Centre for Comparative and Clinical Anatomy, University of Bristol, Bristol, UK.
Spine (Phila Pa 1976). 2013 Aug 1;38(17):1473-81. doi: 10.1097/BRS.0b013e318290f3cc.
Mechanical and morphological studies on cadaveric spines.
To explain how spinal level and age influence disc degeneration arising from endplate fracture.
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.
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.
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).
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.
N/A.
对尸体脊柱进行力学和形态学研究。
解释脊柱水平和年龄如何影响终板骨折引起的椎间盘退变。
椎间盘退变可由椎体终板损伤引起,但尚不清楚为什么终板病变和椎间盘退变模式随脊柱水平和年龄变化如此之大。
对 174 个尸体运动节段(T7-T8 至 L5-S1)进行了受控压缩过载,以损伤椎体。在损伤前后进行了应力轮廓测量,以量化椎间盘内压力和环内压缩应力的变化。然后将 86 个未损伤的椎体在正中矢状面切开,并从微射线照片测量中央骨性终板的厚度。回归分析用于比较脊柱水平、年龄、椎间盘退变和性别对获得结果的相对影响。
压缩过载导致终板骨折的平均力为 3.4 kN,使运动节段高度平均降低 1.88 mm。相邻髓核内的压力损失从 T8-T9 的 93%降低到 L4-L5 的 38%(R = 22%,P < 0.001),并随年龄增加(R = 19%,P < 0.001),尤其是在男性标本中。终板骨折后后环内的应力集中增加,在上段脊柱水平的效果最大(R = 7%,P < 0.001)。终板厚度在 T11 和 L5 之间增加了约 50%(R = 21%,P < 0.001)。
终板骨折在相邻椎间盘中产生异常的应力分布,增加了内部破裂和退变的风险。在下腰椎和年轻标本中,这种影响大大降低,主要是由于核体积和材料特性的差异所致。L4 和 S1 之间的椎间盘退变可能常常与终板骨折无关。
N/A。