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Christopher J Hernandez - One of the best experts on this subject based on the ideXlab platform.
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finite element models predict the location of Microdamage in cancellous bone following uniaxial loading
Journal of Biomechanics, 2015Co-Authors: M G Goff, Floor M Lambers, Christopher J Hernandez, R M Sorna, Tony M KeavenyAbstract:High-resolution finite element models derived from micro-computed tomography images are often used to study the effects of trabecular microarchitecture and loading mode on tissue stress, but the degree to which existing finite element methods correctly predict the location of tissue failure is not well characterized. In the current study, we determined the relationship between the location of highly strained tissue, as determined from high-resolution finite element models, and the location of tissue Microdamage, as determined from three-dimensional fluoroscopy imaging, which was performed after the Microdamage was generated in-vitro by mechanical testing. Fourteen specimens of human vertebral cancellous bone were assessed (8 male donors, 2 female donors, 47-78 years of age). Regions of stained Microdamage, were 50-75% more likely to form in highly strained tissue (principal strains exceeding 0.4%) than elsewhere, and generally the locations of the regions of Microdamage were significantly correlated (p<0.05) with the locations of highly strained tissue. This spatial correlation was stronger for the largest regions of Microdamage (≥1,000,000μm(3) in volume); 87% of large regions of Microdamage were located near highly strained tissue. Together, these findings demonstrate that there is a strong correlation between regions of Microdamage and regions of high strain in human cancellous bone, particularly for the biomechanically more important large instances of Microdamage.
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Finite element models predict the location of Microdamage in cancellous bone following uniaxial loading
Journal of biomechanics, 2015Co-Authors: M G Goff, Floor M Lambers, R M Sorna, Tony M Keaveny, Christopher J HernandezAbstract:High-resolution finite element models derived from micro-computed tomography images are often used to study the effects of trabecular microarchitecture and loading mode on tissue stress, but the degree to which existing finite element methods correctly predict the location of tissue failure is not well characterized. In the current study, we determined the relationship between the location of highly strained tissue, as determined from high-resolution finite element models, and the location of tissue Microdamage, as determined from three-dimensional fluoroscopy imaging, which was performed after the Microdamage was generated in-vitro by mechanical testing. Fourteen specimens of human vertebral cancellous bone were assessed (8 male donors, 2 female donors, 47-78 years of age). Regions of stained Microdamage, were 50-75% more likely to form in highly strained tissue (principal strains exceeding 0.4%) than elsewhere, and generally the locations of the regions of Microdamage were significantly correlated (p
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fatigue induced Microdamage in cancellous bone occurs distant from resorption cavities and trabecular surfaces
Bone, 2015Co-Authors: M G Goff, Floor M Lambers, Clare M Rimnac, Christopher J Hernandez, T M Nguyen, J SungAbstract:Impaired bone toughness is increasingly recognized as a contributor to fragility fractures. At the tissue level, toughness is related to the ability of bone tissue to resist the development of microscopic cracks or other tissue damage. While most of our understanding of Microdamage is derived from studies of cortical bone, the majority of fragility fractures occur in regions of the skeleton dominated by cancellous bone. The development of tissue Microdamage in cancellous bone may differ from that in cortical bone due to differences in microstructure and tissue ultrastructure. To gain insight into how Microdamage accumulates in cancellous bone we determined the changes in number, size and location of Microdamage sites following different amounts of cyclic compressive loading. Human vertebral cancellous bone specimens (n=32, 10 male donors, 6 female donors, age 76 ± 8.8, mean ± SD) were subjected to sub-failure cyclic compressive loading and Microdamage was evaluated in three-dimensions. Only a few large Microdamage sites (the largest 10%) accounted for 70% of all Microdamage caused by cyclic loading. The number of large Microdamage sites was a better predictor of reductions in Young's modulus caused by cyclic loading than overall damage volume fraction (DV/BV). The majority of Microdamage volume (69.12 ± 7.04%) was located more than 30 μm (the average erosion depth) from trabecular surfaces, suggesting that Microdamage occurs primarily within interstitial regions of cancellous bone. Additionally, Microdamage was less likely to be near resorption cavities than other bone surfaces (p<0.05), challenging the idea that stress risers caused by resorption cavities influence fatigue failure of cancellous bone. Together, these findings suggest that reductions in apparent level mechanical performance during fatigue loading are the result of only a few large Microdamage sites and that Microdamage accumulation in fatigue is likely dominated by heterogeneity in tissue material properties rather than stress concentrations caused by micro-scale geometry.
