Objective Adjacent segment disease (ASD) is a recognized long-term complication after anterior cervical discectomy and fusion (ACDF). Cervical disc arthroplasty (CDA) was introduced as a motion-preserving alternative, thought to reduce stress at adjacent levels and lower ASD risk. This study aimed to compare the risk of ASD requiring reoperation after ACDF and CDA and identify factors associated with ASD.
Methods This retrospective cohort study used prospectively collected data from the Swedish Spine Registry (Swespine) and included adult patients undergoing anterior cervical surgery for degenerative cervical disease between 2006 and 2026. ASD was defined as a secondary operation at an adjacent level ≥12 months after the index procedure. Cumulative incidence was estimated using Kaplan-Meier analysis, and associations with ASD were evaluated using multivariable Cox proportional hazards regression. Radiological or conservatively treated ASD were not assessed.
Results A total of 9,338 patients were included (ACDF, n=9,005; CDA, n=333). During 45,666 person-years follow-up, 509 ASD events occurred (incidence rate 11.1 per 1,000 person-years). Cumulative incidence was 4.9% at 5 years and 10.4% at 10 years. CDA was associated with lower ASD hazard than ACDF (hazard ratio [HR], 0.61) though this association was not significant after propensity score matching (HR, 0.88). Multilevel procedures (HR, 0.61), increasing age (HR, 0.96 per year), and radiculopathy were associated with lower risk, while myelopathy or stenosis was associated with higher risk (HR, 1.22).
Conclusion The long-term risk of ASD requiring reoperation was lower than previously reported. After adjustment, CDA was associated with lower ASD risk compared to ACDF, although the absolute difference was small, and the clinical significance remains uncertain.
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A Commentary on “A Nationwide Registry Study Comparing Long-term Risk of Adjacent Segment Disease Requiring Reoperation Following Anterior Cervical Discectomy and Fusion Versus Cervical Disc Arthroplasty” Samuel K. Cho Neurospine.2026; 23(3): 536. CrossRef
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Anterior cervical decompression and fusion for Samartzis Type I Klippel–Feil syndrome complicated by cervical radiculopathy with radiographic spinal cord compression: a case report of sandwich-type interposed mobile segment Baopeng Zeng, Shengxing Liu Frontiers in Surgery.2026;[Epub] CrossRef
Objective This study aimed to investigate the role of the STAT3/POSTN/GSTP1/JNK axis in ferroptosis and extracellular matrix (ECM) metabolic imbalance in nucleus pulposus cells (NPCs) during intervertebral disc degeneration (IDD) and to explore therapeutic strategies targeting this axis.
Methods Using integrated multiomics sequencing, transcriptional regulation assays (chromatin immunoprecipitation, dual‑luciferase reporter), protein interaction analysis (CoIP), and other molecular biology approaches, we systematically elucidated the regulatory role of the STAT3/POSTN/GSTP1/JNK axis in ferroptosis of NPCs during IDD. Functional validation was performed in POSTN‑edited cell and rat models as well as in a needle‑puncture‑
induced rat IDD model. A small‑molecule candidate targeting this axis was identified through virtual screening, molecular docking, and molecular dynamics simulations.
Results Periostin (POSTN) expression increased during ferroptosis and induced ferroptosis and ECM metabolic imbalance in NPCs in a concentration- and time-dependent manner. STAT3 was identified as a transcriptional regulator of POSTN and functionally coupled with POSTN to form a self-amplifying positive feedback loop, accelerating ferroptosis progression. Furthermore, POSTN impaired the binding of the GSTP1/JNK complex, leading to the depletion of cellular glutathione. Chemical screening identified pristimerin (PN) as a potential GSTP1-targeting compound, targeting the STAT3/POSTN/GSTP1/JNK axis and delaying IDD progression.
Conclusion This study identified the important role of the STAT3/POSTN/GSTP1/JNK axis in regulating ferroptosis and ECM metabolism in NPCs and highlighted PN as a promising candidate therapeutic agent for IDD. These findings provide new insights into the molecular mechanisms underlying IDD and offer new targeted therapeutic avenues for IDD.
Objective Transient receptor potential vanilloid 4 (TRPV4), a mechanosensitive ion channel, has been implicated in intervertebral disc homeostasis; however, its role in autophagy regulation remains unclear. This study aimed to investigate whether agonist-induced TRPV4 activation promotes autophagy and extracellular matrix (ECM) synthesis in rat intervertebral discs.
