Spring 2005 Bone Seminar Series

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February 8, 2005 Bone Seminar:
Luis Cardoso Landa PhD on “On the Ultrasonic Characterization of Anisotropic Cancellous Bone: An In Vitro Experimental and Theoretical Study Based on a Modified Biot’s Theory”

March 8, 2005 Bone Seminar:
J. Chris Fritton, PhD candidate, on “Mechanical Loading Induced Adaptations of the Mouse Tibia”

April 12, 2005 Bone Seminar:
X. Edward Guo PhD on “Mechanobiology of Bone: In Vivo and In Vitro Studies”

May 10, 2005 Bone Seminar:
Sheldon Weinbaum PhD “Mechanotransduction and Strain Amplification in Bone Cell Processes”

February 8, 2005 Bone Seminar

Speaker: Luis Cardoso Landa PhD, Postdoctoral Research Fellow, Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY

Topic: On the Ultrasonic Characterization of Anisotropic Cancellous Bone: An In Vitro Experimental and Theoretical Study Based on a Modified Biot’s Theory

Dr. Cardoso Landa’s Research Interests: The bone mechanotransduction processes regulated by osteocytes and the assessment of bone mechanical properties through different experimental, mathematical, and computational approaches.

Abstract
Currently, the approach most widely used to examine bone loss is bone densitometry, which measures bone mass density by x-ray absorptiometry. Recently bone ultrasound attenuation (BUA) has seen wider clinical use. However, osteoporosis is not only characterized by a decreased bone mass density, but also by changes in the microstructure. These mass/density-based approaches cannot show the microarchitectural aspects of cancellous bone that are key to fully describing bone’s mechanical integrity.

In the material sciences field, ultrasonic wave propagation is a widely used nondestructive test to estimate the anisotropic mechanical properties of a media in an accurate manner. An acoustic wave is a mechanical disturbance reflecting the elasticity of the material where it is propagated. In a poroelastic media, wave velocity is affected by the mass quantity and the spatial distribution of the solid and fluid constituting the composite. If the porous media exhibit different mechanical properties for different directions of the space (mechanical anisotropy), it will accordingly exhibit different ultrasonic velocities (acoustic anisotropy), as shown in the figure above.

Nevertheless, a complex relationship exists between acoustic and mechanical properties in cancellous bone. The intimate processes determining the ultrasonic wave propagation phenomena in porous media are not only the consequence of elastic phenomenon, but also reflect inertial and viscous effects due to the interaction between the solid and fluid phases, which are frequency-dependent.

Recently, an experimental and theoretical study to understand ultrasonic wave propagation on anisotropic cancellous bone was developed. In the experimental studies, human and bovine cancellous bones from different skeletal sites, exhibiting a large variability in porosity and microstructure, were evaluated in multiple directions. The porosity (and correlatively the bone mass density) was found to be a low predictor of the velocities and the mechanical properties of cancellous bone. As the variability in measured wave velocities was hypothesized related to the microstructure of bone, a novel architectural-density-based model of wave propagation was developed based on the Biot’s theory. This model describes the velocity of waves as a function of porosity, structural parameters, tissue properties, and frequency of propagated ultrasonic waves.

The predictability of the measured velocities and mechanical properties for the different orthogonal directions of the samples analyzed as a function of density and microstructure was highly improved, when compared to the density-based approach. Better estimation of bone mechanical properties is expected to result in enhanced discrimination of osteoporotic and nonosteoporotic bone. This approach provides the potential to use ultrasound measurements in bone to examine tissue architecture in addition to bone mass.

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March 8, 2005 Bone Seminar

Speaker: J. Chris Fritton, PhD candidate, Laboratory for Biomedical Mechanics, Hospital for Special Surgery, New York, NY

Topic: Mechanical Loading Induced Adaptations of the Mouse Tibia

Dr. Fritton ’s Research Interests: Understanding mechanical and hormonal effects on bone at the organ and tissue level; in vivo mechanical loading; mineral assessment by x-ray techniques such as quantitative microcomputed tomography; mouse models for the study of bone physiology

