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Biology
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Bone Mechanics: From Cells to Organs to Function
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Bone Mechanics: From Cells to Organs to Function

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Physiology".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 3402

Special Issue Editor

Dr. Viviana Toro-Ibacache

E-Mail Website
Guest Editor
Institute for Research in Dental Sciences, Faculty of Dentistry, Universidad de Chile, Santiago 8380544, Chile
Interests: functional morphology; musculoskeletal biology; biomechanics; musculoskeletal pathology

Special Issue Information

Dear Colleagues,

We invite you to contribute original articles to the Special Issue “Bone Mechanics: From Cells to Organs to Function”, with a focus on advancing our understanding of bone physiology and function. As bone serves both mechanical and metabolic roles, studying its response to loads at a cell, tissue and organ level is essential for deciphering research questions across fields such as skeletal adaptation during evolution of species, consequences of ageing in humans, acute and chronic pathologies, among others.

We welcome submissions in basic research exploring bone mechanics in humans and animal models, including comparative studies that shed light on evolutionary patterns or translational relevance. Contributions may address topics such as mechanotransduction, structural analysis, age-related changes, and innovative experimental or computational methods to assess bone response to loads.

This Special Issue aims to bridge disciplines, from biomechanics and histology to evolutionary biology and biomedical engineering, highlighting the importance of research questions, classic and new methods and results, and methodological rigor in the study of skeletal systems.

Join us in deepening the dialogue on how bones grow, adapt, weaken, and fail across the lifespan and among diverse organisms.

Dr. Viviana Toro-Ibacache
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bone mechanics
  • bone remodeling
  • mechanotransduction
  • structural analysis
  • functional morphology
  • bioengineering

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Published Papers (4 papers)

