Low back pain (LBP) is the leading cause of disability worldwide, interfering with an individual's quality of life and work performance. Understanding the degeneration mechanism of the intervertebral disc (IVD), one of the key triggers of LBP, is hence of great interest. Disc degeneration can be mimicked in animal studies using the injection of enzymatic digestion, needle puncture, stab injury, or mechanical over-loading [1]. However, the detailed response of the artificial degenerated disc using needle puncture under physiological dynamic loading in diurnal activities has not yet been analyzed using FE-models. To fill the gap in literature, this study investigates the role of needle puncture injury on the biomechanical response of IVD using a combination of Finite Element (FE) simulations and in-vitro lumbar spine sheep experiments.

16 lumbar motion segments (LMS) were dissected from juvenile sheep lumbar spines. The harvested LMSs were assigned equally to two groups (control group with no incision and an injured group punctured with a 16-gauge needle). All specimens were mounted in a homemade chamber filled with saline solution and underwent a stress-relaxation test using a mechanical testing apparatus (Zwick/Roell, Ulm-Germany). A validated inverse poroelastic FE methodology [2] in conjunction with in-vitro experiments were used to find the elastic modulus and permeability. Subsequently, specimen-specific FE models for the 16 discs were simulated based on daily dynamic physiological activity (i.e., 8h rest followed by a 16h loading phase under compressive loads of 350 N and 1000 N, respectively).

The results of the individual FE models were well fitted with the in-vitro stress-relaxation experiments, with an average error of 7.48 (±2.24)%. The results of the simulations demonstrated that the variation of axial displacement in the control discs was significantly higher than the injured ones (P=0.037). At the end of day, the intradiscal pressure (IDP) was slightly higher in the control group (P=0.061) although the maximum axial stress in the annulus fibrosus (AF) was significantly higher in the injured group (P=0.028). The total fluid loss after 24h was significantly higher in the control group (p<0.001).

We found that needle puncture can decrease the strain range, IDP, and fluid loss in an IVD, although it increases the axial stress. We therefore hypothesize that the fissures, clefts or tears produced by needle puncture alter the saturation time for disc deformation and pore pressure. The collapsed disc structure hinders the fluid flow capability; hence, the total fluid loss decreases for the injured discs, inhibiting the transportation of nutrients. Higher stresses in the AF were observed for the injured group in alignment with previous studies [3]. It is therefore concluded that the needle puncture injury methodology can be effectively used to mimic the degeneration mechanism in animal models. It is a convenient, reproducible, and cost-effective technique. Future work includes exploring degenerated disks induced by needle puncture to investigate potential regenerative therapeutics.