Kayanja Mark Makumbi, Evans Korboi, Milks Ryan, Lieberman Isador Harry
Spine Research Laboratory, Spine Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Spine (Phila Pa 1976). 2006 Oct 1;31(21):E790-7. doi: 10.1097/01.brs.0000238690.09903.4c.
In vitro biomechanics.
To determine if osteoporotic vertebral compression fracture (VCF) augmentation increases adjacent level load transfer.
Osteoporotic VCF subsequent to augmentation may result from disease progression or increased adjacent level load transfer, or both.
There were 11 T3-T7 and 10 T8-T12 divided by lumbar bone mineral density into a normal group (No. 1; n = 11) and an osteoporotic group (No. 2; n = 10). Strain and centrum stress were measured on T4 and T6 (T3-T7), and T9 and T11 (T8-T12) during tests in the intact state, following a centrum defect, during and after an augmented VCF at T5 or T10, and during a subsequent VCF. Stiffness and strength were compared: between groups 1 and 2; among intact, defect, and augmented VCF states; and between the initial and subsequent VCF.
Group 1 was stiffer than 2 in compression (P = 0.01) and flexion (P = 0.07), with no difference in adjacent level load transfer (strain P = 0.72, centrum stress P = 0.36) or strength (P = 0.07). The centrum defect reduced compressive stiffness from the intact (P = 0.001), which was partially restored following VCF augmentation (P = 0.006). There were no differences in flexion stiffness (P > or = 0.14). Adjacent level load transfer in flexion exceeded that in compression (strain P = 0.001, centrum stress P = 0.19). Initial and subsequent VCF occurred at similar forces (P = 0.26) with higher adjacent level load at subsequent (strain and centrum stress P = 0.04).
Augmentation of multilevel spinal segments with VCF produced by combined compression, flexion, and a centrum defect normalizes adjacent level load transfer at physiologic loads. In both normal and osteoporotic spinal segments, as loads approach those of the initial VCF, protection from augmentation is lost, and subsequent adjacent level VCFs occur from extreme loading, and not the augmentation process.
体外生物力学研究。
确定骨质疏松性椎体压缩骨折（VCF）强化术是否会增加相邻节段的负荷传递。
VCF强化术后的骨质疏松性VCF可能是疾病进展或相邻节段负荷传递增加，或两者共同作用的结果。
将11个T3 - T7节段和10个T8 - T12节段根据腰椎骨密度分为正常组（第1组；n = 11）和骨质疏松组（第2组；n = 10）。在完整状态、椎体缺损后、T5或T10椎体压缩骨折强化术期间及术后以及随后发生椎体压缩骨折期间，测量T4和T6（T3 - T7）以及T9和T11（T8 - T12）的应变和椎体应力。比较了刚度和强度：第1组和第2组之间；完整、缺损和强化椎体压缩骨折状态之间；以及初次和随后的椎体压缩骨折之间。
第1组在压缩（P = 0.01）和屈曲（P = 0.07）方面比第2组更硬，相邻节段负荷传递（应变P = 0.72，椎体应力P = 0.36）或强度（P = 0.07）无差异。椎体缺损使完整状态下的压缩刚度降低（P = 0.001），椎体压缩骨折强化术后部分恢复（P = 0.006）。屈曲刚度无差异（P≥0.14）。屈曲时相邻节段负荷传递超过压缩时（应变P = 0.001，椎体应力P = 0.19）。初次和随后的椎体压缩骨折发生时的力相似（P = 0.26），但随后的相邻节段负荷更高（应变和椎体应力P = 0.04）。
通过联合压缩、屈曲和椎体缺损产生的多节段脊柱椎体压缩骨折强化术可使生理负荷下的相邻节段负荷传递正常化。在正常和骨质疏松性脊柱节段中，当负荷接近初次椎体压缩骨折时，强化术的保护作用丧失，随后的相邻节段椎体压缩骨折是由极端负荷引起，而非强化过程所致。