Methods In vitro, rat nucleus pulposus (NP) cells were treated with the TRPV4 agonist (GSK1016790) under normal, serum-deprived, or interleukin-1β-stimulated conditions. Cell viability, intracellular Ca2+ influx, adenosine monophosphate-activated protein kinase/mammalian target of rapamycin (mTOR) (AMPK/mTOR) pathway, autophagy, ECM metabolism, apoptosis, and senescence were evaluated. In vivo, TRPV4 agonist was injected into the caudal discs subjected to temporary static compression, and disc changes were assessed by radiography, histomorphology, and immunofluorescence.
Results In vitro, agonist-induced TRPV4 activation rapidly increased intracellular Ca2+ influx and enhanced AMPK phosphorylation. A noncytotoxic concentration of the TRPV4 agonist (10 nM) was selected after dose-response testing. Under the inflammatory stress, TRPV4 agonist enhanced autophagy, promoted ECM synthesis, and suppressed apoptosis and senescence, leading to improved NP cell viability. In vivo, TRPV4 agonist treatment preserved radiographic disc height (p<0.01), reduced histomorphological degeneration (p<0.01), and increased expression of COL2A1, Brachyury, p-AMPK (phosphorylated AMPK), and autophagy markers (p<0.01) compared with controls.
Conclusion These findings demonstrated that TRPV4 activation promotes autophagy and ECM synthesis via the AMPK/mTOR pathway in rat discs and attenuates stress-induced degeneration, suggesting TRPV4 as a potential therapeutic target for disc degeneration.
Objective Intervertebral disc degeneration (IVDD) is a complex pathological process involving inflammation, oxidative stress, and immune dysregulation. Emerging evidence suggests that neuroimmune interactions contribute to IVDD progression, but the role of neuropeptide-like factors remains poorly understood.
Methods We investigated whether Gαi-interacting protein (GINIP+) sensory neurons infiltrate degenerative discs and secrete TAFA chemokine like family member 4 (TAFA4), a neuron-derived cytokine known to influence macrophage activity. In vivo and in vitro models were used to assess TAFA4 expression, its regulatory effects on macrophage polarization, reactive oxygen species (ROS) production, inflammasome activation, and disc cell phenotype. Knockdown of TAFA4 was achieved via lentiviral transduction in rabbit discs and cell coculture models.
Results TAFA4 was upregulated in IVDD tissues and colocalized with GINIP+ neurons. Knockdown of TAFA4 in vivo exacerbated disc degeneration, increased M1 macrophage presence, elevated ROS levels, and activated the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. In vitro, GINIP+ neurons promoted macrophage M2 polarization and interleukin (IL)-10 production while suppressing tumor necrosis factor-α and IL-1β. These effects were reversed by TAFA4 knockdown. Moreover, TAFA4 attenuated ROS-dependent NLRP3 activation and preserved anabolic marker expression (ACAN [aggrecan], COL II [type II collagen], SOX9 [SRY-box transcription factor 9]), while reducing catabolic and hypertrophic-related markers (MMP13 [matrix metalloproteinase 13], ADAMTS5 [a disintegrin and metalloproteinase with thrombospondin motifs 5], COL X [collagen type X alpha 1 chain], RUNX2 [Runt-related transcription factor 2]) in nucleus pulposus cells.
Conclusion TAFA4 acts as a neuron-derived mediator of neuroimmune crosstalk in IVDD that modulates macrophage polarization and oxidative stress, thereby delaying disc degeneration. This neuron–immune axis represents a potential therapeutic target.
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This study aimed to elucidate the efficacy and safety of mesenchymal stromal cell (MSC) therapy for chronic discogenic low back pain (LBP). A systematic literature search was conducted on PubMed/Medline, Scopus, Cochrane, and ClinicalTrials.gov following PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-analysis) guidelines. Eligible studies included published and ongoing clinical trials assessing intradiscal MSC injections in patients with chronic discogenic LBP unresponsive to conservative treatment. Risk-of-bias (RoB) assessment was performed through MINORS (Methodological Index for Non-randomized Studies) and RoB 2 tools. Within- and between-group differences were expressed as means and 95% confidence intervals. Effect sizes were calculated through Cohen d and g. Data from 10 published clinical studies (n=736; 470 in treatment and 266 in control groups) revealed a mean age of 41.5 years and an average follow-up of 21.6 (range, 6–72) months. Various MSC sources were employed, including autologous and allogeneic bone marrow-derived MSCs and adipose-derived MSCs, with doses ranging from 6×10⁶ to over 50×10⁶ cells/disc. Visual analogue scale, Oswestry Disability Index, and quality-of-life questionnaires indicated modest improvements in pain, disability, and functional status. Additionally, magnetic resonance imaging assessments occasionally demonstrated increased disc hydration and stabilization or improvement of Pfirrmann grade. Data from 8 ongoing trials (n=498 participants; 276 treatment, 222 control) with follow-up periods ranging 6–24 months further corroborate the feasibility and safety of MSC-based interventions. MSC therapy is a biologically-driven approach for managing chronic discogenic LBP. While preliminary data support its potential to alleviate pain and improve disc integrity, further high-quality, standardized trials are necessary to optimize treatment protocols and confirm long-term clinical benefits.