Abstract
Adaptation to mechanical loading has been studied extensively in cortical bone, but not in cancellous bone. However, combined cortical/cancellous sites at the ends of long bones and in the spine are more relevant to osteoporosis and related fracture risk. The experiments to be discussed tested the hypotheses that adaptation to daily, in vivo, cyclic, axial loading of a long bone would (1) inhibit the bone loss associated with androgen hormone deficiency; (2) increase bone mineral content under normal hormone levels; (3) be greater at cancellous than at cortical sites; and (4) possibly depend on the term and level of loading. Compressive loads were applied to the 10-week-old, male C57BL/6 mouse tibia. Adaptation was quantified at the completion of loading by directly comparing volumetric bone mineral content between loaded and contralateral limbs by microcomputed tomography. Increases in mineral content were site-specific with the greatest responses found in the proximal metaphysis. Furthermore, bone volume fraction and average trabecular thickness of cancellous bone in the proximal tibia were increased. Diaphyseal responses, including cross-sectional moments of inertia, generally decreased along the length from proximal to distal. Loading terms (2 vs. 6 weeks) produced similar results. That loading inhibits bone loss and increases bone volume and fraction at a metaphyseal site motivates exploring the use of mechanical loading to attain greater peak bone mass and combat osteoporosis.

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April 12, 2005 Bone Seminar

Speaker: X. Edward Guo PhD, Director, Bone Bioengineering Laboratory, Associate Professor of Bioengineering, Columbia University, New York, NY

Topic: Mechanobiology of Bone: In Vivo and In Vitro Studies

Dr. Guo ’s Research Interests: Mechanobiology of bone, computational mechanics of trabecular bone, micromechanics of bone tissue

Abstract
Bone adapts in response to its mechanical environment. A quantitative characterization of the relationship between bone adaptation and mechanical loading and establishment of underlying cellular and molecular mechanism of bone adaptation are important in the understanding of the etiology of age-related bone fractures, optimal design of total joint replacements, and prevention of bone loss due to microgravity. In our laboratory, we have developed three new model systems for the study of mechanobiology of bone: an in vivo rat tail vertebrae model, an in vitro trabecular bone explant model, and an in vitro micropatterned osteocytic network model. In the first model system, an intact vertebral bone is subjected to controlled mechanical loading, while in the in vitro trabecular bone explant model, osteocytes in their native trabecular bone matrix are maintained alive in vitro and allowed for controlled seeding of osteoblasts and/or osteoclasts. Combining with high-resolution microimage-based finite-element modeling techniques, a quantitative assessment of mechanotransduction mechanisms involving all three types of bone cells can be examined. In the second in vitro system, 2D and 3D osteocytes networks have been developed using modern microfabrication techniques while allowing controlled interactions with osteoblasts and/or osteoclasts. New experimental findings from these new in vivo and in vitro models regarding a century-old hypothesis of trabecular bone adaptation, Wolff's Law, will be presented.

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May 17, 2005 Bone Seminar

Speaker: Sheldon Weinbaum PhD, CUNY Distinguished Professor of Engineering, The City College of New York

Topic: Mechanotransduction and Strain Amplification in Bone Cell Processes

Dr. Weinbaum’s Research Interests: Mechanotransduction in all tissues, including bone, kidney, intestines, cardiovascular system, and ear. In the past Dr. Weinbaum has studied transport and heat transfer in the microcirculation and LDL transport across vascular endothelium in atherogenesis.

Abstract
A paradox in bone tissue is that tissue-level strains due to animal and human locomotion are too small to initiate intracellular chemical responses directly. A model recently was proposed to resolve this paradox, which predicts that the fluid flow through the pericellular matrix in the lacunar-canalicular porosity due to mechanical loading can induce strains in the actin filament bundles of the cytoskeleton that are more than an order of magnitude larger than tissue level strains. In this study, we greatly refine this model by using the latest ultrastructural data for the cell process cytoskeleton, the tethering elements that attach the process to the canalicular wall and their finite flexural rigidity EI. We construct a much more realistic 3D model for the osteocyte process and then use large-deformation “elastica” theory for finite EI to predict the deformed shape of the tethering elements and the hoop strain on the central actin bundle. Our model predicts a cell process that is 3 times stiffer than in a previous study but hoop strain of >0.5% for tissue-level strains of >1,000 microstrain at 1 Hz and >250 microstrain at frequencies >10 Hz. We propose that this strain-amplification model provides a more likely hypothesis for the excitation of osteocytes than the previously proposed fluid-shear hypothesis.

Note: This presentation is based on the paper “Mechanotransduction and strain amplification in osteocyte cell processes and flow across the endothelial glycocalyx” by Y. Han, S. C. Cowin, M. B. Schaffler, and S. Weinbaum, published in 2004 in the Proceedings of the National Academy of Sciences of the United States of America (Volume 101, Issue 47, pages 16689-16694).

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