Study design: Mechanical and morphological studies on cadaveric spines.
Objective: To explain how spinal level and age influence disc degeneration arising from endplate fracture.
Summary of background data: Disc degeneration can be initiated by damage to a vertebral body endplate, but it is unclear why endplate lesions, and patterns of disc degeneration, vary so much with spinal level and age.
Methods: One hundred seventy-four cadaveric motion segments, from T7-T8 to L5-S1 and aged 19 to 96 years, were subjected to controlled compressive overload to damage a vertebral body. Stress profilometry was performed before and after damage to quantify changes in intradiscal pressure, and compressive stresses in the annulus. Eighty-six of the undamaged vertebral bodies were then sectioned in the midsagittal plane, and the thickness of the central bony endplate was measured from microradiographs. Regression analysis was used to compare the relative influences of spinal level, age, disc degeneration, and sex on results obtained.
Results: Compressive overload caused endplate fracture at an average force of 3.4 kN, and reduced motion segment height by an average 1.88 mm. Pressure loss in the adjacent nucleus pulposus decreased from 93% at T8-T9 to 38% at L4-L5 (R = 22%, P < 0.001), and increased with age (R = 19%, P < 0.001), especially in male specimens. Stress concentrations in the posterior annulus increased after endplate fracture, with the effect being greatest at upper spinal levels (R = 7%, P < 0.001). Endplate thickness increased by approximately 50% between T11 and L5 (R = 21%, P < 0.001).
Conclusion: Endplate fracture creates abnormal stress distributions in the adjacent intervertebral disc, increasing the risk of internal disruption and degeneration. Effects are greatly reduced in the lower lumbar spine, and in young specimens, primarily because of differences in nucleus volume, and materials properties, respectively. Disc degeneration between L4 and S1 may often be unrelated to endplate fracture.
Level of evidence: N/A.