How Bone Tissue and Cells Experience Elevated Temperatures During Orthopaedic Cutting: An Experimental and Computational Investigation

Duffy, Garry P.; Vaughan, Ted J.; Niebur, Glen L.; Casey, Conor; Tallon, David; McNamara, Laoise M.

doi:10.1115/1.4026177

Cited by 18 publications

(26 citation statements)

References 46 publications

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“…In this case, temperatures measured on the endosteal surface at point 1 were greater than the threshold temperature of 478C [19]. 3.2.…”

Section: Temperature Validation Of Thermal Injury Modelmentioning

confidence: 70%

“…The specific objectives of this study were to test the effect of clinically relevant temperatures increases (478C or 608C determined previously [6,19]) on osteocyte apoptosis and gene expression responses in vivo. Immunohistochemistry (IHC) staining was used to determine the spatial distribution of apoptotic signalling marker cleaved caspase-3 in osteocytes in the damage region.…”

Section: Introductionmentioning

confidence: 99%

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Thermally induced osteocyte damage initiates pro-osteoclastogenic gene expression in vivo

Duffy

Tallon

Cheung

et al. 2016

J. R. Soc. Interface.

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Bone is often subject to harsh temperatures during orthopaedic procedures resulting in thermally induced bone damage, which may affect the healing response. Postsurgical healing of bone is essential to the success of surgery, therefore, an understanding of the thermally induced responses of bone cells to clinically relevant temperatures in vivo is required. Osteocytes have been shown to be integrally involved in the bone remodelling cascade, via apoptosis, in micro-damage systems. However, it is unknown whether this relationship is similar following thermal damage. Sprague-Dawley rat tibia were exposed to clinically relevant temperatures (478C or 608C) to investigate the role of osteocytes in modulating remodelling related factors. Immunohistochemistry was used to quantify osteocyte thermal damage (activated caspase-3). Thermally induced pro-osteoclastogenic genes (Rankl, Opg and M-csf ), in addition to genes known to mediate osteoblast and osteoclast differentiation via prostaglandin production (Cox2), vascularization (Vegf ) and inflammatory (Il1a) responses, were investigated using gene expression analysis. The results demonstrate that heat-treatment induced significant bone tissue and cellular damage. Pro-osteoclastogenic genes were upregulated depending on the amount of temperature elevation compared with the control. Taken together, the results of this study demonstrate the in vivo effect of thermally induced osteocyte damage on the gene expression profile.

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“…In this case, temperatures measured on the endosteal surface at point 1 were greater than the threshold temperature of 478C [19]. 3.2.…”

Section: Temperature Validation Of Thermal Injury Modelmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Thermally induced osteocyte damage initiates pro-osteoclastogenic gene expression in vivo

Duffy

Tallon

Cheung

et al. 2016

J. R. Soc. Interface.

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“…While the cell necrosis of nerve tissue can be permanent, bone cell necrosis seems to be reversible. Dolan et al (2015) show that osteocyte thermal damage (apoptosis) initiates a bone remodelling cascade. However, the effects of osteonecrosis on implant fixation (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…Other researchers use finite element models (FEM) to investigate how bone cells with different thermal conductivities would experience a temperature rise in the mineralised bone matrix, but only a small temperature difference (0.001 °C) is found between the embedded cells and the surrounding mineralised matrix (Dolan et al, 2014). Overall, there is a lack of reliable thermal conductivity values reported for cancellous bone or human cortical bone.…”

