Division of Biomechanics and Engineering Design, K.U. Leuven, Celestijnenlaan 300C (2419), 3001, Leuven, Belgium.
Biomech Model Mechanobiol. 2010 Dec;9(6):713-24. doi: 10.1007/s10237-010-0208-8. Epub 2010 Mar 24.
Both mechanical and biological factors play an important role in normal as well as impaired fracture healing. This study aims to provide a mathematical framework in which both regulatory mechanisms are included. Mechanics and biology are coupled by making certain parameters of a previously established bioregulatory model dependent on local mechanical stimuli. To illustrate the potential added value of such a framework, this coupled model was applied to investigate whether local mechanical stimuli influencing only the angiogenic process can explain normal healing as well as overload-induced nonunion development. Simulation results showed that mechanics acting directly on angiogenesis alone was not able to predict the formation of overload-induced nonunions. However, the direct action of mechanics on both angiogenesis and osteogenesis was able to predict overload-induced nonunion formation, confirming the hypotheses of several experimental studies investigating the interconnection between angiogenesis and osteogenesis. This study shows that mathematical models can assist in testing hypothesis on the nature of the interaction between biology and mechanics.
在正常和受损的骨折愈合中，机械因素和生物因素都起着重要作用。本研究旨在提供一个数学框架，其中包括这两种调节机制。通过使先前建立的生物调节模型中的某些参数依赖于局部机械刺激，将力学和生物学联系起来。为了说明这种框架的潜在附加值，将该耦合模型应用于研究仅影响血管生成过程的局部机械刺激是否可以解释正常愈合以及过载引起的不愈合的发展。模拟结果表明，仅直接作用于血管生成的力学本身并不能预测过载引起的不愈合的形成。然而，力学对血管生成和成骨作用的直接作用能够预测过载引起的不愈合的形成，证实了一些研究血管生成和成骨之间相互联系的实验研究的假设。本研究表明，数学模型可以辅助检验生物学和力学之间相互作用的本质的假说。
