Microstructural investigation of compression-induced disruption of the flexed lumbar disc.
To provide a microstructural analysis of the mechanisms of annular wall failure in healthy discs subjected to flexion and an elevated rate of compression.
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.
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.
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.
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
The relationship between flexion, compression rate, and traumatic disc failure was investigated. High physiological flexion combined with an elevated rate of compression produced herniations that were initiated by subtle tearing of the mid-then-outer annular region where the fiber strains are likely to be highest due to endplate curvature.
*Department of Chemical and Materials Engineering, Experimental Tissue Mechanics Laboratory, University of Auckland, New Zealand; and
†Department of Orthopaedic Surgery, Auckland City Hospital, New Zealand.
Address correspondence and reprint requests to Neil D. Broom, PhD, Department of Chemical and Materials Engineering, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand; E-mail: firstname.lastname@example.org
Acknowledgment date: October 11, 2013. Revision date: January 20, 2014. Acceptance date: January 25, 2014.
The manuscript submitted does not contain information about medical device(s)/drug(s).
AO Foundation (project S-12-24B) grant funds were received in support of this work.
Relevant financial activities outside the submitted work: consultancy, grants, patents, royalties.