneous intracranial hypotension (SIH) is commonly caused by cerebrospinal fluid (CSF) leakage, resulting in epidural CSF accumulation. Although bony spurs and disc degeneration are traditionally implicated, SIH frequently affects younger individuals, suggesting that additional anatomical or biomechanical factors may contribute. We hypothesized that cervical spinal alignment, particularly reduced lordosis, may influence CSF retention patterns and contribute to SIH pathophysiology. A retrospective analysis was conducted on 30 SIH patients and 30 age- and sex-matched healthy controls. Cervical Cobb angles were measured from lateral MRI images, and CSF accumulation was evaluated for thickness, distribution (ventral vs. dorsal), and spinal level. Correlations were assessed between these variables. Group comparisons were performed using the Wilcoxon rank sum test. Pearson's correlation coefficient was used to evaluate associations between quantitative variables. A p-value of < 0.05 was considered statistically significant. SIH patients had significantly smaller Cobb angles than controls (p = 0.011), indicating reduced cervical lordosis or a straight neck alignment. A strong association was found between smaller Cobb angles and dorsal CSF accumulation (p < 0.001). Ventral retention was more common in the lower cervical spine, while dorsal retention predominated in the mid-thoracic region. No significant correlation was observed between Cobb angle and CSF thickness or patient age. Reduced cervical lordosis is associated with distinct CSF retention patterns in SIH, particularly dorsal accumulation. Despite the limited sample size due to the rarity of SIH, consistent and statistically significant trends were observed. These findings support the clinical relevance of assessing spinal alignment in SIH and suggest that anatomical factors may influence dural vulnerability. Further research should explore whether alignment-based interventions can mitigate dural stress and reduce CSF leakage risk.

Study Design: Systematic review and meta-analysis. Objective: To systematically review and meta-analyze spine magnetic resonance imaging (MRI) data from military personnel to characterize occupational risk factors for disc degeneration before spaceflight. Summary of Background Data: Approximately 60% of NASA astronauts have military backgrounds, potentially predisposing them to higher risk of spinal pathology. We evaluated data on disc degeneration in military personnel compared with an asymptomatic civilian population to estimate spinal pathology prevalence among NASA astronauts with military backgrounds. Methods: PubMed, Scopus, and Google Scholar databases were systematically queried in April 2024 using the MeSH terms: military personnel, spine, and MRI. Studies involving asymptomatic civilians from a prior systematic review served as a control population. A mixed-effects meta-analysis and linear regression were conducted to compare disc degeneration and average age between military and civilian populations. Results: There was a significant group effect, with military personnel showing higher overall prevalence of disc degeneration compared with civilians ( =0.999; 95% CI: 0.588, 1.4110; P <0.001). Age was also a significant predictor, with each additional year associated with an increase in the prevalence of disc degeneration [ =0.108; 95% CI: 0.075, 0.140; P <0.001]. Linear regression estimated that nearly all military personnel (∼100%) at the average age of first spaceflight (∼40 years old) exhibited at least one level of disc degeneration compared with ∼71% of civilians. Conclusions: Military personnel have a higher prevalence of disc degeneration compared with civilians, likely associated to their relative increased physical demands of military service. The extent of disc degeneration may even be underestimated, because our analyses included only young military personnel with a relatively short service duration. The current findings inform baseline expectations for disc degeneration in asymptomatic civilians and military personnel for more accurate interpretation of spine imaging before spaceflight. Level of Evidence: Level 3—systematic review of level 3 evidence

mModPoEs: Multimodal posture estimation and feedback-driven correction of load-bearing human movements using wearable sensors and computer vision.

Retrospective cohort study based on a multicenter adult spinal deformity (ASD) database. To characterize distinct patterns of proximal junctional failure (PJF) beyond kyphosis-based definitions and evaluate their morphology, timing, and clinical implications. Proximal junctional kyphosis (PJK) is commonly defined by angular measurements, yet many patients develop other junctional complications-such as vertebral fractures, disc degeneration, or instrumentation failure-without measurable kyphosis. These "non-kyphotic" failures are under-recognized in current classification systems, limiting clinical decision-making and preventive strategies. Data from 185 ASD patients who either met Lovecchio's radiographic PJK criteria or underwent revision surgery with proximal extension were retrospectively reviewed. Three independent readers qualitatively classified failure morphology at the proximal junction. Free-text reports were standardized and categorized into vertebral, soft-tissue/disc, or diffuse degenerative failure modes. An unsupervised cluster analysis was used to identify failure patterns based on imaging features and time to onset. Relationships between failure types, UIV level, prophylactic measures, and timing were analyzed. Among 1,506 enrolled patients, 185 (12.3%) developed proximal junctional complications (median age 67.5 yr; 86.5% female). Failure modes included vertebral (66%), soft tissue/disc (64.9%), and diffuse degeneration (22.2%). Notably, 27% of patients exhibited no kyphotic angulation. Cluster analysis identified three patterns: type 1 (acute vertebral fracture, median onset 73.5 days), type 2 (disc/soft tissue failure, 368 days), and type 3 (degeneration, 670 days). Proximal junctional failure is not synonymous with kyphosis. This study identifies three distinct, temporally and morphologically defined failure modes, including a significant proportion of non-kyphotic cases. These findings support expanding PJF definitions and adopting individualized, mechanism-based preventive strategies in ASD surgery. Level III.