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Fatigue-induced Microdamage in cancellous bone occurs distant from resorption cavities and trabecular surfaces.
Bone, 2015Co-Authors: M G Goff, Floor M Lambers, Clare M Rimnac, T M Nguyen, J Sung, Christopher J HernandezAbstract:Impaired bone toughness is increasingly recognized as a contributor to fragility fractures. At the tissue level, toughness is related to the ability of bone tissue to resist the development of microscopic cracks or other tissue damage. While most of our understanding of Microdamage is derived from studies of cortical bone, the majority of fragility fractures occur in regions of the skeleton dominated by cancellous bone. The development of tissue Microdamage in cancellous bone may differ from that in cortical bone due to differences in microstructure and tissue ultrastructure. To gain insight into how Microdamage accumulates in cancellous bone we determined the changes in number, size and location of Microdamage sites following different amounts of cyclic compressive loading. Human vertebral cancellous bone specimens (n=32, 10 male donors, 6 female donors, age 76 ± 8.8, mean ± SD) were subjected to sub-failure cyclic compressive loading and Microdamage was evaluated in three-dimensions. Only a few large Microdamage sites (the largest 10%) accounted for 70% of all Microdamage caused by cyclic loading. The number of large Microdamage sites was a better predictor of reductions in Young's modulus caused by cyclic loading than overall damage volume fraction (DV/BV). The majority of Microdamage volume (69.12 ± 7.04%) was located more than 30 μm (the average erosion depth) from trabecular surfaces, suggesting that Microdamage occurs primarily within interstitial regions of cancellous bone. Additionally, Microdamage was less likely to be near resorption cavities than other bone surfaces (p
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the effects of tensile compressive loading mode and microarchitecture on Microdamage in human vertebral cancellous bone
Journal of Biomechanics, 2014Co-Authors: Floor M Lambers, Amanda R Bouman, Christopher J Hernandez, Tony M Keaveny, Evgeniy V TkachenkoAbstract:The amount of Microdamage in bone tissue impairs mechanical performance and may act as a stimulus for bone remodeling. Here we determine how loading mode (tension vs. compression) and microstructure (trabecular microarchitecture, local trabecular thickness, and presence of resorption cavities) influence the number and volume of Microdamage sites generated in cancellous bone following a single overload. Twenty paired cylindrical specimens of human vertebral cancellous bone from 10 donors (47–78 years) were mechanically loaded to apparent yield in either compression or tension, and imaged in three dimensions for microarchitecture and Microdamage (voxel size 0.7×0.7×5.0 μm3). We found that the overall proportion of damaged tissue was greater (p=0.01) for apparent tension loading (3.9±2.4%, mean±SD) than for apparent compression loading (1.9±1.3%). Individual Microdamage sites generated in tension were larger in volume (p<0.001) but not more numerous (p=0.64) than sites in compression. For both loading modes, the proportion of damaged tissue varied more across donors than with bone volume fraction, traditional measures of microarchitecture (trabecular thickness, trabecular separation, etc.), apparent Young׳s modulus, or strength. Microdamage tended to occur in regions of greater trabecular thickness but not near observable resorption cavities. Taken together, these findings indicate that, regardless of loading mode, accumulation of Microdamage in cancellous bone after monotonic loading to yield is influenced by donor characteristics other than traditional measures of microarchitecture, suggesting a possible role for tissue material properties.
David B. Burr - One of the best experts on this subject based on the ideXlab platform.
