“Surprise” Loading in Flexion Increases the Risk of Disc Herniation Due to Annulus-Endplate Junction Failure: A Mechanical and Microstructural Investigation

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Study Design.

Microstructural investigation of compression-induced herniation of the flexed lumbar disc.


To provide a microstructural analysis of the mechanisms of annular wall failure in healthy discs subjected to flexion and a rate of compression comparable with the maximum rate at which the muscles of the spinal column can generate a force.

Summary of Background Data.

Clinical evidence indicates the involvement of the endplate in herniation. It is known that both an elevated rate of compression and a flexed posture are necessary to cause disc failure either within the midspan of the annulus or at the annular-endplate interface. However, the question of what effect a sudden or “surprise” loading might have on the mode of failure is, as yet, unanswered.


Twenty-four healthy mature ovine lumbar motion segments were compressed to failure in high physiological flexion (10º). This occurred over approximately 5 mm of crosshead displacement in 0.75 seconds that resulted in a displacement rate of 400 mm/min (defined as a “surprise” rate) and was intended to simulate the maximum rate at which the muscles of the spinal column can generate a force. The damaged discs were then analyzed microstructurally.


Fifty-eight percent of discs suffered annular-endplate junction rupture, 25% suffered midspan annular rupture, and the balance of 17% endplate fracture. Microstructural analysis indicated that annular rupture initiated at the endplate apical ridge in the mid-to-outer region of the annulus in both annular-endplate and midspan annulus rupture.


Motion segments subjected to a “surprise” loading rate are likely to fail via some form of annular rupture. Failure under such sudden loading occurs mostly via rupture of the annular-endplate junction and is thought to arise from a rate-induced mechanostructural imbalance between the annulus and the endplate.


Level of Evidence: N/A

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