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Symmetry breaking and effects of nutrient walkway in time-dependent bone remodeling incorporating poroelasticity

Bone is an extraordinary biological material that continuously adapts its hierarchical microstructure to respond to static and dynamic loads for offering optimal mechanical features, in terms of stiffness and toughness, across different scales, from the sub-microscopic constituents within osteons—wh...

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Autores principales: Esposito, L., Minutolo, V., Gargiulo, P., Fraldi, M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9132879/
https://www.ncbi.nlm.nih.gov/pubmed/35394267
http://dx.doi.org/10.1007/s10237-022-01573-6
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author Esposito, L.
Minutolo, V.
Gargiulo, P.
Fraldi, M.
author_facet Esposito, L.
Minutolo, V.
Gargiulo, P.
Fraldi, M.
author_sort Esposito, L.
collection PubMed
description Bone is an extraordinary biological material that continuously adapts its hierarchical microstructure to respond to static and dynamic loads for offering optimal mechanical features, in terms of stiffness and toughness, across different scales, from the sub-microscopic constituents within osteons—where the cyclic activity of osteoblasts, osteoclasts, and osteocytes redesigns shape and percentage of mineral crystals and collagen fibers—up to the macroscopic level, with growth and remodeling processes that modify the architecture of both compact and porous bone districts. Despite the intrinsic complexity of the bone mechanobiology, involving coupling phenomena of micro-damage, nutrients supply driven by fluid flowing throughout hierarchical networks, and cells turnover, successful models and numerical algorithms have been presented in the literature to predict, at the macroscale, how bone remodels under mechanical stimuli, a fundamental issue in many medical applications such as optimization of femur prostheses and diagnosis of the risk fracture. Within this framework, one of the most classical strategies employed in the studies is the so-called Stanford’s law, which allows uploading the effect of the time-dependent load-induced stress stimulus into a biomechanical model to guess the bone structure evolution. In the present work, we generalize this approach by introducing the bone poroelasticity, thus incorporating in the model the role of the fluid content that, by driving nutrients and contributing to the removal of wastes of bone tissue cells, synergistically interacts with the classical stress fields to change homeostasis states, local saturation conditions, and reorients the bone density rate, in this way affecting growth and remodeling. Through two paradigmatic example applications, i.e. a cylindrical slice with internal prescribed displacements idealizing a tract of femoral diaphysis pushed out by the pressure exerted by a femur prosthesis and a bone element in a form of a bent beam, it is highlighted that the present model is capable to catch more realistically both the transition between spongy and cortical regions and the expected non-symmetrical evolution of bone tissue density in the medium–long term, unpredictable with the standard approach. A real study case of a femur is also considered at the end in order to show the effectiveness of the proposed remodeling algorithm.
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spelling pubmed-91328792022-05-27 Symmetry breaking and effects of nutrient walkway in time-dependent bone remodeling incorporating poroelasticity Esposito, L. Minutolo, V. Gargiulo, P. Fraldi, M. Biomech Model Mechanobiol Original Paper Bone is an extraordinary biological material that continuously adapts its hierarchical microstructure to respond to static and dynamic loads for offering optimal mechanical features, in terms of stiffness and toughness, across different scales, from the sub-microscopic constituents within osteons—where the cyclic activity of osteoblasts, osteoclasts, and osteocytes redesigns shape and percentage of mineral crystals and collagen fibers—up to the macroscopic level, with growth and remodeling processes that modify the architecture of both compact and porous bone districts. Despite the intrinsic complexity of the bone mechanobiology, involving coupling phenomena of micro-damage, nutrients supply driven by fluid flowing throughout hierarchical networks, and cells turnover, successful models and numerical algorithms have been presented in the literature to predict, at the macroscale, how bone remodels under mechanical stimuli, a fundamental issue in many medical applications such as optimization of femur prostheses and diagnosis of the risk fracture. Within this framework, one of the most classical strategies employed in the studies is the so-called Stanford’s law, which allows uploading the effect of the time-dependent load-induced stress stimulus into a biomechanical model to guess the bone structure evolution. In the present work, we generalize this approach by introducing the bone poroelasticity, thus incorporating in the model the role of the fluid content that, by driving nutrients and contributing to the removal of wastes of bone tissue cells, synergistically interacts with the classical stress fields to change homeostasis states, local saturation conditions, and reorients the bone density rate, in this way affecting growth and remodeling. Through two paradigmatic example applications, i.e. a cylindrical slice with internal prescribed displacements idealizing a tract of femoral diaphysis pushed out by the pressure exerted by a femur prosthesis and a bone element in a form of a bent beam, it is highlighted that the present model is capable to catch more realistically both the transition between spongy and cortical regions and the expected non-symmetrical evolution of bone tissue density in the medium–long term, unpredictable with the standard approach. A real study case of a femur is also considered at the end in order to show the effectiveness of the proposed remodeling algorithm. Springer Berlin Heidelberg 2022-04-08 2022 /pmc/articles/PMC9132879/ /pubmed/35394267 http://dx.doi.org/10.1007/s10237-022-01573-6 Text en © The Author(s) 2022, corrected publication 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Original Paper
Esposito, L.
Minutolo, V.
Gargiulo, P.
Fraldi, M.
Symmetry breaking and effects of nutrient walkway in time-dependent bone remodeling incorporating poroelasticity
title Symmetry breaking and effects of nutrient walkway in time-dependent bone remodeling incorporating poroelasticity
title_full Symmetry breaking and effects of nutrient walkway in time-dependent bone remodeling incorporating poroelasticity
title_fullStr Symmetry breaking and effects of nutrient walkway in time-dependent bone remodeling incorporating poroelasticity
title_full_unstemmed Symmetry breaking and effects of nutrient walkway in time-dependent bone remodeling incorporating poroelasticity
title_short Symmetry breaking and effects of nutrient walkway in time-dependent bone remodeling incorporating poroelasticity
title_sort symmetry breaking and effects of nutrient walkway in time-dependent bone remodeling incorporating poroelasticity
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9132879/
https://www.ncbi.nlm.nih.gov/pubmed/35394267
http://dx.doi.org/10.1007/s10237-022-01573-6
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