Vertebral end plates (EP) are essential for disc homeostasis due to their dual role of structural load distributor and a nutritional interface. Focal EP defects are frequently observed clinically, but their true biomechanical significance in vivo is unknown. Finite Element (FE) analysis offers a unique opportunity to simulate specific anatomical changes and can quantify the consequences of the mechanical disruption. We employed a validated FE Model of L4-L5 functional unit and investigated the effects of physiological compression and pure moments on models simulating: (1) Healthy discs with intact EP, (2) Four EP defect models, and (3) Graded anatomical EP damage based on Integrated Total Endplate Score (I-TEPS). Stress distribution on cartilage end plate (CEP), bony end plate (BEP), annulus fibrosus (AF), nucleus pulposus (NP), and subchondral bone was documented. In the intact healthy model, stress was uniformly distributed without focal concentrations. In contrast, all EP defect models demonstrated significant, non-linear stress elevation across the motion segment. Incremental analysis based on I-TEPS revealed a ‘mechanical tipping point’ phenomenon: stresses remained relatively stable until score three but increased sharply once the score reached four, coinciding with the onset of BEP involvement. Focal EP defects, irrespective of their location, cause stress extensions beyond the defect zone, causing cascading mechanical disruption of the disc environment. Combined CEP and BEP defects (I-TEPS ≥ 4) represent synergistic mechanical failure, characterized by abnormal NP pressure, annular tension, and subchondral bone stress. These findings demonstrate that EP integrity is one of the primary determinants of segmental spine stability.
The management of upper cervical spine (UCS) fractures is unclear concerning the role of fusion versus non-fusion fixation and the need for implant removal following fracture healing. This international AO Spine expert survey (Level IV study) evaluated the current trends, and practice preferences among experienced surgeons in the management of UCS fractures. A structured questionnaire was answered by AO Spine Knowledge Forum Trauma and Infection (KF T I) members (n = 24). The survey collected data regarding demographics, classification use, fixation vs. fusion preferences, and implant removal practices for UCS fractures (C1, C2 odontoid, and Hangman’s fractures). Descriptive statistics were analysed. Majority were from North America and Europe (54
Study DesignRetrospective.ObjectiveTo evaluate the association between mechanical instability and neurological deficit in spinal tuberculosis (TB), and compare it against previously recognized radiological parameters.MethodsClinical and radiological data of patients with active thoracic spinal TB were evaluated. Instability was assessed using the Spinal Tuberculosis Instability Scoring System (STISS) by Rajasekaran et al. Neurological status and radiological parameters were analysed to identify the factors associated with neurological deficit.ResultsA total of 122 patients were included. The average age was 51 ± 18 years, and 54.9% were males. 40 (32.8%) patients had neurological deficits at presentation. Based on the STISS, 71 (58%) patients were categorised as stable, 10 (8.2%) as potentially unstable, and 41 (34%) as definitely unstable. On MRI, cord signal changes and epidural compression were noted in 18% and 64% of the patients, respectively. Definite instability was found to be the strongest independent association of neurological deficit (OR 9.77, 95% CI 2.85-38.9, P < 0.001), followed by greater canal encroachment area (CEA) (OR 1.08, 95% CI 1.03-1.13, P = 0.002). In a stable spine with epidural compression, the predicted probability of neurological deficit is 27%. In an unstable spine, the likelihood of neurological deficit is 50% even without epidural compression, and highest (63%) when instability was associated with epidural compression.ConclusionMechanical instability is the strongest independent association of neurological deficit in spinal TB, even in the absence of epidural compression. Incorporating the Spine Instability Scoring System into routine clinical evaluation improves risk stratification, enables timely decision-making, and can prevent irreversible neurological deficits.
BACKGROUND:Aging and degeneration are biologically distinct processes in intervertebral discs, but are difficult to differentiate radiologically. Metabolomics reflects real-time biochemical activity, and age-stratified metabolomic profiling of normal and degenerated discs may identify preclinical degeneration and reveal molecular signatures distinguishing normal aging from degeneration. PURPOSE:To characterize the metabolomic changes in the MRI-normal healthy lumbar intervertebral disc and compare them with degenerated discs to identify metabolomic signatures that differentiate normal aging from degeneration. STUDY DESIGN AND SETTING:Comparative metabolomics study using human nucleus pulposus tissue from organ donors and surgical specimens, conducted at a tertiary spine care center and an affiliated research laboratory. PATIENT SAMPLE:Nucleus pulposus tissue from 21 healthy organ donors (Pfirrmann grade I) was stratified by age: young (20-30 years), middle-aged (31-50 years), and old (>50 years), and compared with 40 degenerated discs (grades III-V) from surgical specimens. OUTCOME MEASURES:Primary outcome measures included differential metabolite abundance (metabolites with [VIP] Variable Importance in Projection scores>1), pathway enrichment profiles, and identification of age-specific versus degeneration-specific metabolic signatures. METHODS:Untargeted ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) was performed in both positive and negative ionization modes. Metabolites were identified using Compound Discoverer v3.7, with reference to Human Metabolome Database (HMDB) and Kyoto Genome Encyclopedia (KEGG). Statistical and pathway enrichment analyses were performed using MetaboAnalyst 6.0. RESULTS:Untargeted UHPLC-MS/MS analysis revealed 831 significant metabolites (VIP>1), contributing to group separation in the partial least squares discriminant analysis (PLS-DA) model. Lipids and lipid-like molecules, especially sphingolipids, fatty acyls, and steroids, constituted 39%. MRI normal organ donor discs in progressive age periods demonstrated 4 distinct metabolic trends: (i) progressive decline of antioxidants (ubiquinone, glutathione, N-acetyl seretonin); (ii) increased oxidative/inflammatory markers (4-HNE, prostaglandin E₂ ethanolamide, N1-acetylspermidine); (iii) transient midlife antioxidant elevation; (4OH benozoic acid, 4OH phenylpyruvic acid); (iv) partial recovery in older discs (Hypoxanthine, Paraxanthine, CerP(d18:1/18:0)). In old-aged discs, accumulation of sphingolipids (sphingosine, ceramides) and redox drift indicated enhanced senescence and energy imbalance. Degenerated discs exhibited a different profile, characterized by the suppression of bioactive lipids, particularly resolvins, PGE2, and SOFAs, accompanied by disrupted sphingolipid metabolism and reduced redox capacity. CONCLUSION:Distinct metabolomic signatures differentiate physiological aging from disc degeneration. Degeneration is characterized by disrupted sphingolipid and redox homeostasis, suggesting a pathobiological process beyond normal senescence. These data provide a metabolic framework for future translational studies to identify disc degeneration even at the preclinical stage and in therapeutic stratification.
