Multi-Scale Micro-Mechanical Poroelastic Modeling of Fluid Flow in Cortical Bone

Materials ◽  
2004 ◽  
Author(s):  
Colby C. Swan ◽  
Hyung-Joo Kim

To explore the potential role that load-induced fluid flow plays as a mechano-transduction mechanism in bone adaptation, a lacunar-canalicular scale bone poroelasticity model is developed and exercised. The model uses micromechanics to homogenize the pericanalicular bone matrix, a system of straight circular cylinders in the bone matrix through which bone fluids can flow, as a locally anisotropic poroelastic medium. In this work, a simplified two-dimensional model of a periodic array of lacunae and their surrounding systems of canaliculi is developed and exercised to quantify local fluid flow characteristics in the vicinity of a single lacuna. When the cortical bone model is loaded, microscale stress and strain concentrations occur in the vicinity of individual lacunae and give rise to microscale spatial variations in the pore fluid pressure field. Consequently, loading of cortical bone can induce fluid flow in the canaliculi and exchange of fluid between canaliculi and lacunae. For realistic bone morphology parameters, and a range of loading frequencies, fluid pressures and fluid-solid shear stresses in the canalicular bone are computed and the associated energy dissipation in the models compared to that measured in physical in vitro experiments on human cortical bone. For realistic volume fractions of canaliculi, deformation-induced fluid flow is found to have a much larger characteristic time constant than deformation-induced flow in the Haversian system.

2003 ◽  
Vol 125 (1) ◽  
pp. 25-37 ◽  
Author(s):  
C. C. Swan ◽  
R. S. Lakes ◽  
R. A. Brand ◽  
K. J. Stewart

To explore the hypothesis that load-induced fluid flow in bone is a mechano-transduction mechanism in bone adaptation, unit cell micro-mechanical techniques are used to relate the microstructure of Haversian cortical bone to its effective poroelastic properties. Computational poroelastic models are then applied to compute in vitro Haversian fluid flows in a prismatic specimen of cortical bone during harmonic bending excitations over the frequency range of 100 to 106Hz. At each frequency considered, the steady state harmonic response of the poroelastic bone specimen is computed using complex frequency-domain finite element analysis. At the higher frequencies considered, the breakdown of Poisueille flow in Haversian canals is modeled by introduction of a complex fluid viscosity. Peak bone fluid pressures are found to increase linearly with loading frequency in proportion to peak bone stress up to frequencies of approximately 10 kHz. Haversian fluid shear stresses are found to increase linearly with excitation frequency and loading magnitude up until the breakdown of Poisueille flow. Tan δ values associated with the energy dissipated by load-induced fluid flow are also compared with values measured experimentally in a concurrent broadband spectral analysis of bone. The computational models indicate that fluid shear stresses and fluid pressures in the Haversian system could, under physiologically realistic loading, easily reach the level of a few Pascals, which have been shown in other works to elicit cell responses in vitro.


2001 ◽  
Author(s):  
Yixian Qin ◽  
Anita Saldanha ◽  
Tamara Kaplan

Abstract Load-generated intracortical fluid flow is proposed to be an important mediator for regulating bone mass and morphology [1]. Although the mechanism of cellular response to induced flow parameters, i.e., fluid pressure, pressure gradient, velocity, and fluid shear stress, are not yet clear, interstitial fluid flow driven by loading may be necessary to explain the adaptive response of bone, which is either coupled with load-induced strain magnitude or independent with matrix strain per se [2]. It has been demonstrated that load-induced intracortical fluid flow is contributed by both bone matrix deformation and induced intramedullary (IM) pressure [3]. To examine the hypothesis of fluid flow generated adaptation, it is necessary to test the mechanism under the circumstances of solely fluid induced bone adaptation in the absence of matrix deformation. While our previous data has demonstrated that bone fluid flow and its associated streaming potential product can be influenced by the dynamic IM pressure quantitatively [4], the objective of this study was to evaluate fluid induced bone adaptation in an avian ulna model using oscillatory IM fluid pressure loading in the absence of bone matrix strain. The potential fluid pathway was measured in the model.


2000 ◽  
Vol 122 (4) ◽  
pp. 387-393 ◽  
Author(s):  
J. You ◽  
C. E. Yellowley ◽  
H. J. Donahue ◽  
Y. Zhang ◽  
Q. Chen ◽  
...  

Although it is well accepted that bone tissue metabolism is regulated by external mechanical loads, it remains unclear to what load-induced physical signals bone cells respond. In this study, a novel computer-controlled stretch device and parallel plate flow chamber were employed to investigate cytosolic calcium Ca2+i mobilization in response to a range of dynamic substrate strain levels (0.1–10 percent, 1 Hz) and oscillating fluid flow (2 N/m2, 1 Hz). In addition, we quantified the effect of dynamic substrate strain and oscillating fluid flow on the expression of mRNA for the bone matrix protein osteopontin (OPN). Our data demonstrate that continuum strain levels observed for routine physical activities (<0.5 percent) do not induce Ca2+i responses in osteoblastic cells in vitro. However, there was a significant increase in the number of responding cells at larger strain levels. Moreover, we found no change in osteopontin mRNA level in response to 0.5 percent strain at 1 Hz. In contrast, oscillating fluid flow predicted to occur in the lacunar–canalicular system due to routine physical activities (2 N/m2, 1 Hz) caused significant increases in both Ca2+i and OPN mRNA. These data suggest that, relative to fluid flow, substrate deformation may play less of a role in bone cell mechanotransduction associated with bone adaptation to routine loads. [S0148-0731(00)01204-8]


Author(s):  
Kridsanapong Boonpen ◽  
Pruet Kowitwarangkul ◽  
Patiparn Ninpetch ◽  
Nadnapang Phophichit ◽  
Piyapat Chuchuay ◽  
...  

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