ArticleJOR spine2026
Combined Flexion, Torsion and Compression Drive Distinct Intervertebral Disc Failure Mechanisms Under Asymmetric, High-Cycle Loading.
Article in JOR spine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Recent advancements in next-generation bioreactors have substantially improved the simulation of complex, detrimental spinal mechanics in ex vivo intervertebral disc models. This study investigated intervertebral disc responses to combined flexion, torsion, and static compression. A range of loading frequencies, magnitudes, and patterns was applied to identify conditions that contribute to disc degeneration under complex motion. Methods: Twelve bovine coccygeal intervertebral discs (mean age 9 months) were subjected to three distinct loading regimes, with four samples per condition. Static compression of 0.1 MPa was combined with: (1) symmetrical 3° flexion/extension and 2° torsion, (2) symmetrical 6° flexion/extension and 4° torsion, and (3) asymmetrical 6° flexion and 4° torsion. Loading frequencies and durations ranged from 0.2 Hz for 1 h in symmetrical loading to 1 Hz for 2 h in asymmetrical loading over a 14-day period. Structural integrity, cell viability, tissue composition, and molecular responses were evaluated using histology, biochemical assays, and gene expression analysis. Results: Lower-cycle symmetrical flexion/extension and torsion, regardless of magnitude, preserved disc structure and maintained a high cell viability (88% ± 14%) across all disc regions. Higher cycle numbers and asymmetrical loading induced significant fissures in the outer annulus fibrosus (AF) on the tensed side ( Conclusions: Under conditions of asymmetrical and more frequent loading, complex motion involving flexion, torsion, and compression led to structural damage in the outer disc regions and promoted cell death in inner regions. These region-specific responses suggest the independent development of distinct failure mechanisms contributing to disc degeneration. They also underscore the importance of developing targeted strategies that address both structural integrity and cellular resilience in degeneration models and therapeutic interventions.
Identifiers
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Registered trials
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