Body Mass Index as a Risk Factor for Recurrence and Frequency of Re-surgery after Lumbar Spine Surgery.

Duhuo mitigates intervertebral disc degeneration by activating PI3K/AKT to inhibit ferroptosis in nucleus pulposus cells.

A novel bicortical alternating screw exchange lagging technique for reduction of cervical spinal deformity.

Duhuo Jisheng decoction alleviates intervertebral disc degeneration by inhibiting nucleus pulposus cell pyroptosis via gallic acid-mediated downregulation of HIF-1α.

Human nucleus pulposus cells (HNPCs), the primary cellular constituents of the intervertebral disc, are central to the pathogenesis of intervertebral disc degeneration (IVDD). Oxidative stress-induced mitochondrial dysfunction leads to intracellular metabolic imbalance and has been implicated in IVDD. This study investigated the role and molecular mechanism of glutamate dehydrogenase 1 (GLUD1) in hydrogen peroxide (H2O2)-challenged HNPCs relevant to IVDD. HNPCs were exposed to H2O2 to establish an oxidative stress model. Cell viability was assessed using the CCK-8 assay. Mitochondrial function was evaluated by measuring the oxygen consumption rate (OCR) and mitochondrial membrane potential. GLUD1 expression was quantified by qRT-PCR and Western blotting. The regulatory relationship between METTL3 and GLUD1 was examined by MeRIP-qPCR and a luciferase reporter assay. H2O2 treatment decreased OCR and mitochondrial membrane potential in HNPCs and reduced alpha-ketoglutarate (α-KG) levels and GLUD1 expression. GLUD1 knockdown exacerbated H2O2-induced mitochondrial dysfunction, whereas GLUD1 overexpression alleviated it. METTL3 regulated GLUD1 mRNA stability by inducing GLUD1 m6A modification via YTHDF2, thereby modulating H2O2-induced mitochondrial dysfunction. GLUD1 protects HNPCs from H2O2-induced mitochondrial dysfunction through the glutamate/α-KG metabolic axis.

Intervertebral disc degeneration (IVDD) is an age-related degenerative spinal disorder, with age as the primary independent risk factor. To investigate the key pathogenic mechanisms of IVDD, we conducted biochemical analyses on IVD specimens from elderly and young groups. In this study, we found that methylmalonic acid (MMA) levels are significantly elevated within the discs of the elderly group, suggesting that MMA may be a critical metabolite involved in aging-induced IVDD. In invitro experiments, we observed that MMA treatment of nucleus pulposus cells (NPCs) upregulated the expression of extracellular matrix catabolic markers and downregulated the expression of anabolic markers. Further validation in an invivo mouse model of needle puncture-induced IVDD confirmed that MMA accelerates IVDD progression. Mechanistically, we demonstrated that MMA upregulates the expression of C-C motif chemokine ligand 7 (CCL7) in NPCs. CCL7 acts as a chemoattractant, further enhancing Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling transduction, ultimately leading to upregulated vascular endothelial growth factor (VEGF) expression. This promotes abnormal growth of vascular endothelial cells, resulting in disc vascularization. Additional invivo and invitro experiments confirmed that disc vascularization is a key progression factor in IVDD. As a rescue strategy, we administered lenvatinib, a VEGF receptor inhibitor, which delayed IVDD progression. Therefore, VEGF and disc vascularization represent a promising therapeutic target for IVDD, offering an innovative approach to addressing IVDD treatment in clinical practice.

Piezo1 at the crossroads: Mediating inflammation and mechanical stress in joint disorders.