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Objective Intervertebral disc degeneration (IDD), a prevalent musculoskeletal disorder, imposes significant socioeconomic and health care burdens worldwide. Despite its clinical impact, the molecular mechanisms driving IDD pathogenesis remain poorly characterized, and effective pharmacological interventions are urgently needed. This study elucidated the molecular mechanisms underlying IDD progression through multiomics integration.
Methods We performed systematic transcriptomic, proteomic, metabolomic, and lipidomic profiling of human degenerated nucleus pulposus (NP) tissues to identify disease-associated molecular signatures and therapeutic targets. Functional validation experiments were conducted using in vitro and ex vivo models of IDD.
Results Multiomics analyses revealed that lysosomal membrane lipid remodeling plays a critical role in IDD progression. Dysregulation of lysosomal phosphatidylcholine (PC) metabolism caused by reduced lysophosphatidylcholine acyltransferase 1 (LPCAT1) expression led to lysosomal membrane permeabilization (LMP) and subsequent ferroptosis in NP cells. Mechanistically, the LPCAT1-PC axis was identified as a key regulatory pathway: LPCAT1 downregulation in IDD correlated with decreased lysosomal PC content, impaired membrane stability and increased LMP-driven ferroptosis. Conversely, LPCAT1 overexpression increased the number of endoplasmic reticulum-lysosome contact sites, facilitating phospholipid transfer and lysosomal membrane repair. This restoration of lysosomal integrity effectively suppressed ferroptotic cell death.
Conclusion Our findings establish the LPCAT1-PC axis as a potential protective mechanism against IDD by maintaining lysosomal homeostasis through interorganellar lipid trafficking. This study provides the first evidence linking lysosomal lipid composition, membrane stability, and ferroptosis in NP cells, offering new therapeutic strategies targeting lipid metabolism and organelle crosstalk for IDD management.
Objective The precise mechanisms driving intervertebral disc degeneration (IVDD) development remain unclear, but evidence suggests a significant involvement of gut microbiota (GM) and blood metabolites. We aimed to investigate the causal relationships between GM, IVDD, and blood metabolites using Mendelian randomization (MR) analysis.
Methods We utilized the summary statistics of GM from the MiBioGen consortium, 1400 blood metabolites from the genome-wide association studies (GWAS) Catalog, and IVDD data from the FinnGen repository, which are sourced from the largest GWAS conducted to date. Employing bidirectional MR analyses, we investigated the causal relationships between GM and IVDD. Additionally, we conducted 2 mediation analyses, 2-step MR and multivariable MR (MVMR), to identify potential mediating metabolites.
Results Five bacterial genera were causally associated with IVDD, while IVDD did not show a significant causal effect on GM. In the 2-step MR analysis, Eubacteriumfissicatenagroup, RuminococcaceaeUCG003, Lachnoclostridium, and Marvinbryantia genera, along with metabolites X-24949, Pimeloylcarnitine/3-methyladipoylcarnitine (C7-DC), X-24456, histidine, 2-methylserine, Phosphocholine, and N-delta-acetylornithine, were all significantly associated with IVDD (all p < 0.05). MVMR analysis revealed that the associations between Eubacteriumfissicatenagroup genus and IVDD were mediated by X-24949 (8.1%, p = 0.024); Lachnoclostridium genus and IVDD were mediated by histidine (18.1%, p = 0.013); and RuminococcaceaeUCG003 genus and IVDD were mediated by C7-DC (-7.5%, p = 0.041).
Conclusion The present MR study offers evidence supporting the causal relationships between several specific GM taxa and IVDD, as well as identifying potential mediating metabolites.