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microcrack associated bone remodeling is rarely observed in biopsies from athletes with medial tibial stress syndrome
Journal of Bone and Mineral Metabolism, 2019Co-Authors: Marinus Winters, David B. Burr, Henk Van Der Hoeven, Keith W Condon, Johan Bellemans, Maarten H MoenAbstract:The pathology of medial tibial stress syndrome (MTSS) is unknown. Studies suggest that MTSS is a bony overload injury, but histological evidence is sparse. The presence of Microdamage, and its potential association with targeted remodeling, could provide evidence for the pathogenesis of MTSS. Understanding the pathology underlying MTSS could contribute to effective preventative and therapeutic interventions for MTSS. Our aim was to retrospectively evaluate biopsies, previously taken from the painful area in athletes with MTSS, for the presence of linear microcracks, diffuse Microdamage and remodeling. Biopsies, previously taken from athletes with MTSS, were evaluated at the Department of Anatomy and Cell Biology at the Indiana University. After preparing the specimens by en bloc staining, one investigator evaluated the presence of linear microcracks, diffuse Microdamage and remodeling in the specimens. A total of six biopsies were evaluated for the presence of Microdamage and remodeling. Linear microcracks were found in 4 out of 6 biopsies. Cracking in one of these specimens was artefactual due to the biopsy procedure. No diffuse Microdamage was seen in any of the specimens, and only one potential remodeling front in association with the microcracks. We found only linear microcracks in vivo in biopsies taken from the painful area in 50% of the athletes with MTSS, consistent with the relationship between linear cracks and fatigue-associated overloading of bone. The nearly universal absence of a repair reaction was notable. This suggests that unrepaired Microdamage accumulation may underlie the pathophysiological basis for MTSS in athletes.
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suppressed bone turnover by bisphosphonates increases Microdamage accumulation and reduces some biomechanical properties in dog rib
Journal of Bone and Mineral Research, 2010Co-Authors: Tasuku Mashiba, Mark R Forwood, Charles H Turner, T Hirano, Conrad C Johnston, David B. BurrAbstract:It has been hypothesized that suppression of bone remodeling allows Microdamage to accumulate, leading to increased bone fragility. This study evaluated the effects of reduced bone turnover produced by bisphosphonates on Microdamage accumulation and biomechanical properties of cortical bone in the dog rib. Thirty-six female beagles, 1-2 years old, were divided into three groups. The control group (CNT) was treated daily for 12 months with saline vehicle. The remaining two groups were treated daily with risedronate (RIS) at a dose of 0.5 mg/kg per day or alendronate (ALN) at 1.0 mg/kg per day orally. After sacrifice, the right ninth rib was assigned to cortical histomorphometry or Microdamage analysis. The left ninth rib was tested to failure in three-point bending. Total cross-sectional bone area was significantly increased in both RIS and ALN compared with CNT, whereas cortical area did not differ significantly among groups. One-year treatment with RIS or ALN significantly suppressed intracortical remodeling (RIS, 53%; ALN, 68%) without impairment of mineralization and significantly increased Microdamage accumulation in both RIS (155%) and ALN (322%) compared with CNT. Although bone strength and stiffness were not significantly affected by the treatments, bone toughness declined significantly in ALN (20%). Regression analysis showed a significant nonlinear relationship between suppressed intracortical bone remodeling and Microdamage accumulation as well as a significant linear relationship between Microdamage accumulation and reduced toughness. This study showed that suppression of bone turnover by high doses of bisphosphonates is associated with Microdamage accumulation and reduced some mechanical properties of bone.
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Teriparatide Reduces Bone Microdamage Accumulation in Postmenopausal Women Previously Treated With Alendronate
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2009Co-Authors: Harald Dobnig, David B. Burr, Jan J. Stepan, Dana Michalska, Adrien Sipos, Helmut Petto, Astrid Fahrleitner-pammer, Imre PavoAbstract:Suppression of bone turnover by bisphosphonates is associated with increased bone Microdamage accumulation in animal models. Our objective was to study the effects of teriparatide treatment on changes in Microdamage accumulation at the iliac crest in previously treatment-naive patients or in those switched from alendronate to teriparatide. Sixty-six postmenopausal women with osteoporosis (mean age, 68.0 yr; and mean BMD T-score of −2.8 at lumbar spine and −1.7 at total hip; 62% with prevalent fractures) entered this prospective, nonrandomized study and started with 24-mo 20 μg/d subcutaneous teriparatide treatment in monotherapy: 38 patients stopped previous alendronate treatment (10 mg/d or 70 mg/wk for a mean duration of 63.6 mo) and switched to teriparatide, whereas 28 were previously treatment naive. Thirty-one paired biopsies with two intact cortices were collected and analyzed for microstructure and Microdamage accumulation at baseline and after 24 mo of teriparatide administration. After 24 mo of teriparatide treatment, crack density (Cr.Dn), crack surface density (Cr.S.Dn), and crack length (Cr.Le) were decreased in previously alendronate-treated patients, whereas only Cr.Le was reduced in former treatment-naive patients. Patients with lower initial femoral neck BMD also showed a higher reduction of Microdamage accumulation. Better bone microarchitecture correlated positively, whereas bone turnover markers and age did not correlate with reduced Microdamage accumulation on teriparatide. In conclusion, teriparatide reduces Microdamage accumulation in the iliac crest of patients previously treated with alendronate. There is insufficient evidence to suggest that age or bone turnover would be associated with this change.