Targeting the ROS-senescence-fibrosis axis: A dual-pronged strategy against intervertebral disc degeneration

As a chronic musculoskeletal disorder, intervertebral disc degeneration (IDD) is a leading cause of low back pain. Inflammatory response plays a key role in the IDD progression. Albiflorin (AF), a bioactive compound derived from Paeonia lactiflora, exhibits anti-inflammatory effects in various diseases. However, the effects of AF on IDD remain unexplored. This study explored the protective effect of AF against IDD and elucidate its possible mechanisms. Nucleus pulposus (NP) cells were stimulated with lipopolysaccharide (LPS ) for 24 h to establish the IDD cell model, followed by AF or p38MAPK agonist (P79350) treatment. Cell viability and apoptosis were evaluated using 5-ethynyl-2'-deoxyuridine (EdU) assay and flow cytometry analysis, respectively. Levels of the Inflammatory cytokines (tumor necrosis factor alpha, TNF-α; interleukin-1beta, IL-1β; IL-6) were assessed by enzyme-linked immunosorbent assay (ELISA). The mRNA levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-Associated X (Bax), aggrecan, and collagen type II was analyzed by reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR), while their protein levels were determined by western blot assay. LPS induction remarkably inhibited NP cell proliferation (p < 0.001) and induced apoptosis (p < 0.001), which were significantly reversed by AF dose-dependently. Furthermore, AF treatment dose-dependently decreased extracellular matrix (ECM) degradation and inflammatory factors secretion in LPS-induced NP cells, evidenced by enhanced aggrecan and collagen type II protein expression (all p < 0.01), and reduced TNF-α, IL-1β, and IL-6 section (all p < 0.05). Mechanistically, AF exerted its protective effects by suppressing the p38 mitogen-activated protein kinase (MAPK)/nuclear factor κB (NF-κB) signaling pathway, as evidenced by reduced phosphorylation of p38 and p65 (all p < 0.01). Notably, co-treatment with P79350 partially abolished the protective effects of AF against LPS-induced NP cell damage. AF relieved IDD through repressing NP cell apoptosis, inflammatory response, and ECM degradation through the p38 MAPK/NF-κB pathway, indicating that it is a potential IDD therapeutic agent.

The word Gridhrasi is derived from the Sanskrit word ‘Gridhra’ which means the name of bird i.e. Vulture. Gridhrasi is a Vataj Nanatmaja Vikara. Ruk (pain), Toda (pricking feeling), Muhuspandana (tingling sensation), and Stambha (stiffness) in the Sphik, Kati, Uru, Janu, Jangha, and Pada are the four primary symptoms of Gridhrasi. In modern medicine, this condition can be correlated with Sciatica, Sciatica is a common clinical condition resulting from lumbar nerve root compression and may lead to chronic pain/radiating pain, restricted mobility, and secondary muscular disuse. Prolonged radicular pain often causes avoidance of limb usage, which may progress to disuse atrophy of the affected muscles. In this case a 47- year old female patient with chronic low back pain radiating to the left lower limb, associated with difficulty in walking as well as sitting position and visible reduction in thigh muscle bulk reported for treatment. Radiological evaluation of the lumbar spine revealed reduced intervertebral disc space at the L4–L5 level with mild alteration of lumbar lordosis, suggestive of degenerative disc disease. The patient was treated with Integrative Ayurvedic interventions incluiding Sarvanga Abhayanga, Shastik Shali Pind Swedana and Mustadi Rajyapan basti. Post treatment assessment showed significant reduction in pain, improvement in gait and functional mobility and gradual improvement in thigh circumference. The patient also reported enhanced quality of life.

Lactate accumulation is a hallmark and contributing factor of intervertebral disc degeneration (IVDD), while the role of protein lactylation caused by lactate accumulation in IVDD remains unclear. Via metabolomics, single-cell RNA-sequencing analysis, and lactylation proteomics, we reveal the lactylome landscape in IVDD and identified superoxide dismutase 1 (SOD1) lactylation at lysine 123 (SOD1K123la) as crucial for IVDD aggravation. Using in vitro site-directed mutagenesis, in vivo generation of SOD1K123R mutant male rats, and in silico molecular dynamics simulations, we find that SOD1K123la alters SOD1 conformation and impairs its enzymatic activity, and induces oxidative damage, and activates p53 pathway in nucleus pulposus cells (NPCs). Notably, we identify a small molecule ZL-01 that inhibits SOD1K123la. NPC-targeted delivery of ZL-01 via collagen type II-targeted peptide-modified extracellular vesicles alleviated IVDD in male rats. Together, these findings clarify the mechanism by which SOD1K123la promotes IVDD aggravation and provide a promising therapeutic strategy for IVDD.

Comparative Outcomes of Anterior Cervical Discectomy and Fusion Vs Hybrid Surgery in Multilevel Cervical Degenerative Disc Disease: A Systematic Review and Meta-analysis.

