Topic
Mechanical load
About: Mechanical load is a research topic. Over the lifetime, 1642 publications have been published within this topic receiving 26732 citations. The topic is also known as: load.
Papers published on a yearly basis
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Papers
TL;DR: A computational model of the metabolic process in bone is presented that confirms that cell coupling is governed by feedback from mechanical load transfer, and can explain the emergence and maintenance of trabecular architecture as an optimal mechanical structure, as well as its adaptation to alternative external loads.
Abstract: The architecture of trabecular bone, the porous bone found in the spine and at articulating joints, provides the requirements for optimal load transfer, by pairing suitable strength and stiffness to minimal weight according to rules of mathematical design1,2,3,4,5,6. But, as it is unlikely that the architecture is fully pre-programmed in the genes7, how are the bone cells informed about these rules, which so obviously dictate architecture? A relationship exists between bone architecture and mechanical usage8—while strenuous exercise increases bone mass9, disuse, as in microgravity and inactivity, reduces it10. Bone resorption cells (osteoclasts) and bone formation cells (osteoblasts) normally balance bone mass in a coupled homeostatic process of remodelling, which renews some 25% of trabecular bone volume per year. Here we present a computational model of the metabolic process in bone that confirms that cell coupling is governed by feedback from mechanical load transfer11,12,13.This model can explain the emergence and maintenance of trabecular architecture as an optimal mechanical structure, as well as its adaptation to alternative external loads.
1,221 citations
TL;DR: Mechanotransduction plays a crucial role in the physiology of many tissues including bone and some hormones may interact with local mechanical signals to change the sensitivity of the sensor or effector cells to mechanical load.
Abstract: Mechanotransduction plays a crucial role in the physiology of many tissues including bone. Mechanical loading can inhibit bone resorption and increase bone formation in vivo. In bone, the process of mechanotransduction can be divided into four distinct steps: (1) mechanocoupling, (2) biochemical coupling, (3) transmission of signal, and (4) effector cell response. In mechanocoupling, mechanical loads in vivo cause deformations in bone that stretch bone cells within and lining the bone matrix and create fluid movement within the canaliculae of bone. Dynamic loading, which is associated with extracellular fluid flow and the creation of streaming potentials within bone, is most effective for stimulating new bone formation in vivo. Bone cells in vitro are stimulated to produce second messengers when exposed to fluid flow or mechanical stretch. In biochemical coupling, the possible mechanisms for the coupling of cell-level mechanical signals into intracellular biochemical signals include force transduction through the integrin-cytoskeleton-nuclear matrix structure, stretch-activated cation channels within the cell membrane, G protein-dependent pathways, and linkage between the cytoskeleton and the phospholipase C or phospholipase A pathways. The tight interaction of each of these pathways would suggest that the entire cell is a mechanosensor and there are many different pathways available for the transduction of a mechanical signal. In the transmission of signal, osteoblasts, osteocytes, and bone lining cells may act as sensors of mechanical signals and may communicate the signal through cell processes connected by gap junctions. These cells also produce paracrine factors that may signal osteoprogenitors to differentiate into osteoblasts and attach to the bone surface. Insulin-like growth factors and prostaglandins are possible candidates for intermediaries in signal transduction. In the effector cell response, the effects of mechanical loading are dependent upon the magnitude, duration, and rate of the applied load. Longer duration, lower amplitude loading has the same effect on bone formation as loads with short duration and high amplitude. Loading must be cyclic to stimulate new bone formation. Aging greatly reduces the osteogenic effects of mechanical loading in vivo. Also, some hormones may interact with local mechanical signals to change the sensitivity of the sensor or effector cells to mechanical load.
988 citations
TL;DR: It is concluded that application of the techniques investigated here can lead to a better prediction of the bone failure load for bone in vivo than is possible from DXA measurements, structural parameters, or a combination thereof.
642 citations
TL;DR: This review highlights current insights in bone adaptation to external mechanical loading, with an emphasis on how a mechanical load placed on whole bones is translated and amplified into a mechanical signal that is subsequently sensed by the osteocytes.
569 citations
TL;DR: In this paper, the authors use the chemical potential of the solvent and the deformation gradient of the network as independent variables of the free energy function, and show that the boundary value problem of the swollen gel is equivalent to that of a hyperelastic solid.
549 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 2 |
| 2024 | 3 |
| 2023 | 7 |
| 2022 | 22 |
| 2021 | 73 |
| 2020 | 83 |