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Skeletal Microdamage: Less About Biomechanics and More About Remodeling
Clinical Reviews in Bone and Mineral Metabolism, 2008Co-Authors: Matthew R. Allen, David B. BurrAbstract:The mechanical consequences of skeletal Microdamage have been clearly documented using various experimental methods, yet recent experiments suggest that physiological levels of Microdamage accumulation are not sufficient to compromise the bones’ biomechanical properties. While great advances have been made in our understanding of the biomechanical implications of Microdamage, less is known concerning the physiological role of Microdamage in bone remodeling. Microdamage has been shown to act as a signal for bone remodeling, likely through a disruption of the osteocyte-canalicular network. Interestingly, age-related increases in Microdamage are not accompanied by increases in bone remodeling suggesting that the physiological mechanisms which link Microdamage and remodeling are compromised with aging.
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three years of alendronate treatment results in similar levels of vertebral Microdamage as after one year of treatment
Journal of Bone and Mineral Research, 2007Co-Authors: Matthew R. Allen, David B. BurrAbstract:Three years of daily alendronate treatment increases Microdamage in vertebral bone but does not significantly increase it beyond levels of Microdamage found after 1 yr of treatment. This suggests Microdamage accumulation peaks during the early period of bisphosphonate treatment and does not continue to accumulate with longer periods of treatment. Introduction: Clinically relevant doses of alendronate increase vertebral Microdamage by 4- to 5-fold in skeletally mature beagles after 1 yr of treatment. The goal of this study was to determine whether Microdamage would continue to accumulate with 3 yr of alendronate treatment in an intact beagle dog model. Materials and Methods: One-year-old female beagles were treated with daily oral doses of vehicle (VEH, 1 ml/kg/d) or alendronate (ALN, 0.2 or 1.0 mg/kg/d) for 3 yr. These ALN doses were chosen to approximate, on a milligram per kilogram basis, those used to treat osteoporosis (ALN0.2) and Paget's disease (ALN1.0). Microdamage accumulation, static and dynamic histomorphometry, densitometry, and mechanical properties of lumbar vertebrae were assessed. Comparisons were made among the three groups treated for 3 yr and also within each treatment group to animals treated under the same conditions for 1 yr. Results: Overall Microdamage accumulation (crack surface density) was not significantly higher in animals treated for 3 yr with either dose of ALN, whereas crack density increased significantly (100%; p < 0.05) with the higher dose of ALN compared with VEH. Both ALN doses significantly suppressed the rate of bone turnover (−60% versus VEH). There was no difference among groups for any of the structural biomechanical properties-ultimate load, stiffness, or energy absorption. However, when adjusted for areal BMD, ALN-treated animals had significantly lower energy absorption (−20%) compared with VEH. Toughness, the energy absorption capacity of the bone tissue, was significantly lower than VEH for both ALN0.2 (−27%) and ALN1.0 (−33%). Compared with animals treated for 1 yr, there was no significant difference in Microdamage accumulation for either ALN dose. VEH-treated animals had significantly lower bone turnover (−58%) and significantly higher levels of Microdamage (+300%) compared with values in 1-yr animals. Toughness was significantly lower in animals treated for 3 yr with ALN1.0 (−18%) compared with animals treated for 1 yr, whereas there was no difference in toughness between the two treatment durations for either VEH or ALN0.2. Conclusions: Although 3 yr of ALN treatment resulted in higher microcrack density in vertebral trabecular bone compared with control dogs, the amount of Microdamage was not significantly higher than animals treated for 1 yr with similar doses. This suggests that bisphosphonate-associated increases in Microdamage occur early in treatment. Because toughness continued to decline significantly over 3 yr of treatment at the higher ALN dose, decreases in toughness are probably not dependent on damage accumulation.
Floor M Lambers - One of the best experts on this subject based on the ideXlab platform.
