椎体前缘楔形畸形的发病机制:一个两阶段过程?
Pathogenesis of Vertebral Anterior Wedge Deformity: A 2-Stage Process?
作者信息
Landham Priyan R, Gilbert Samuel J, Baker-Rand Holly L A, Pollintine Phillip, Robson Brown Katharine A, Adams Michael A, Dolan Patricia
机构信息
*Centre for Comparative and Clinical Anatomy, University of Bristol, Bristol, England; and †School of Archaeology and Anthropology, University of Bristol, Bristol, England.
出版信息
Spine (Phila Pa 1976). 2015 Jun 15;40(12):902-8. doi: 10.1097/BRS.0000000000000905.
STUDY DESIGN
Biomechanical and radiographical study on cadaveric spines.
OBJECTIVE
To explain the pathogenesis of vertebral "anterior wedge" deformity, which causes senile kyphosis.
SUMMARY OF BACKGROUND DATA
This deformity arises with minimal trauma and is difficult to reproduce in cadaveric spines. We hypothesize that wedging is created by a 2-stage process. First, excessive loading damages a vertebral endplate and decompresses the adjacent intervertebral disc. This alters load sharing between the vertebral body cortex and trabeculae so that subsequent cyclic loading causes progressive collapse of the unsupported anterior cortex.
METHODS
Thirty-four cadaveric thoracolumbar "motion segments," aged 70 to 98 years, were positioned in flexion and overloaded in compression. Physiologically reasonable cyclic compressive loading was then applied to each flexed specimen, at progressively higher loads, for up to 2 hours. Before and after initial overload and again after cyclic loading, the distribution of loading on the vertebra was assessed from measurements of compressive stress within the adjacent disc. These "stress profiles" were repeated in the neutral, flexed, and extended postures. Progressive vertebral body deformity was assessed radiographically.
RESULTS
Compressive overload induced endplate fracture at an average force of 2.31 kN. There was minimal anterior wedging, but pressure in the adjacent disc nucleus (in flexion) fell by an average of 55% and neural arch load bearing increased by 166%. Subsequent cyclic loading exaggerated these changes and concentrated compressive stress within the anterior annulus. After both stages, height of the anterior and posterior vertebral cortexes was reduced by 32% and 12%, respectively, so that anterior wedging of the vertebral body increased from 5.0° to 11.4° on average. All changes were highly significant (P < 0.001).
CONCLUSION
Anterior wedge deformities can be created consistently by a 2-stage process involving initial endplate damage, followed by progressive collapse of the anterior cortex. Detecting initial endplate damage may be important to minimize vertebral deformity in patients with osteoporosis.
LEVEL OF EVIDENCE
N/A.
研究设计
对尸体脊柱进行生物力学和影像学研究。
目的
解释导致老年驼背的椎体“前楔形”畸形的发病机制。
背景资料总结
这种畸形在受到极小创伤时就会出现,且难以在尸体脊柱上重现。我们假设楔形是由一个两阶段过程造成的。首先,过度负荷会损伤椎体终板并使相邻椎间盘减压。这会改变椎体皮质和小梁之间的负荷分担,从而使随后的循环负荷导致未支撑的前皮质逐渐塌陷。
方法
34个年龄在70至98岁的尸体胸腰段“运动节段”被置于屈曲位并进行压缩过载。然后对每个屈曲的标本施加生理上合理的循环压缩负荷,负荷逐渐增加,持续2小时。在初始过载前后以及循环负荷后,通过测量相邻椎间盘内的压缩应力来评估椎体上的负荷分布。这些“应力分布”在中立位、屈曲位和伸展位重复进行。通过影像学评估椎体的渐进性畸形。
结果
压缩过载平均在2.31 kN的力作用下导致终板骨折。前楔形畸形最小,但相邻椎间盘髓核内的压力(在屈曲位)平均下降了55%,神经弓的负荷增加了166%。随后的循环负荷加剧了这些变化,并使前环内的压缩应力集中。在两个阶段之后,椎体前皮质和后皮质的高度分别降低了32%和12%,椎体的前楔形平均从5.0°增加到11.4°。所有变化均具有高度显著性(P < 0.001)。
结论
前楔形畸形可通过一个两阶段过程持续产生,该过程包括初始终板损伤,随后前皮质逐渐塌陷。检测初始终板损伤对于将骨质疏松症患者的椎体畸形降至最低可能很重要。
证据水平
无。