Section: Introductionmentioning

confidence: 99%

The thermal conductivity of cortical and cancellous bone

Feldmann

Wili²,

Maquer³

et al. 2018

eCM

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Surgical interventions close to vulnerable structures, such as nerves, require precise handling of surgical instruments and tools. These tools not only pose the risk of mechanical damage to soft tissues, but they also generate heat, which can lead to thermal necrosis of bone or soft tissues. Researchers and engineers are trying to improve those tools through experimentation and simulations. To simulate temperature distributions in anatomical structures, reliable material constants are needed. Therefore, this study aimed at investigating the thermal conductivity of cortical and cancellous bone. Accordingly, a custom-made steady-state experimental setup was designed and validated. 6 bovine and 3 human cortical bone samples, as well as 32 bovine cancellous bone samples, with variable bone volume fraction were tested. The cancellous bone samples were scanned by micro-computed tomography (µCT) and micro-finite element (µFE) voxel models were created to calculate iteratively the thermal conductivity of the bone marrow. The experimental results provided 0.64 ± 0.04 W/ mK for bovine cortical bone and 0.68 ± 0.01 W/mK for human cortical bone. A linear dependency of thermal conductivity on bone volume fraction was found for cancellous bone [R-square (R 2 ) = 0.8096, standard error of the estimates (SEE) = 0.0355 W/mK]. The thermal conductivity of the bone marrow was estimated to be 0.42 ± 0.05 W/mK. These results will help to improve thermal finite element simulations of the human skeleton and aid the development of new surgical tools or procedures.Keywords: Thermal conductivity of compact and trabecular bone, specific heat of bone, thermal bone necrosis, temperature of cutting or drilling of bone.

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“…A node-based submodeling procedure, similar to Refs. [36,38], was used whereby the boundary conditions applied to the cellular submodel were interpolated from the nodal displacements that were resolved in the tissue-level model. In this case, the solution for the tissuelevel trabecular unit cell is determined a priori and this was used to impart deformation on the relevant boundaries of the cellular submodel, allowing an accurate prediction of global to local behavior.…”

Section: Tissue Level: Trabecular Unitmentioning

confidence: 99%

Multiscale Modeling of Trabecular Bone Marrow: Understanding the Micromechanical Environment of Mesenchymal Stem Cells During Osteoporosis

Vaughan

Voisin

Niebur

et al. 2015

Journal of Biomechanical Engineering

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Mechanical loading directs the differentiation of mesenchymal stem cells (MSCs) in vitro and it has been hypothesized that the mechanical environment plays a role in directing the cellular fate of MSCs in vivo. However, the complex multicellular composition of trabecular bone marrow means that the precise nature of mechanical stimulation that MSCs experience in their native environment is not fully understood. In this study, we developed a multiscale model that discretely represents the cellular constituents of trabecular bone marrow and applied this model to characterize mechanical stimulation of MCSs in vivo.We predicted that cell-level strains in certain locations of the trabecular marrow microenvironment were greater in magnitude (maximum e12¼24,000 le) than levels that have been found to result in osteogenic differentiation of MSCs in vitro (>8000 le),which may indicate that the native mechanical environment of MSCs could direct cellular fate in vivo. The results also showed that cell–cell adhesions could play an important role in mediating mechanical stimulation within the MSC population in vivo. The model was applied to investigate how changes that occur during osteoporosis affected mechanical stimulation in the cellular microenvironment of trabecular bone marrow. Specifically,a reduced bone volume (BV) resulted in an overall increase in bone deformation, leading to greater cell-level mechanical stimulation in trabecular bone marrow (maximume12¼48,000 le). An increased marrow adipocyte content resulted in slightly lower levels of stimulation within the adjacent cell population due to a shielding effect caused by the more compliant behavior of adipocytes (maximum e12¼41,000 le). Despite this reduction, stimulation levels in trabecular bone marrow during osteoporosis remained much higher than those predicted to occur under healthy conditions. It was found that compensatory mechanobiological responses that occur during osteoporosis, such as increased trabecular stiffness and axial alignment of trabeculae, would be effective in returning MSC stimulation in trabecular marrow to normal levels. These results have provided novel insight into the mechanical stimulation of the trabecular marrow MSC population in both healthy and osteoporotic bone, and could inform the design three dimensional(3D) in vitro bioreactor strategies techniques, which seek to emulate physiological conditions.

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How Bone Tissue and Cells Experience Elevated Temperatures During Orthopaedic Cutting: An Experimental and Computational Investigation

Cited by 18 publications

References 46 publications

Thermally induced osteocyte damage initiates pro-osteoclastogenic gene expression in vivo

Thermally induced osteocyte damage initiates pro-osteoclastogenic gene expression in vivo

The thermal conductivity of cortical and cancellous bone

Multiscale Modeling of Trabecular Bone Marrow: Understanding the Micromechanical Environment of Mesenchymal Stem Cells During Osteoporosis

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