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Research

19 pages, 1995 KB  
Article
Microscopic and Geometric Changes in the Mandibular Condylar Head in Response to Subtle Secondary Overload: In Search of a Mechanical Origin of Condylar Hyperplasia
by Viviana Toro-Ibacache, Sonja Buvinic, Julián Balanta-Melo, Valeria Caro, Felipe Zúñiga, Ricardo Miranda-Krause, Léo Botton-Divet, John A. Nyakatura, Veronica Iturriaga and Bélgica Vásquez
Biology 2026, 15(10), 809; https://doi.org/10.3390/biology15100809 (registering DOI) - 20 May 2026
Abstract
In condylar hyperplasia (CH), one of the condylar processes of the mandible (CPs) grows more than its counterpart, leading to facial asymmetry. Using a mouse model of asymmetric masticatory loading, we investigated a possible mechanical origin of CH by evaluating the association between [...] Read more.
In condylar hyperplasia (CH), one of the condylar processes of the mandible (CPs) grows more than its counterpart, leading to facial asymmetry. Using a mouse model of asymmetric masticatory loading, we investigated a possible mechanical origin of CH by evaluating the association between morphometric parameters of CP cartilage and bone and the mandibular load regime. Thirty-nine adult male and female mouse hemimandibles that underwent different loading regimes were used: underloaded (UL), overloaded (OL), and symmetrically loaded (SL) controls. Micro-CTs were used to assess macroscopic shape and trabecular bone (TB) parameters, and articular cartilage features were studied histologically. Data were compared using multivariate and pairwise statistics. Principal component analysis showed that OL CPs exhibit a wide range of shape variation and show thicker cartilage but display TB features indicative of ongoing remodeling. Female OL tended to show more variable and larger parameters than males. However, differences in traits between sexes and load groups were not always statistically significant. We conclude that an asymmetric increase in mandibular loading may be associated with changes in the macro-/microscopic structure of the CP, affecting males and females differently. Signs of cartilage growth and bone remodeling are found in OL individuals, which are compatible with CH features. Full article
(This article belongs to the Special Issue Bone Mechanics: From Cells to Organs to Function)
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26 pages, 16545 KB  
Article
A Specimen-Based Comparative MicroCT–FEA Analysis of Vertebral Trabecular Bone Microarchitecture and Mechanical Response in Two South American Cervids: The Patagonian Huemul (Hippocamelus bisulcus) and the Southern Pudu (Pudu puda)
by Danae Tapia, Álvaro González, Fernando Vidal and Paulo Salinas
Biology 2026, 15(9), 722; https://doi.org/10.3390/biology15090722 - 2 May 2026
Viewed by 672
Abstract
The Patagonian huemul (Hippocamelus bisulcus) and the Southern pudu (Pudu puda) are native South American cervids that differ in body size, ecology, and conservation status. However, quantitative evidence linking vertebral trabecular microarchitecture with biomechanical behavior in these species remains [...] Read more.
The Patagonian huemul (Hippocamelus bisulcus) and the Southern pudu (Pudu puda) are native South American cervids that differ in body size, ecology, and conservation status. However, quantitative evidence linking vertebral trabecular microarchitecture with biomechanical behavior in these species remains scarce. This study aimed to comparatively characterize vertebral trabecular bone structure and its mechanical response using an integrative, non-destructive approach. Vertebral bodies from cervical, thoracic, and lumbar regions were analyzed using high-resolution micro-computed tomography to quantify structural parameters, followed by finite element analysis to estimate deformation and von Mises stress under standardized axial compression. Both specimens exhibited consistent regional variation, with cervical vertebrae showing lower density and organization, and thoracic–lumbar vertebrae displaying denser trabecular networks. The Southern pudu specimen appeared to present a more homogeneous microarchitecture and a relatively uniform mechanical response along the vertebral column. In contrast, the Patagonian huemul specimen tended to show greater structural heterogeneity, with apparently higher deformation and stress values, particularly in the cervical region. These findings suggest that trabecular organization may contribute to the differences in vertebral mechanical behavior observed between the analyzed specimens. This study provides a preliminary comparative baseline for understanding skeletal adaptation and structural vulnerability in South American cervid species. This exploratory analysis is based on single specimens per species and should be interpreted as preliminary evidence rather than population-level inference. Full article
(This article belongs to the Special Issue Bone Mechanics: From Cells to Organs to Function)
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22 pages, 6755 KB  
Article
Weight-Bearing Ladder Climbing Exercise Improves Bone Loss and Bone Microstructural Damage While Promoting Bone Injury Healing in OVX Rats
by Yiting Kang, Nan Li, Yanan Yu, Dingkang Wang, Tingting Zhao, Lijun Sun, Changjiang Liu and Liang Tang
Biology 2026, 15(1), 55; https://doi.org/10.3390/biology15010055 - 28 Dec 2025
Cited by 1 | Viewed by 783
Abstract
