Diego A. Garzón-Alvarado, Carlos A. Duque-Daza, Dorian L. Linero, Boumediene Nedjar, Abdelghani May, Estevam Barbosa Las Casas, Salah Ramtani
{"title":"Integration of Bone Remodeling and Damage Accumulation: A Preliminary Computational Framework for Physiological and Pathological Responses","authors":"Diego A. Garzón-Alvarado, Carlos A. Duque-Daza, Dorian L. Linero, Boumediene Nedjar, Abdelghani May, Estevam Barbosa Las Casas, Salah Ramtani","doi":"10.1007/s10441-026-09522-x","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>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.</p>\n </div>","PeriodicalId":7057,"journal":{"name":"Acta Biotheoretica","volume":"74 3","pages":""},"PeriodicalIF":1.5000,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10441-026-09522-x.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Biotheoretica","FirstCategoryId":"99","ListUrlMain":"https://link.springer.com/article/10.1007/s10441-026-09522-x","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MATHEMATICAL & COMPUTATIONAL BIOLOGY","Score":null,"Total":0}
引用次数: 0
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.
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.