ArticleBMC musculoskeletal disorders2025
Fatigue-induced biomechanical decoupling at L4-S1 discs: mechanism of disc degeneration in chronic low back pain.
Article in BMC musculoskeletal disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Reduced lumbar myofascial mobility in chronic low back pain quantified using MR elastography-based slip interface imaging.European radiology experimental · 2026Article
- Pathophysiology, diagnosis, and management of discogenic low back pain: a phenotype-driven precision framework for surgical and interventional decision-making.Frontiers in surgery · 2026Review
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8 authors.
Funding
Abstract
objectiveThis study aims to quantitatively compare segment-specific disc kinematics, height changes, and strain patterns in the lumbar spine between patients with chronic low back pain (CLBP) and asymptomatic controls during weight-bearing flexion-extension, before and after fatigue loading.
methodsA total of 29 patients with CLBP and 24 asymptomatic controls were included. All participants underwent dual fluoroscopic imaging system (DFIS) and computed tomography (CT) imaging. Weight-bearing kinematic sequences from maximum extension to approximately 45° flexion were captured pre- and post-fatigue. A validated geometric deformation model based on supine CT scans was used to quantify intervertebral kinematics from L1 to S1. Disc height variations and strain (axial and shear) were computed using computational morphometry and kinematic correspondence tracking. Statistical analyses included paired and independent t-tests for within- and between-group comparisons, with significance set at p < 0.05.
resultsComputational morphometry revealed distinct degenerative features associated with CLBP. Compared with controls, L4/5 discs in CLBP patients showed significantly reduced baseline height (p < 0.05), which may indicate a predisposition to early degeneration. At L5/S1, disc height was significantly reduced after fatigue loading across all postures in the CLBP group (p < 0.01), a change not observed in controls. Strain analysis demonstrated segment-dependent alterations in mechanical behavior. During flexion, both groups exhibited posterior tensile and anterior compressive strains from L4 to S1. However, after fatigue, CLBP patients developed a distinct strain pattern at L5/S1, characterized by high compressive strain and reduced shear strain. More broadly, fatigue loading in CLBP patients led to impaired shear strain dissipation and accumulation of compressive strain within the L4–S1 segments. In contrast, the upper lumbar segments (L1–L3) in both groups maintained physiological strain gradients that were unaffected by fatigue.
conclusionsThis study provides in vivo evidence of fatigue-induced biomechanical alterations in the L4–S1 discs of CLBP patients, marked by increased compressive strain and reduced capacity for shear strain redistribution. The preserved biomechanical behavior in the upper lumbar segments underscores the particular vulnerability of the lumbosacral junction to mechanical deficits. These findings support the value of segment-specific biomechanical assessment for identifying early degenerative changes and inform the development of targeted load-management strategies in CLBP. However, further research is needed to account for potential confounding variables and to validate these observations in larger cohorts.
trial registrationChinese Clinical Trial Registry Registration number ChiCTR2000036039. Registered 21 August 2020.
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