Abstract
Introduction
The “weak link” in the thoracolumbar spine is the vertebral body endplate, which is easily damaged in compression. Vertebral endplate fracture can decompress the adjacent intervertebral disk and allow the annulus to collapse inwards.1 This can lead to disk degeneration in animal models2 and in patients.3 However, population MRI studies indicate that endplate damage is strongly associated with adjacent disk degeneration only in the upper lumbar spine.4 We hypothesize that lower lumbar disks are less affected by endplate fracture.
Materials and Methods
Mechanical experiments were performed on cadaveric “motion segments” comprising two vertebrae and the intervening disk and ligaments. Each specimen was compressed to failure, until the elastic limit was just exceeded, and measurements of intradiscal (nucleus) pressure were compared before and after failure, at a reference load of 1 kN. Pressure measurements were made with a strain-gauged pressure transducer side-mounted near the tip of a 1.3-mm-diameter catheter. Multiple linear regression (SPSS v16) was used to analyze factors that influence the fall in nucleus pressure.
Results
A total of 143 specimens aged 19 to 96 years (mean 67 years) were tested, from all spinal levels between T7-8 and L5-S1. Radiographs confirmed the endplate as the site of compressive failure, and damage caused an average specimen height loss of 1.9 mm (STD 0.9 mm). The resulting fall in nucleus pressure averaged 59% (STD 37%), and increased with age and (pre-existing) disk degeneration (p < 0.001). Apart from specimen height loss, the greatest determinant of nucleus decompression was spinal level, with decompression averaging 70 to 90% in the lower thoracic spine, and falling linearly from T11-12 to just 6% at L5-S1. Spinal level explained 28% of the variance in nucleus decompression (p < 0.001).
Conclusion
The relatively small effects observed in lower lumbar disks may be due to the relatively large height and anteroposterior diameter of the nucleus at L4-5 and L5-S1: a larger nucleus volume would lead to a smaller drop in pressure for the same amount of endplate damage. Results suggest that compressive overload may well initiate disk degeneration in the upper lumbar and thoracic spine, explaining the strong relationship between disk degeneration and Schmorl's nodes at these levels.4 At L4-5 and L5-S1, however, another mechanism is likely to be important: these lower lumbar disks are particularly susceptible to radial fissure formation, leading to disk prolapse, in response to high loading in bending.1 The concept of two distinct mechanisms of disc degeneration (‘annulus-driven’ in the lower lumbar spine, and “endplate-driven” at higher spinal levels) may explain why the genetic influence in disk degeneration varies with spinal level.5
Yes
None declared
Adams MA, Freeman BJ, Morrison HP, Nelson IW, Dolan P. Mechanical initiation of intervertebral disc degeneration. Spine 2000;25(13):1625–1636
Holm S, Holm AK, Ekstrom L, Karladani A, Hansson T. Experimental disc degeneration due to endplate injury. Journal of Spinal Disorder and Techniques 2004;17(1):64–71
Kerttula LI, Serlo WS, Tervonen OA, Paakko EL, Vanharanta HV. Post-traumatic findings of the spine after earlier vertebral fracture in young patients: clinical and MRI study. Spine 2000;25(9):1104–1108
Mok FP, Samartzis D, Karppinen J, Luk KD, Fong DY, Cheung KM. ISSLS prize winner: Prevalence, determinants, and association of Schmorl nodes of the lumbar spine with disc degeneration: a population-based study of 2449 individuals. Spine (Phila Pa 1976) 2010;35(21):1944–1952
Battie MC, Videman T, Levalahti E, Gill K, Kaprio J. Genetic and environmental effects on disc degeneration by phenotype and spinal level: a multivariate twin study. Spine 2008;33(25):2801–2808