The annual prevalence of intervertebral disc (IVD) degeneration is 27.3%[1]. During IVD degeneration, the nucleus pulposus (NP) undergoes changes, including the transformation of notochordal cells into chondrocyte-like cells, leading to reduced collagen II and proteoglycan[2] production. This results in dehydration, altering pressurization and load distribution in the NP[3]. NP allograft can preserve disc structure[4], however its mechanical properties remain underexplored[5]. This study examines the viscoelastic properties and dynamic loading response of IVDs supplemented with NP allograft.
2.1. Stress relaxation study
Human IVD was punctured with an 8mm biopsy punch to simulate tissue loss and degeneration. Twelve points across the AF, inner AF, and NP were subjected to a 3-step stress relaxation protocol using the Mach-1 mechanical tester (MA001). After supplementing the hole with NP allograft and incubating overnight, the same loading regimen was applied the next day. Stress relaxation curves were analyzed with Mach-1 analysis software (MA726) to compare peak forces and aggregate modulus before and after NP allograft supplementation.
2.2. Dynamic mechanical loading study
Three IVDs with similar geometry underwent 10 cycles of dynamic loading (5% strain at 1 Hz). The top endplate was drilled, NP removed, and the loading regimen repeated. NP allograft was then placed to supplement the IVD, and dynamic loading was applied again (Figure 2).
3.1. Stress relaxation study
The stress relaxation test performed on all 12 points of the degenerated IVD, before and after NP allograft supplementation, showed an increase in peak force and aggregate modulus at all points.
3.2. Dynamic mechanical loading study
Figure 4 demonstrates that creating a puncture in the IVD significantly reduces the peak force of dynamic loading in each sample. Peak force is significantly restored by adding the NP allograft to the IVD.
The results of this study indicate that NP allograft supplementation in degenerated IVDs enhances mechanical properties in non-defected regions (Figure 3), while at the same time restores the mechanical strength impacted by tissue loss and desiccation (Figure 4).
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