Slomka Noa, Diamant Idit, Gefen Amit
Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv, Israel.
Technol Health Care. 2008;16(1):47-60.
Vertebral compression fractures are a potentially severe injury, which is characteristic to osteoporotic elderly. Despite being a significant healthcare problem, the etiology of compression fractures is not fully understood, and there are no biomechanical models in the literature that describe the development of these fractures based on cancellous bone failure accumulation. The objective of this study was therefore to develop a computational model of tissue-level failure accumulation in vertebral cancellous bone, which eventually leads to compression fractures. The model predicts the accumulated percentage of broken trabeculae delta in a vertebral region of interest (ROI) over 60 years, by employing Euler's theory for elastic buckling. The accumulated failure delta is calculated as function of the daily activity characteristics and rate of annual bone loss (RABL) with aging. An RABL of unity represents the normal bone loss attributed to aging per se, whereas RABL>1 is assumed to represent pathological bone metabolism such as osteoporosis. Simulations were conducted for a range of RABLs, to determine the effect of changes in bone metabolism on the accumulation of bone failure. Results showed that bone failure rapidly increased with RABL. Generally, trabecular failure was shown to become more severe for RABL>4. Total failure was exhibited at RABL=7.5 for the central ROI, and at RABL=8.5 for the sub-endplate ROI. We concluded that vertebral compression fractures advance monotonically between the age of 50-55 years and 70 years, and may accelerate thereafter if RABL is high (~8). Additionally, the model identified weight lifting as the action that most dramatically accelerated the destruction of osteoporotic spinal cancellous bone. The present biomechanical model is useful for understanding the etiology of compression fractures, and potentially, depending on further experimental characterization of RABL, for considering the effects of medications that influence bone metabolism on patient prognosis.
椎体压缩性骨折是一种潜在的严重损伤，是骨质疏松老年人的特征性表现。尽管这是一个重大的医疗保健问题，但压缩性骨折的病因尚未完全明确，而且文献中没有基于松质骨失效累积来描述这些骨折发展过程的生物力学模型。因此，本研究的目的是建立一个椎体松质骨组织水平失效累积的计算模型，该模型最终会导致压缩性骨折。该模型通过应用欧拉弹性屈曲理论预测在60年时间里感兴趣的椎体区域（ROI）内小梁骨折的累积百分比。累积失效量δ是根据日常活动特征和随年龄增长的年骨丢失率（RABL）计算得出的。RABL为1表示因衰老本身导致的正常骨丢失，而RABL>1则被认为代表骨质疏松等病理性骨代谢。针对一系列RABL值进行了模拟，以确定骨代谢变化对骨失效累积的影响。结果表明，骨失效随RABL迅速增加。一般来说，当RABL>4时，小梁失效会变得更严重。中央ROI在RABL=7.5时出现完全失效，而在RABL=8.5时终板下ROI出现完全失效。我们得出结论，椎体压缩性骨折在50 - 55岁至70岁之间呈单调进展，如果RABL较高（约为8），此后可能会加速发展。此外，该模型确定举重是最显著加速骨质疏松性脊柱松质骨破坏的行为。目前的生物力学模型有助于理解压缩性骨折的病因，并且根据RABL的进一步实验特征，有可能用于考虑影响骨代谢的药物对患者预后的影响。
