Measurement of microstructural strain in cortical bone

Abstract

It is well known that mechanical factors affect bone remodeling such that increased mechanical demand results in net bone formation, whereas decreased demand results in net bone resorption. Current theories suggest that bone modeling and remodeling is controlled at the cellular level through signals mediated by osteocytes. The objective of this study was to investigate how macroscopically applied bone strains similar in magnitude to those that occur in vivo are manifest at the microscopic level in the bone matrix. Using a digital image correlation strain measurement technique, experimentally determined bone matrix strains around osteocyte lacuna resulting from macroscopic strains of approximately 2,000 microstrain (0.2%) reach levels of over 30,000 microstrain (3%) over fifteen times greater than the applied macroscopic strain. Strain patterns were highly heterogeneous and in some locations similar to observed microdamage around osteocyte lacuna indicating the resulting strains may represent the precursors to microdamage. This information may lead to a better understanding of how bone cells are affected by whole bone functional loading.

Strain amplification in bone mechanobiology: a computational investigation of the in vivo mechanics of osteocytes

“…However, these studies did not investigate direct mechanical loading more than 5000 m1. Therefore, it is possible that the elevated strain levels (more than 10 000 m1) predicted in our models and previous experimental studies [11][12][13] may also stimulate these biochemical osteogenic responses, particularly owing to the strain amplification effects of the PCM and ECM projections.…”

“…It must be noted that those experimental studies characterized strain in the lacunae, as opposed to strain measured in the cell [11][12][13], and also that the authors proposed that microdamage artefacts might be exacerbating local tissue deformation [11][12][13]. Therefore, it is unlikely that such high strain levels would indeed be experienced by the osteocyte in vivo, and our results correlate better with average strains between 7500 and 20 000 m1 reported in experimental studies [11][12][13]. Our results demonstrate that the in vivo geometrical characteristics of the surrounding ECM and PCM lead to a high degree of strain transfer into the cell body and must be considered for understanding mechanotransduction in osteocytes in vivo.…”

Noninvasive Determination of Ligament Strain with Deformable Image Registration

“…Practical implementation for strain measurement requires manual alignment of images to account for rigid body rotation. 34 For Hyperelastic Warping, the constitutive model is unaffected by rigid body rotations by design. A limitation of Hyperelastic Warping is that the computational expense associated with solving the equations emanating from the combined energy functional is considerably higher than that associated with analyses based on texture correlation.…”

“…Techniques that have been used for noninvasive strain measurement in soft tissues include texture correlation 5,6,18 and magnetic resonance (MR) tagging. 33,35,50 Texture correlation requires the presence of well-defined textural details that can be tracked between image pairs and does not provide any constraint to ensure diffeomorphic mappings for large deformations, 34 while MR tagging is limited to loadings that can be repeated cyclically because of the need to tag and then acquire MR data along separate spatial directions sequentially. 33 Historically, even invasive measurement of ligament strain has proven to be challenging because constraints in access and visibility to the ligament limit the application of traditional optical or strain gauge techniques.…”

Letter to the Editor commenting on “Multilevel finite element modeling for the prediction of local cellular deformation in bone,” Deligianni DD and Apostolopoulos CA (2008) Biomech Model Mechanobiol 7(2):151–159

“…We currently have no reasons to believe that the ultimate strain of the mineralised extracellular matrix at the cells scale should be anyway different. Given this, if the amplification Deligianni and Apostolopoulos (2008) predict is true (which seems to be supported by some recent experimental data; Nicolella et al 2005), physiological loading would produce microfractures of the extracellular matrix, before direct mechanotransduction to cells. Microfractures disrupt the canaliculi (O'Brien et al 2005) and there are evidences that they also break the osteocytarian processes inside the canaliculi (Hazenberg et al 2006).…”