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finite element models predict the location of Microdamage in cancellous bone following uniaxial loading
Journal of Biomechanics, 2015Co-Authors: M G Goff, Floor M Lambers, Christopher J Hernandez, R M Sorna, Tony M KeavenyAbstract:High-resolution finite element models derived from micro-computed tomography images are often used to study the effects of trabecular microarchitecture and loading mode on tissue stress, but the degree to which existing finite element methods correctly predict the location of tissue failure is not well characterized. In the current study, we determined the relationship between the location of highly strained tissue, as determined from high-resolution finite element models, and the location of tissue Microdamage, as determined from three-dimensional fluoroscopy imaging, which was performed after the Microdamage was generated in-vitro by mechanical testing. Fourteen specimens of human vertebral cancellous bone were assessed (8 male donors, 2 female donors, 47-78 years of age). Regions of stained Microdamage, were 50-75% more likely to form in highly strained tissue (principal strains exceeding 0.4%) than elsewhere, and generally the locations of the regions of Microdamage were significantly correlated (p<0.05) with the locations of highly strained tissue. This spatial correlation was stronger for the largest regions of Microdamage (≥1,000,000μm(3) in volume); 87% of large regions of Microdamage were located near highly strained tissue. Together, these findings demonstrate that there is a strong correlation between regions of Microdamage and regions of high strain in human cancellous bone, particularly for the biomechanically more important large instances of Microdamage.
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Finite element models predict the location of Microdamage in cancellous bone following uniaxial loading
Journal of biomechanics, 2015Co-Authors: M G Goff, Floor M Lambers, R M Sorna, Tony M Keaveny, Christopher J HernandezAbstract:High-resolution finite element models derived from micro-computed tomography images are often used to study the effects of trabecular microarchitecture and loading mode on tissue stress, but the degree to which existing finite element methods correctly predict the location of tissue failure is not well characterized. In the current study, we determined the relationship between the location of highly strained tissue, as determined from high-resolution finite element models, and the location of tissue Microdamage, as determined from three-dimensional fluoroscopy imaging, which was performed after the Microdamage was generated in-vitro by mechanical testing. Fourteen specimens of human vertebral cancellous bone were assessed (8 male donors, 2 female donors, 47-78 years of age). Regions of stained Microdamage, were 50-75% more likely to form in highly strained tissue (principal strains exceeding 0.4%) than elsewhere, and generally the locations of the regions of Microdamage were significantly correlated (p
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fatigue induced Microdamage in cancellous bone occurs distant from resorption cavities and trabecular surfaces
Bone, 2015Co-Authors: M G Goff, Floor M Lambers, Clare M Rimnac, Christopher J Hernandez, T M Nguyen, J SungAbstract:Impaired bone toughness is increasingly recognized as a contributor to fragility fractures. At the tissue level, toughness is related to the ability of bone tissue to resist the development of microscopic cracks or other tissue damage. While most of our understanding of Microdamage is derived from studies of cortical bone, the majority of fragility fractures occur in regions of the skeleton dominated by cancellous bone. The development of tissue Microdamage in cancellous bone may differ from that in cortical bone due to differences in microstructure and tissue ultrastructure. To gain insight into how Microdamage accumulates in cancellous bone we determined the changes in number, size and location of Microdamage sites following different amounts of cyclic compressive loading. Human vertebral cancellous bone specimens (n=32, 10 male donors, 6 female donors, age 76 ± 8.8, mean ± SD) were subjected to sub-failure cyclic compressive loading and Microdamage was evaluated in three-dimensions. Only a few large Microdamage sites (the largest 10%) accounted for 70% of all Microdamage caused by cyclic loading. The number of large Microdamage sites was a better predictor of reductions in Young's modulus caused by cyclic loading than overall damage volume fraction (DV/BV). The majority of Microdamage volume (69.12 ± 7.04%) was located more than 30 μm (the average erosion depth) from trabecular surfaces, suggesting that Microdamage occurs primarily within interstitial regions of cancellous bone. Additionally, Microdamage was less likely to be near resorption cavities than other bone surfaces (p<0.05), challenging the idea that stress risers caused by resorption cavities influence fatigue failure of cancellous bone. Together, these findings suggest that reductions in apparent level mechanical performance during fatigue loading are the result of only a few large Microdamage sites and that Microdamage accumulation in fatigue is likely dominated by heterogeneity in tissue material properties rather than stress concentrations caused by micro-scale geometry.
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Fatigue-induced Microdamage in cancellous bone occurs distant from resorption cavities and trabecular surfaces.