Introduction Intervertebral disc degeneration (IDD) is a major cause of low back pain and disability. While MRI remains the standard diagnostic tool, it provides limited insight into the cellular and molecular changes underlying IDD. Histological analysis offers a complementary approach to characterizing the degenerative process in human intervertebral discs (IVDs). This systematic review aims to provide a comprehensive analysis of histological and immunohistochemical changes across the IVD, nucleus pulposus (NP), and cartilage endplate (CEP) in degenerated human discs. Methods A literature search was conducted in PubMed, Scopus, and Web of Science for studies published between 2015 and 2025. A total of 45 human studies were included. Histological features, protein expression profiles, and grading systems were analyzed. Differentially expressed proteins were mapped into protein–protein interaction (PPI) networks using the STRING database. Results Common histopathological features included ECM disorganization, proteoglycan depletion, fibrosis, neovascularization, and cell clustering. Molecular data revealed upregulation of catabolic enzymes, inflammatory cytokines, apoptotic mediators, and angiogenic factors. Conversely, regenerative and protective markers were significantly downregulated. PPI analysis revealed region-specific pathways: ECM remodeling and BMP/VEGF signaling in the IVD, inflammation and mechanotransduction in the NP, and ossification and prostaglandin signaling in the CEP. Conclusion Histology reveals spatially distinct yet converging degenerative pathways across IVD regions. These findings identify potential biomarkers and therapeutic targets, supporting histological analysis as an essential complement to imaging for accurate IDD characterization.

Intervertebral disc degeneration (IVDD) is a major contributor to low back pain, influenced by various factors including cellular senescence, apoptosis, oxidative stress, and inflammation. Metallothionein-2A (MT2A), due to its unique metal-binding and antioxidant capacity, plays a critical role in various diseases. This research sought to clarify how MT2A inhibits the progression of IVDD. Single-cell sequencing analysis revealed that ferroptosis was involved in IVDD, and MT2A was significantly upregulated in the degenerated nucleus pulposus tissue. In vitro, Tert-Butyl Hydroperoxide (TBHP) treatment induced MT2A expression. Knockdown of MT2A exacerbated TBHP-induced ferroptosis, whereas MT2A overexpression or treatment with ferrostatin-1 reversed ferroptosis, lipid peroxidation, and mitochondrial damage. In vivo, AAV-mediated MT2A overexpression significantly alleviated puncture-induced IVDD in rats. Mechanistically, MT2A overexpression activated PI3K/AKT/mTOR pathway, and this protective effect was significantly attenuated upon treatment with specific pathway inhibitors. In Conclusion, our findings demonstrate that MT2A is protectively upregulated in IVDD and mitigates ferroptosis of NP cells and IVDD progression through activation of the PI3K/AKT/mTOR pathway, which designates MT2A as a promising target for therapy in IVDD.

Background and Objectives: Long spinal fusion terminating at L5 remains controversial because of the risk of postoperative junctional failure. Although degeneration of the residual L5-S1 disc has been suggested as a contributing factor, the relative impact of disc degeneration versus sagittal spinopelvic alignment on different junctional failure patterns has not been fully clarified. Materials and Methods: This retrospective cohort study included 47 patients aged ≥60 years who underwent ≥5-level thoracolumbar fusion ending at L5 with a minimum follow-up of 2 years. Junctional failures were classified as proximal junctional failure (PJF) or distal junctional failure (DJF). Preoperative L5-S1 disc degeneration was assessed using modified Weiner and Pfirrmann classifications. Spinopelvic parameters were measured preoperatively, postoperatively, and at final follow-up. Junctional failure-free survival was analyzed using the Kaplan-Meier method, and risk factors were explored using Cox proportional hazards models. Results: Junctional failures occurred in 28 patients (59.6%), including 16 PJFs (34.0%) and 10 DJFs (21.3%). Lower grades of L5-S1 disc degeneration (Weiner grades 0-1) were more frequently associated with PJFs, whereas higher grades (≥2) were predominantly associated with DJFs (p = 0.024). Multivariate analysis showed that preoperative thoracolumbar kyphosis (hazard ratio [HR] = 1.164), preoperative T1 pelvic angle (HR = 1.269), and postoperative pelvic incidence-lumbar lordosis mismatch (HR = 0.877) as significant risk factors for PJF. Postoperative proximal junctional angle (HR = 0.899) and lumbar lordosis (HR = 0.920) were independently associated with DJF. Conclusions: Sagittal spinopelvic alignment parameters appear to have a greater influence on junctional failure patterns than residual L5-S1 disc degeneration in long fusions terminating at L5. Adequate sagittal correction should be prioritized to reduce the risk of both proximal and distal junctional failures.