It is well known that microcracks act as a stimulus for bone remodelling, initiating resorption by osteoclasts and new bone formation by osteoblasts. Moreover, microcracks are likely to alter the fluid flow and convective transport through the bone tissue. This paper proposes a quantitative evaluation of the strain-induced interstitial fluid velocities developing in osteons in presence of a microcrack in the interstitial bone tissue. Based on Biot theory in the low-frequency range, a poroelastic model is carried out to study the hydro-mechanical behaviour of cracked osteonal tissue. The finite element results show that the presence of a microcrack in the interstitial osteonal tissue may drastically reduce the fluid velocity inside the neighbouring osteons. This fluid inactive zone inside osteons can cover up to 10% of their surface. Consequently, the fluid environment of bone mechano-sensitive cells is locally modified.
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http://dx.doi.org/10.1007/s10237-011-0287-1 | DOI Listing |
Acta Biomater
January 2025
Biomedical Engineering, College of Engineering, Mathematics and Physical Sciences, University of Exeter, UK. Electronic address:
The biomechanical properties of articular cartilage arise from a complex bioenvironment comprising hierarchically organised collagen networks within the extracellular matrix (ECM) that interact with the proteoglycan-rich interstitial fluid. This network features a depth-dependent fibril organisation across different zones. Understanding how collagen fibrils respond to external loading is key to elucidating the mechanisms behind lesion and managing degenerative conditions like osteoarthritis.
View Article and Find Full Text PDFPLoS Genet
January 2025
Mater Research Institute-University of Queensland, Translational Research Institute, Woolloongabba, Brisbane, Australia.
Adaptation to existence outside the womb is a key event in the life of a mammal. The absence of macrophages in rats with a homozygous mutation in the colony-stimulating factor 1 receptor (Csf1r) gene (Csf1rko) severely compromises pre-weaning somatic growth and maturation of organ function. Transfer of wild-type bone marrow cells (BMT) at weaning rescues tissue macrophage populations permitting normal development and long-term survival.
View Article and Find Full Text PDFJ Heart Lung Transplant
January 2025
Department of Medicine, University Health Network and Sinai Health System, University of Toronto, Toronto, ON, Canada; Toronto General Hospital Research Institute, University Health Network, Toronto, ON, Canada; Joint Department of Medical Imaging, University of Toronto, Toronto, ON, Canada. Electronic address:
Bone health after lung transplantation has not been comprehensively reviewed in over two decades. This narrative review summarizes available literature on bone health in the context of lung transplantation, including epidemiology, presentation and post-operative management. Osteoporosis is reported in approximately 30-50% of lung transplant candidates, largely due to disease-related impact on bone and lifestyle, and corticosteroid-related effects during end-stage lung disease (interstitial lung diseases, chronic obstructive pulmonary disease, and historically cystic fibrosis).
View Article and Find Full Text PDFJBMR Plus
February 2025
Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 22529 Hamburg, Germany.
Advanced glycation end products (AGEs) accumulate in various tissues, including bone, due to aging and conditions like diabetes mellitus. To investigate the effects of AGEs on bone material quality and biomechanical properties, an study utilizing human tibial cortex, sectioned into 90 beams, and randomly assigned to three mechanical test groups was performed. Each test group included ribose ( = 0.
View Article and Find Full Text PDFJ Cancer Res Clin Oncol
January 2025
Department of Internal Medicine III, University Hospital Ulm, Ulm, Germany.
Background: Li-Fraumeni syndrome (LFS) is an autosomal dominant tumor predisposition syndrome characterized by a high familial incidence of various malignancies. It results from pathogenic/likely pathogenic heterozygous constitutional variants of the TP53 gene. Due to impaired DNA damage repair, conventional cytotoxic therapies or radiotherapy should be avoided whenever feasible to mitigate the high incidence of treatment-related secondary malignancies in these patients.
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