Integration of Bone Remodeling and Damage Accumulation: A Preliminary Computational Framework for Physiological and Pathological Responses

IF 1.5 4区 生物学 Q4 MATHEMATICAL & COMPUTATIONAL BIOLOGY
Diego A. Garzón-Alvarado, Carlos A. Duque-Daza, Dorian L. Linero, Boumediene Nedjar, Abdelghani May, Estevam Barbosa Las Casas, Salah Ramtani
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Abstract

This study presents a computational model that integrates bone remodeling dynamics with damage accumulation, focusing on both physiological and pathological conditions. Building upon Komarova’s classical model of osteoclast and osteoblast interactions, this work introduces fatigue-induced damage using a stress-life (S-N) approach. By simulating bone responses under sinusoidal and random mechanical loads, the model captures the cyclical nature of bone turnover. The results show that under normal physiological conditions, bone is able to repair microdamage and maintain structural integrity. However, in pathological scenarios such as osteoporosis and tumors, the remodeling cycle is disrupted, leading to an increase in damage accumulation and eventual structural failure. Through numerical simulations, the study also demonstrates the significant impact of fatigue on bone health, showing that repetitive mechanical loads, even below critical stress levels, can result in bone degradation over time. By capturing the accumulation of microdamage and its repair, the model offers potential applications in personalized medicine to assess fracture risks in varying stress and health scenarios. This approach provides a framework for understanding how different stress patterns contribute to bone damage and offers insights into the progression of bone diseases. The model could be extended using metabolic and age-related characteristics and serves as a potential tool for personalized medicine, helping to predict bone failure risks in individuals when they are submitted to repetitive mechanical loads.

Abstract Image

骨重塑和损伤积累的整合:生理和病理反应的初步计算框架
本研究提出了一个计算模型,将骨重塑动力学与损伤积累结合起来,关注生理和病理条件。在Komarova的经典破骨细胞和成骨细胞相互作用模型的基础上,本研究采用应力-寿命(S-N)方法引入疲劳引起的损伤。通过模拟骨在正弦和随机机械载荷下的反应,该模型捕捉到了骨更替的周期性。结果表明,在正常生理条件下,骨具有修复微损伤和维持结构完整性的能力。然而,在骨质疏松和肿瘤等病理情况下,重塑周期被破坏,导致损伤积累增加,最终导致结构失效。通过数值模拟,该研究还证明了疲劳对骨骼健康的显著影响,表明随着时间的推移,即使低于临界应力水平,重复的机械负荷也会导致骨骼退化。通过捕获微损伤的积累及其修复,该模型在个性化医疗中提供了潜在的应用,以评估不同应力和健康情况下的骨折风险。这种方法为理解不同的应力模式如何导致骨损伤提供了一个框架,并为骨疾病的进展提供了见解。该模型可以利用代谢和年龄相关特征进行扩展,并作为个性化医疗的潜在工具,帮助预测个体在承受重复性机械负荷时的骨衰竭风险。
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来源期刊
Acta Biotheoretica
Acta Biotheoretica 生物-生物学
CiteScore
2.70
自引率
7.70%
发文量
19
审稿时长
3 months
期刊介绍: Acta Biotheoretica is devoted to the promotion of theoretical biology, encompassing mathematical biology and the philosophy of biology, paying special attention to the methodology of formation of biological theory. Papers on all kind of biological theories are welcome. Interesting subjects include philosophy of biology, biomathematics, computational biology, genetics, ecology and morphology. The process of theory formation can be presented in verbal or mathematical form. Moreover, purely methodological papers can be devoted to the historical origins of the philosophy underlying biological theories and concepts. Papers should contain clear statements of biological assumptions, and where applicable, a justification of their translation into mathematical form and a detailed discussion of the mathematical treatment. The connection to empirical data should be clarified. Acta Biotheoretica also welcomes critical book reviews, short comments on previous papers and short notes directing attention to interesting new theoretical ideas.
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