How healthy discs herniate: a biomechanical and microstructural study investigating the combined effects of compression rate and flexion.

STUDY DESIGN: Microstructural investigation of compression-induced disruption of the flexed lumbar disc.

OBJECTIVE: To provide a microstructural analysis of the mechanisms of annular wall failure in healthy discs subjected to flexion and an elevated rate of compression.

SUMMARY OF BACKGROUND DATA: At the level of the motion segment failure of the disc in compression has been extensively studied. However, at the microstructural level the exact mechanisms of disc failure are still poorly understood, especially in relation to loading posture and rate.

METHODS: Seventy-two healthy mature ovine lumbar motion segments were compressed to failure in either a neutral posture or in high physiological flexion (10°) at a displacement rate of either 2 mm/min (low) or 40 mm/min (high). Testing at the high rate was terminated at stages ranging from initial wall tearing through to facet fracture so as to capture the evolution of failure up to full herniation. The damaged discs were then analyzed microstructurally.

RESULTS: Approximately, 50% of the motion segments compressed in flexion at the high rate experienced annulus or annulus-endplate junction failure, the remainder failed via endplate fracture with no detectable wall damage. The average load to induce disc failure in flexion was 18% lower (P < 0.05) than that required to induce endplate fracture. Microstructural analysis indicated that wall rupture occurred first in the posterior mid-then-outer annulus.

CONCLUSION: Disc wall failure in healthy motion segments requires both flexion and an elevated rate of compression. Damage is initiated in the mid-then-outer annular fibers, this a likely consequence of the higher strain burden in these same fibers arising from endplate curvature. Given the similarity in geometry between ovine and human endplates, it is proposed that comparable mechanisms of damage initiation and herniation occur in human lumbar discs.

LEVEL OF EVIDENCE: N/A.