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Degenerative cervical myelopathy (DCM) is the leading cause of spinal cord dysfunction in adults, representing substantial morbidity and significant financial and resource burdens. Typically, patients with progressive DCM will eventually receive surgical treatment. Nonetheless, despite advancements in pharmacotherapeutics, evidence for pharmacological therapy remains limited. Health professionals from various fields would find interest in pharmacological agents that could benefit patients with mild DCM or enhance surgical outcomes. This review aims to consolidate all clinical and experimental evidence on the pharmacological treatment of DCM. We conducted a comprehensive narrative review that presents all pharmacological agents that have been investigated for DCM treatment in both humans and animal models. Riluzole exhibits effectiveness solely in rat models, but not in treating mild DCM in humans. Cerebrolysin emerges as a potential neuroprotective agent for myelopathy in animals but had contradictory results in clinical trials. Limaprost alfadex demonstrates motor function improvement in animal models and exhibits promising outcomes in a small clinical trial. Glucocorticoids not only fail to provide clinical benefits but may also lead to adverse events. Cilostazol, anti-Fas ligand antibody, and Jingshu Keli display promise in animal studies, while erythropoietin, granulocyte colony-stimulating factor and limaprost alfadex exhibit potential in both animal and human research. Existing evidence mainly rests on weak clinical data and animal experimentation. Current pharmacological efforts target ion channels, stem cell differentiation, inflammatory, vascular, and apoptotic pathways. The inherent nature and pathogenesis of DCM offer substantial prospects for developing neurodegenerative or neuroprotective therapies capable of altering disease progression, potentially delaying surgical intervention, and optimizing outcomes for those undergoing surgical decompression.
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Neurospine 2024;21(1):204-211. Published online March 31, 2024
Objective To evaluate the global practice pattern of wound dressing use after lumbar fusion for degenerative conditions.
Methods A survey issued by AO Spine Knowledge Forums Deformity and Degenerative was sent out to AO Spine members. The type of postoperative dressing employed, timing of initial dressing removal, and type of subsequent dressing applied were investigated. Differences in the type of surgery and regional distribution of surgeons’ preferences were analyzed.
Results Right following surgery, 60.6% utilized a dry dressing, 23.2% a plastic occlusive dressing, 5.7% glue, 6% a combination of glue and polyester mesh, 2.6% a wound vacuum, and 1.2% other dressings. The initial dressing was removed on postoperative day 1 (11.6%), 2 (39.2%), 3 (20.3%), 4 (1.7%), 5 (4.3%), 6 (0.4%), 7 or later (12.5%), or depending on drain removal (9.9%). Following initial dressing removal, 75.9% applied a dry dressing, 17.7% a plastic occlusive dressing, and 1.3% glue, while 12.1% used no dressing. The use of no additional coverage after initial dressing removal was significantly associated with a later dressing change (p < 0.001). Significant differences emerged after comparing dressing management among different AO Spine regions (p < 0.001).
Conclusion Most spine surgeons utilized a dry or plastic occlusive dressing initially applied after surgery. The first dressing was more frequently changed during the first 3 postoperative days and replaced with the same type of dressing. While dressing policies tended not to vary according to the type of surgery, regional differences suggest that actual practice may be based on personal experience rather than available evidence.
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Objective To compare the long-term clinical and radiographic outcomes of transforaminal endoscopic lumbar discectomy (TELD) versus microdiscectomy (MD).
Methods The data of 154 patients with lumbar disc herniation (LDH) who underwent TELD (n = 89) or MD (n = 65) were retrospectively analyzed. The patients’ clinical outcomes were evaluated using visual analogue scales for leg and low back pain, the Japanese Orthopaedic Association (JOA) score, and the Oswestry Disability Index (ODI). The evolution of radiographic manifestations was observed during follow-up. Potential risk factors for a poor clinical outcome were investigated.
Results During a mean follow-up of 5.5 years (range, 5–7 years), the recurrence rate was 4.49% in the TELD group and 1.54% in the MD group. All scores significantly improved from preoperatively to postoperatively in both groups (p < 0.01). The improvement in the ODI and JOA scores was significantly greater in the TELD than MD group (p < 0.05). Forty-seven patients (52.8%) in the TELD group and 32 (49.2%) in the MD group had Modic changes before surgery, most of which showed no changes at the last follow-up. The degeneration grades of 292 discs (71.0%) were unchanged at the last follow-up, while 86 (20.9%) showed improvement, mostly at the upper adjacent segment. No significant difference was observed in the intervertebral height index or paraspinal muscle-disc ratio.
