TY - JOUR
T1 - Modeling the onset and propagation of trabecular bone microdamage during low-cycle fatigue
AU - Kosmopoulos, Victor
AU - Schizas, Constantin
AU - Keller, Tony S.
N1 - Funding Information:
The research was supported by the United States Department of Energy's Experimental Program to Stimulate Competitive Research (DOE EPSCoR) and the National Aeronautics and Space Administration's (NASA) EPSCoR.
PY - 2008
Y1 - 2008
N2 - Relatively small amounts of microdamage have been suggested to have a major effect on the mechanical properties of bone. A significant reduction in mechanical properties (e.g. modulus) can occur even before the appearance of microcracks. This study uses a novel non-linear microdamaging finite-element (FE) algorithm to simulate the low-cycle fatigue behavior of high-density trabecular bone. We aimed to investigate if diffuse microdamage accumulation and concomitant modulus reduction, without the need for complete trabecular strut fracture, may be an underlining mechanism for low-cycle fatigue failure (defined as a 30% reduction in apparent modulus). A μCT constructed FE model was subjected to a single cycle monotonic compression test, and constant and variable amplitude loading scenarios to study the initiation and accumulation of low-cycle fatigue microdamage. Microcrack initiation was simulated using four damage criteria: 30%, 40%, 50% and 60% reduction in bone element modulus (el-MR). Evaluation of structural (apparent) damage using the four different tissue level damage criteria resulted in specimen fatigue failure at 72, 316, 969 and 1518 cycles for the 30%, 40%, 50% and 60% el-MR models, respectively. Simulations based on the 50% el-MR model were consistent with previously published experimental findings. A strong, significant non-linear, power law relationship was found between cycles to failure (N) and effective strain (Δσ/E0): N=1.394×10-25(Δσ/E0)-12.17, r2=0.97, p<0.0001. The results suggest that microdamage and microcrack propagation, without the need for complete trabecular strut fracture, are mechanisms for high-density trabecular bone failure. Furthermore, the model is consistent with previous numerical fatigue simulations indicating that microdamage to a small number of trabeculae results in relatively large specimen modulus reductions and rapid failure.
AB - Relatively small amounts of microdamage have been suggested to have a major effect on the mechanical properties of bone. A significant reduction in mechanical properties (e.g. modulus) can occur even before the appearance of microcracks. This study uses a novel non-linear microdamaging finite-element (FE) algorithm to simulate the low-cycle fatigue behavior of high-density trabecular bone. We aimed to investigate if diffuse microdamage accumulation and concomitant modulus reduction, without the need for complete trabecular strut fracture, may be an underlining mechanism for low-cycle fatigue failure (defined as a 30% reduction in apparent modulus). A μCT constructed FE model was subjected to a single cycle monotonic compression test, and constant and variable amplitude loading scenarios to study the initiation and accumulation of low-cycle fatigue microdamage. Microcrack initiation was simulated using four damage criteria: 30%, 40%, 50% and 60% reduction in bone element modulus (el-MR). Evaluation of structural (apparent) damage using the four different tissue level damage criteria resulted in specimen fatigue failure at 72, 316, 969 and 1518 cycles for the 30%, 40%, 50% and 60% el-MR models, respectively. Simulations based on the 50% el-MR model were consistent with previously published experimental findings. A strong, significant non-linear, power law relationship was found between cycles to failure (N) and effective strain (Δσ/E0): N=1.394×10-25(Δσ/E0)-12.17, r2=0.97, p<0.0001. The results suggest that microdamage and microcrack propagation, without the need for complete trabecular strut fracture, are mechanisms for high-density trabecular bone failure. Furthermore, the model is consistent with previous numerical fatigue simulations indicating that microdamage to a small number of trabeculae results in relatively large specimen modulus reductions and rapid failure.
KW - Cancellous bone
KW - Finite element
KW - Low-cycle fatigue
KW - Microdamage
KW - Trabecular bone
UR - http://www.scopus.com/inward/record.url?scp=38749123943&partnerID=8YFLogxK
U2 - 10.1016/j.jbiomech.2007.10.020
DO - 10.1016/j.jbiomech.2007.10.020
M3 - Article
C2 - 18076887
AN - SCOPUS:38749123943
SN - 0021-9290
VL - 41
SP - 515
EP - 522
JO - Journal of Biomechanics
JF - Journal of Biomechanics
IS - 3
ER -