Evidence map›Paper›PMID 42080929›Full record

ArticleActa biotheoretica2026

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

Diego A Garzón-Alvarado, Carlos A Duque-Daza, Dorian L Linero, Boumediene Nedjar, Abdelghani May, Estevam Barbosa Las Casas, Salah Ramtani

Abstract read
In one paragraph

Article in Acta biotheoretica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Diego A Garzón-AlvaradoBiotechnology Institute, Universidad Nacional de Colombia, Bogotá, Colombia. dagarzona@unal.edu.co.
Carlos A Duque-DazaGNUM, Universidad Nacional de Colombia, Bogotá, Colombia.
Dorian L LineroCivil and Agricultural Engineering Department, Universidad Nacional de Colombia, Bogotá, Colombia.
Boumediene NedjarUniversité d'Evry, Paris-Saclay, LMEE, 91020, Evry, France.
Abdelghani MayEcole Mil Polytech, Mech Syst Design Lab, BP 17, 16214, Algiers, Algeria.
Estevam Barbosa Las CasasDepartamento de Engenharia de Estruturas, Escola de Engenharia, Universidade Federal de Minas Gerais - UFMG - Belo Horizonte (MG), Belo Horizonte, Brasil.
Salah RamtaniLaboratoire CB3S, equipe BEST, CNRS (UMR 7244), Université Sorbonne Paris Nord, Villetaneuse, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Bone and BonesBone RemodelingComputer SimulationModels, BiologicalAnimalsHumansOsteoblastsOsteoclastsStress, MechanicalAccumulated damageBone remodelingFatigueKomarova’s modelOsteoblastsOsteoclastsPersonalized medicine

Identifiers

PMID42080929
PMCPMC13139263

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.