Conclusion Both TELD and MD provide generally satisfactory long-term clinical outcomes for patients with LDH. TELD can be used as a reliable alternative to MD with less surgical trauma. Modic type II changes, decreased preoperative intervertebral height, and a high body mass index are predictors of a poor prognosis.
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Objective The ‘‘disc degeneration precedes facet joint osteoarthritis’’ hypothesis and multidimensional analysis were actively discussed in lumbar spine. However, in cervical spine degeneration, the multifactorial analyzes of disc degeneration (DD), Modic changes (Mcs), facet degeneration, and endplate degeneration (ED) is still limited. In this cross-sectional study, we aimed to analyze the prevalence and interrelationship of cervical DD parameters.
Methods We retrospectively recruited 62 patients aged between 60 and 70 years. The disc height, segmental angle, ossified posterior longitudinal ligament (OPLL), ED, facet joint degeneration (FD), uncovertebral joint degeneration (UD), DD, spinal stenosis (SS), Mc, and cord signal change (CS) were evaluated using a previously well-known grading system.
Results The prevalence of cervical degenerative parameters were DD (grade 1, 1.2%; grade 2, 13.3%; grade 3, 54.8%; grade 4, 19.0%; grade 5, 11.7%), OPLL (26.2%), SS (grade 0, 7.7%; grade 1, 42.3%; grade 2, 26.2%; grade 3, 23.8%), UD (39.1%), ED (normal, 69.0%; focal defect, 9.7%; corner defect, 11.7%; erosion, 6.9%; sclerosis, 2.8%), and FD (normal, 48.8%; narrowing, 27.0%; hypertrophied, 24.2%). The interrelationship of degenerative parameters showed close relation between UD, SS, DD, OPLL, Mc. ED, and CS has partial relation with degenerative finding. FD only has relation with UD, and Mc.
Conclusion Our results may indicate that FD is a degeneration that occurs independently, rather than as a result of other degenerative factors.
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Neurospine 2020;17(1):190-203. Published online March 31, 2020
Objective To assess the impact of Modic changes (MC) on preoperative symptoms, and postoperative outcomes in anterior cervical discectomy and fusion (ACDF) patients.
Methods We performed a retrospective study of prospectively collected data of ACDF patients at a single institution. Preoperative magnetic resonance imagings were used to assess the presence of MC. MC were stratified by type and location, and compared to patients without MC. Associations with symptoms, patient-reported measures, and surgical outcomes were assessed.
Results A total of 861 patients were included, with 356 patients with MC (41.3%). MC more frequently occurred at C5–6 (15.1%), and type II was the most common type (61.2%). MC were associated with advanced age (p < 0.001), more levels fused (p < 0.001), a longer duration of symptoms, but not with specific symptoms. MC at C7–T1 resulted in higher postoperative disability (p < 0.001), but did not increase risk of adjacent segment degeneration or reoperation.
Conclusion This study is the first to systematically examine the impact of cervical MC, stratified by type and location, on outcomes in ACDF patients. Patients with MC were generally older, required larger fusions, and had longer duration of preoperative symptoms. While MC may not affect specific outcomes following ACDF, they may indicate a more debilitating preoperative state for patients.
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Methods Lumbar AF cells of 6- to 8-month-old female New Zealand white rabbits were harvested and exposed to combinations of inflammatory (interleukin-1β) and mechanical (6% or 18%) tensile stress using the Flexcell System. NPY concentrations were measured in the media via enzyme-linked immunosorbent assay. The presence of NPY receptor-type 1 (NPY-1R) in AF cells of rabbit intervertebral discs was also analyzed via immunohistochemistry and immunofluorescence.
Results Exposure to inflammatory stimuli showed a significant increase in the amount of NPY expression compared to control AF cells. Mechanical strain alone did not result in a significant difference in NPY expression. While combined inflammatory and mechanical stress did not demonstrate an increase in NPY expression at low (6%) levels of strain, at 18% strain, there was a large—though not statistically significant—increase in NPY expression under conditions of inflammatory stress. Lastly, immunofluorescence and immunohistochemistry of AF cells and tissue, respectively, demonstrated the presence of NPY-1R.
Conclusion These findings demonstrate that rabbit AF cells are capable of expressing NPY, and expression is enhanced in response to inflammatory and mechanical stress. Because both inflammatory and mechanical stress contribute to intervertebral disc degeneration (IDD), this observation raises the potential of a mechanistic link between low back pain and IDD.
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