Abstract
As the average age of the population has increased, the incidence of age-related bone fracture has also increased. While some of the increase of fracture incidence with age is related to loss of bone mass, a significant part of the risk is unexplained and may be caused by changes in intrinsic material properties of the hard tissue. This investigation focused on understanding how changes to the intrinsic damage properties affect bone fragility. We hypothesized that the intrinsic (μm) damage properties of bone tissue strongly and nonlinearly affect mechanical behavior at the apparent (whole tissue, cm) level. The importance of intrinsic properties on the apparent level behavior of trabecular bone tissue was investigated using voxel based finite element analysis. Trabecular bone cores from human T12 vertebrae were scanned using microcomputed tomography (μ'CT) and the images used to build nonlinear finite element models. Isotropic and initially homogenous material properties were used for all elements. The elastic modulus (Ei) of individual elements was reduced with a secant damage rule relating only principal tensile tissue strain to modulus damage. Apparent level resistance to fracture as a function of changes in the intrinsic damage properties was measured using the mechanical energy to failure per unit volume (apparent toughness modulus, W a) and the apparent yield strength (σay, calculated using the 0.2% offset). Intrinsic damage properties had a profound nonlinear effect on the apparent tissue level mechanical response. Intrinsic level failure occurs prior to apparent yield strength (σay). Apparent yield strength (σay) and toughness vary strongly (1200% and 400%, respectively) with relatively small changes in the intrinsic damage behavior. The range of apparent maximum stresses predicted by the models was consistent with those measured experimentally for these trabecular bone cores from the experimental axial compressive loading (experimental: σmax=3.0- 4.3 MPa; modeling: σmax=2-16 MPa). This finding differs significantly from previous studies based on nondamaging intrinsic material models. Further observations were that this intrinsic damage model reproduced important experimental apparent level behaviors including softening after peak load, microdamage accumulation before apparent yield (0.2% offset), unload softening, and sensitivity of the apparent level mechanical properties to variability of the intrinsic properties.
| Original language | English (US) |
|---|---|
| Article number | 011004 |
| Journal | Journal of Biomechanical Engineering |
| Volume | 135 |
| Issue number | 1 |
| DOIs | |
| State | Published - 2013 |
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ASJC Scopus subject areas
- Biomedical Engineering
- Physiology (medical)
Cite this
The importance of intrinsic damage properties to bone fragility : A finite element study. / Hardisty, M. R.; Zauel, R.; Stover, Susan M; Fyhrie, David P.
In: Journal of Biomechanical Engineering, Vol. 135, No. 1, 011004, 2013.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The importance of intrinsic damage properties to bone fragility
T2 - A finite element study
AU - Hardisty, M. R.
AU - Zauel, R.
AU - Stover, Susan M
AU - Fyhrie, David P
PY - 2013
Y1 - 2013
N2 - As the average age of the population has increased, the incidence of age-related bone fracture has also increased. While some of the increase of fracture incidence with age is related to loss of bone mass, a significant part of the risk is unexplained and may be caused by changes in intrinsic material properties of the hard tissue. This investigation focused on understanding how changes to the intrinsic damage properties affect bone fragility. We hypothesized that the intrinsic (μm) damage properties of bone tissue strongly and nonlinearly affect mechanical behavior at the apparent (whole tissue, cm) level. The importance of intrinsic properties on the apparent level behavior of trabecular bone tissue was investigated using voxel based finite element analysis. Trabecular bone cores from human T12 vertebrae were scanned using microcomputed tomography (μ'CT) and the images used to build nonlinear finite element models. Isotropic and initially homogenous material properties were used for all elements. The elastic modulus (Ei) of individual elements was reduced with a secant damage rule relating only principal tensile tissue strain to modulus damage. Apparent level resistance to fracture as a function of changes in the intrinsic damage properties was measured using the mechanical energy to failure per unit volume (apparent toughness modulus, W a) and the apparent yield strength (σay, calculated using the 0.2% offset). Intrinsic damage properties had a profound nonlinear effect on the apparent tissue level mechanical response. Intrinsic level failure occurs prior to apparent yield strength (σay). Apparent yield strength (σay) and toughness vary strongly (1200% and 400%, respectively) with relatively small changes in the intrinsic damage behavior. The range of apparent maximum stresses predicted by the models was consistent with those measured experimentally for these trabecular bone cores from the experimental axial compressive loading (experimental: σmax=3.0- 4.3 MPa; modeling: σmax=2-16 MPa). This finding differs significantly from previous studies based on nondamaging intrinsic material models. Further observations were that this intrinsic damage model reproduced important experimental apparent level behaviors including softening after peak load, microdamage accumulation before apparent yield (0.2% offset), unload softening, and sensitivity of the apparent level mechanical properties to variability of the intrinsic properties.
AB - As the average age of the population has increased, the incidence of age-related bone fracture has also increased. While some of the increase of fracture incidence with age is related to loss of bone mass, a significant part of the risk is unexplained and may be caused by changes in intrinsic material properties of the hard tissue. This investigation focused on understanding how changes to the intrinsic damage properties affect bone fragility. We hypothesized that the intrinsic (μm) damage properties of bone tissue strongly and nonlinearly affect mechanical behavior at the apparent (whole tissue, cm) level. The importance of intrinsic properties on the apparent level behavior of trabecular bone tissue was investigated using voxel based finite element analysis. Trabecular bone cores from human T12 vertebrae were scanned using microcomputed tomography (μ'CT) and the images used to build nonlinear finite element models. Isotropic and initially homogenous material properties were used for all elements. The elastic modulus (Ei) of individual elements was reduced with a secant damage rule relating only principal tensile tissue strain to modulus damage. Apparent level resistance to fracture as a function of changes in the intrinsic damage properties was measured using the mechanical energy to failure per unit volume (apparent toughness modulus, W a) and the apparent yield strength (σay, calculated using the 0.2% offset). Intrinsic damage properties had a profound nonlinear effect on the apparent tissue level mechanical response. Intrinsic level failure occurs prior to apparent yield strength (σay). Apparent yield strength (σay) and toughness vary strongly (1200% and 400%, respectively) with relatively small changes in the intrinsic damage behavior. The range of apparent maximum stresses predicted by the models was consistent with those measured experimentally for these trabecular bone cores from the experimental axial compressive loading (experimental: σmax=3.0- 4.3 MPa; modeling: σmax=2-16 MPa). This finding differs significantly from previous studies based on nondamaging intrinsic material models. Further observations were that this intrinsic damage model reproduced important experimental apparent level behaviors including softening after peak load, microdamage accumulation before apparent yield (0.2% offset), unload softening, and sensitivity of the apparent level mechanical properties to variability of the intrinsic properties.
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U2 - 10.1115/1.4023090
DO - 10.1115/1.4023090
M3 - Article
C2 - 23363215
AN - SCOPUS:84871913387
VL - 135
JO - Journal of Biomechanical Engineering
JF - Journal of Biomechanical Engineering
SN - 0148-0731
IS - 1
M1 - 011004
ER -