Colloca Michele, Ito Keita, van Rietbergen Bert
J Biomech Eng. 2014 Mar;136(3):031004. doi: 10.1115/1.4026227.
Simulation of bone remodeling at the bone cell level can predict changes in bone microarchitecture and density due to bone diseases and drug treatment. Their clinical application, however, is limited since bone microarchitecture can only be measured in the peripheral skeleton of patients and since the simulations are very time consuming. To overcome these issues, we have developed an analytical model to predict bone density adaptation at the organ level, in agreement with our earlier developed bone remodeling theory at the cellular level. Assuming a generalized geometrical model at the microlevel, the original theory was reformulated into an analytical equation that describes the evolution of bone density as a function of parameters that describe cell activity, mechanotransduction and mechanical loading. It was found that this analytical model can predict changes in bone density due to changes in these cell-level parameters that are in good agreement with those predicted by the earlier numerical model that implemented a detailed micro-finite element (FE) model to represent the bone architecture and loading, at only a fraction of the computational costs. The good agreement between analytical and numerical density evolutions indicates that the analytical model presented in this study can predict well bone functional adaptation and, eventually, provide an efficient tool for simulating patient-specific bone remodeling and for better prognosis of bone fracture risk.
在骨细胞水平上对骨重塑进行模拟，可以预测由于骨疾病和药物治疗导致的骨微结构和密度变化。然而，它们的临床应用受到限制，因为骨微结构只能在患者的外周骨骼中测量，而且模拟非常耗时。为了克服这些问题，我们开发了一个分析模型来预测器官水平上的骨密度适应性，这与我们早期在细胞水平上开发的骨重塑理论一致。假设在微观层面有一个广义几何模型，原始理论被重新表述为一个分析方程，该方程描述了骨密度随描述细胞活动、机械转导和机械负荷的参数的变化而演变。结果发现，这个分析模型能够预测由于这些细胞水平参数的变化而导致的骨密度变化，这与早期数值模型所预测的结果高度吻合，早期数值模型采用详细的微观有限元（FE）模型来表示骨结构和负荷，而本分析模型的计算成本仅为其一小部分。分析模型和数值模型的骨密度演变结果之间的良好一致性表明，本研究中提出的分析模型能够很好地预测骨功能适应性，并最终为模拟患者特异性骨重塑以及更好地预测骨折风险提供一个有效的工具。
