Tzermiadianos Michael N, Renner Susan M, Phillips Frank M, Hadjipavlou Alexander G, Zindrick Michael R, Havey Robert M, Voronov Michael, Patwardhan Avinash G
Department of Orthopaedic Surgery and Rehabilitation, Loyola University Medical Center, Maywood, IL 60153, USA.
Eur Spine J. 2008 Nov;17(11):1522-30. doi: 10.1007/s00586-008-0775-x. Epub 2008 Sep 16.
This study investigated the effect of endplate deformity after an osteoporotic vertebral fracture in increasing the risk for adjacent vertebral fractures. Eight human lower thoracic or thoracolumbar specimens, each consisting of five vertebrae were used. To selectively fracture one of the endplates of the middle VB of each specimen a void was created under the target endplate and the specimen was flexed and compressed until failure. The fractured vertebra was subjected to spinal extension under 150 N preload that restored the anterior wall height and vertebral kyphosis, while the fractured endplate remained significantly depressed. The VB was filled with cement to stabilize the fracture, after complete evacuation of its trabecular content to ensure similar cement distribution under both the endplates. Specimens were tested in flexion-extension under 400 N preload while pressure in the discs and strain at the anterior wall of the adjacent vertebrae were recorded. Disc pressure in the intact specimens increased during flexion by 26 +/- 14%. After cementation, disc pressure increased during flexion by 15 +/- 11% in the discs with un-fractured endplates, while decreased by 19 +/- 26.7% in the discs with the fractured endplates. During flexion, the compressive strain at the anterior wall of the vertebra next to the fractured endplate increased by 94 +/- 23% compared to intact status (p < 0.05), while it did not significantly change at the vertebra next to the un-fractured endplate (18.2 +/- 7.1%, p > 0.05). Subsequent flexion with compression to failure resulted in adjacent fracture close to the fractured endplate in six specimens and in a non-adjacent fracture in one specimen, while one specimen had no adjacent fractures. Depression of the fractured endplate alters the pressure profile of the damaged disc resulting in increased compressive loading of the anterior wall of adjacent vertebra that predisposes it to wedge fracture. This data suggests that correction of endplate deformity may play a role in reducing the risk of adjacent fractures.
本研究调查了骨质疏松性椎体骨折后终板畸形对增加相邻椎体骨折风险的影响。使用了8个人类下胸椎或胸腰段标本,每个标本由5个椎体组成。为了选择性地骨折每个标本中间椎体的一个终板,在目标终板下方创建一个空隙,然后将标本弯曲并压缩直至破坏。对骨折椎体施加150 N预载荷下的脊柱伸展,以恢复前壁高度和椎体后凸,而骨折终板仍明显凹陷。在完全清除其小梁内容物后,向椎体内注入骨水泥以稳定骨折,以确保两个终板下骨水泥分布相似。在400 N预载荷下对标本进行屈伸测试,同时记录椎间盘压力和相邻椎体前壁的应变。完整标本在屈曲过程中椎间盘压力增加26±14%。骨水泥注入后,未骨折终板的椎间盘在屈曲过程中压力增加15±11%,而骨折终板的椎间盘压力下降19±26.7%。在屈曲过程中,与完整状态相比,骨折终板相邻椎体前壁的压缩应变增加了94±23%(p<0.05),而在未骨折终板相邻椎体处未显著变化(18.2±7.1%,p>0.05)。随后的屈曲加压缩至破坏导致6个标本在靠近骨折终板处发生相邻骨折,1个标本发生非相邻骨折,而1个标本未发生相邻骨折。骨折终板的凹陷改变了受损椎间盘的压力分布,导致相邻椎体前壁的压缩负荷增加,使其易发生楔形骨折倾向。该数据表明,纠正终板畸形可能在降低相邻骨折风险中起作用。