Abstract

The annulus fibrosus (AF), a permeable, hydrated, and fiber-reinforced soft tissue, exhibits complex responses influenced by fluid pressure, osmotic pressure, and structural mechanics. Existing models struggle to comprehensively represent these intricate interactions and the heterogeneous solid responses within the AF. Additionally, the mechanisms driving differential damage accumulation between non-degenerative and degenerative intervertebral discs remain poorly understood. In this study, we introduce a biphasic-swelling damage model for the AF. We conceptually develop and rigorously validate this model through tissue-level tests employing various loading modes, consistently aligning model predictions with experimental data. Leveraging parametric geometric algorithms and custom Python scripts, we construct models simulating both non-degenerative and degenerative discs. Following calibration, we subject these models to viscous loading protocols. Our findings reveal the posterior AF’s susceptibility to damage, contingent upon loading rate and water content. We elucidate the underlying mechanisms by examining the temporal evolution of fluid pressure, osmotic pressure, and the regionally dependent fiber network. This research presents a highly accurate model of the AF, providing valuable insights into disc damage. Future research endeavors should expand this model to incorporate ionic transport and diffusion, enabling a more profound exploration of intervertebral disc mechanobiology. This comprehensive model contributes to a better understanding of AF behavior and may inform therapeutic strategies for disc-related pathologies. Statement of significanceThis research presents a comprehensive model of the annulus fibrosus (AF), a crucial component of the intervertebral disc that provides structural support and resists deformation. The study introduces a biphasic-swelling damage model for the AF and validates it through tissue-level tests. The model accounts for fluid pressure, osmotic pressure, and matrix mechanics, providing a more accurate representation of the AF’s behavior. The study also investigates the differential damage accumulation between non-degenerative and degenerative discs, shedding light on the mechanisms driving disc degeneration. The findings have significant implications for medical treatments and interventions, as they highlight the posterior AF’s susceptibility to damage. This research is of great interest to readers interested in biomechanics, tissue engineering, and medical treatments for disc degeneration.

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