Osteoporosis is highly prevalent in postmenopausal women, causing chronic pain, fractures, and limited mobility that burden individuals and society. While resistance exercise benefits bone health, its role in osteoporotic bone injury healing and underlying mechanisms remain unclear. This study aimed to explore the [...] Read more.
Osteoporosis is highly prevalent in postmenopausal women, causing chronic pain, fractures, and limited mobility that burden individuals and society. While resistance exercise benefits bone health, its role in osteoporotic bone injury healing and underlying mechanisms remain unclear. This study aimed to explore the effects of 10-week weight-bearing ladder climbing exercise on ovariectomy (OVX)-induced osteoporosis and subsequent bone injury healing, and to investigate whether these effects are associated with the myostatin (MSTN) and Wnt/β-catenin pathways. Fifty-four 12-week-old female SD rats were randomized into Sham, OVX, and OVX + EX groups. Rats in the OVX and OVX + EX groups underwent ovariectomy to induce postmenopausal osteoporosis, and those in the OVX + EX group received 10-week weight-bearing ladder climbing. After the exercise intervention, 6 rats in each group were sacrificed; the remaining rats underwent femoral midshaft drilling to establish bone injury. The improvement in osteoporosis was evaluated via Micro-CT, biomechanical tests, RT-qPCR for mRNA detection, and Western blot for measuring protein levels of MSTN and Wnt/β-catenin pathway-related molecules at post-exercise and 21 days post-injury. Bone healing was reflected by the bone volume fraction at the bone injury site detected via Micro-CT at 10 and 21 days post-injury. This exercise significantly enhanced muscle strength and improved femoral bone mineral density (BMD), trabecular microstructure, and biomechanical properties in OVX rats. Meanwhile, the level of MSTN in the OVX + EX group was decreased, the expression of its downstream signaling pathways was inhibited, and the mRNA and protein expressions of Wnt/β-catenin were upregulated. Moreover, 21 days after exercise intervention, the biomechanical properties and bone microstructure of the OVX + EX group were still significantly superior to those of the OVX group, and the aforementioned molecular regulatory effect remained. In addition, pre-conducted exercise was able to promote increases in bone volume fraction at the bone injury site 10 and 21 days after drilling, which was conducive to bone injury healing. Ten-week weight-bearing ladder climbing ameliorates OVX-induced bone loss and promotes osteoporotic bone repair via regulating the MSTN/ActRIIB/Smad3 and Wnt/β-catenin pathways, providing evidence for exercise as a safe non-pharmacological intervention. Full article
(This article belongs to the Special Issue Bone Mechanics: From Cells to Organs to Function)
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23 pages, 13904 KB  
Article
Total Flavonoids of Rhizoma drynariae Enhance Bone Marrow Mesenchymal Stem Cell-Mediated Tendon–Bone Healing by Promoting Tissue Regeneration, Angiogenesis, and Modulation of Cytokine Expression
by Gaoyuan Yang, Yu Wang, Xianyan Xie, Ziyan Li, Shuqi Qin, Weitong Zhang, Zixi Chenyuan, Peizhong Cao, Huiguo Wang and Lin Zhu
Biology 2025, 14(11), 1593; https://doi.org/10.3390/biology14111593 - 14 Nov 2025
Viewed by 1275
Abstract
(1) Objective: This study aimed to investigate the synergistic effect and underlying mechanisms of Total Flavonoids of Rhizoma drynariae (TFRD) in combination with Bone Marrow Mesenchymal Stem Cells (BMSCs) in the repair of tendon–bone injuries. (2) Methods: The effects of TFRD on the [...] Read more.
(1) Objective: This study aimed to investigate the synergistic effect and underlying mechanisms of Total Flavonoids of Rhizoma drynariae (TFRD) in combination with Bone Marrow Mesenchymal Stem Cells (BMSCs) in the repair of tendon–bone injuries. (2) Methods: The effects of TFRD on the proliferation and migration of BMSCs were assessed using CCK-8 and scratch assays, and its potential to promote osteogenic and chondrogenic differentiation was evaluated. Concurrently, the pro-angiogenic effect of TFRD on Human Umbilical Vein Endothelial Cells (HUVECs) was observed. In vivo, a rat model of Achilles tendon–bone injury was established and animals were divided into four groups: SHAM, Model, BMSCs, and BMSCs + TFRD. After an 8-week intervention, the level of functional recovery was evaluated through histological analysis, immunohistochemistry, serum biochemical analysis, and biomechanical testing. (3) Results: A concentration of 5.0 μg/mL TFRD significantly promoted the proliferation, migration, and differentiation of BMSCs and enhanced the tube formation capacity of HUVECs. In the BMSCs + TFRD group, histological analysis revealed well-organized collagen fibers, increased cartilage deposition, and an optimized tendon–bone interface (TBI) structure. Immunohistochemistry showed upregulated expression of COL I, COL II, and SOX-9, alongside downregulated VEGFA. Furthermore, serum IL-6 levels were decreased, while IL-10 and TGF-β levels were elevated. The biomechanical properties were also significantly improved in this group. (4) Conclusions: TFRD promotes tendon–bone healing and functional recovery by enhancing BMSC functions, promoting angiogenesis, and improving the local microenvironment. Full article
(This article belongs to the Special Issue Bone Mechanics: From Cells to Organs to Function)
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