Bone, 2015Co-Authors: M G Goff, Floor M Lambers, Clare M Rimnac, T M Nguyen, J Sung, Christopher J HernandezAbstract:Impaired bone toughness is increasingly recognized as a contributor to fragility fractures. At the tissue level, toughness is related to the ability of bone tissue to resist the development of microscopic cracks or other tissue damage. While most of our understanding of Microdamage is derived from studies of cortical bone, the majority of fragility fractures occur in regions of the skeleton dominated by cancellous bone. The development of tissue Microdamage in cancellous bone may differ from that in cortical bone due to differences in microstructure and tissue ultrastructure. To gain insight into how Microdamage accumulates in cancellous bone we determined the changes in number, size and location of Microdamage sites following different amounts of cyclic compressive loading. Human vertebral cancellous bone specimens (n=32, 10 male donors, 6 female donors, age 76 ± 8.8, mean ± SD) were subjected to sub-failure cyclic compressive loading and Microdamage was evaluated in three-dimensions. Only a few large Microdamage sites (the largest 10%) accounted for 70% of all Microdamage caused by cyclic loading. The number of large Microdamage sites was a better predictor of reductions in Young's modulus caused by cyclic loading than overall damage volume fraction (DV/BV). The majority of Microdamage volume (69.12 ± 7.04%) was located more than 30 μm (the average erosion depth) from trabecular surfaces, suggesting that Microdamage occurs primarily within interstitial regions of cancellous bone. Additionally, Microdamage was less likely to be near resorption cavities than other bone surfaces (p
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the effects of tensile compressive loading mode and microarchitecture on Microdamage in human vertebral cancellous bone
Journal of Biomechanics, 2014Co-Authors: Floor M Lambers, Amanda R Bouman, Christopher J Hernandez, Tony M Keaveny, Evgeniy V TkachenkoAbstract:The amount of Microdamage in bone tissue impairs mechanical performance and may act as a stimulus for bone remodeling. Here we determine how loading mode (tension vs. compression) and microstructure (trabecular microarchitecture, local trabecular thickness, and presence of resorption cavities) influence the number and volume of Microdamage sites generated in cancellous bone following a single overload. Twenty paired cylindrical specimens of human vertebral cancellous bone from 10 donors (47–78 years) were mechanically loaded to apparent yield in either compression or tension, and imaged in three dimensions for microarchitecture and Microdamage (voxel size 0.7×0.7×5.0 μm3). We found that the overall proportion of damaged tissue was greater (p=0.01) for apparent tension loading (3.9±2.4%, mean±SD) than for apparent compression loading (1.9±1.3%). Individual Microdamage sites generated in tension were larger in volume (p<0.001) but not more numerous (p=0.64) than sites in compression. For both loading modes, the proportion of damaged tissue varied more across donors than with bone volume fraction, traditional measures of microarchitecture (trabecular thickness, trabecular separation, etc.), apparent Young׳s modulus, or strength. Microdamage tended to occur in regions of greater trabecular thickness but not near observable resorption cavities. Taken together, these findings indicate that, regardless of loading mode, accumulation of Microdamage in cancellous bone after monotonic loading to yield is influenced by donor characteristics other than traditional measures of microarchitecture, suggesting a possible role for tissue material properties.
Clare M Rimnac - One of the best experts on this subject based on the ideXlab platform.
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fatigue induced Microdamage in cancellous bone occurs distant from resorption cavities and trabecular surfaces
Bone, 2015Co-Authors: M G Goff, Floor M Lambers, Clare M Rimnac, Christopher J Hernandez, T M Nguyen, J SungAbstract:Impaired bone toughness is increasingly recognized as a contributor to fragility fractures. At the tissue level, toughness is related to the ability of bone tissue to resist the development of microscopic cracks or other tissue damage. While most of our understanding of Microdamage is derived from studies of cortical bone, the majority of fragility fractures occur in regions of the skeleton dominated by cancellous bone. The development of tissue Microdamage in cancellous bone may differ from that in cortical bone due to differences in microstructure and tissue ultrastructure. To gain insight into how Microdamage accumulates in cancellous bone we determined the changes in number, size and location of Microdamage sites following different amounts of cyclic compressive loading. Human vertebral cancellous bone specimens (n=32, 10 male donors, 6 female donors, age 76 ± 8.8, mean ± SD) were subjected to sub-failure cyclic compressive loading and Microdamage was evaluated in three-dimensions. Only a few large Microdamage sites (the largest 10%) accounted for 70% of all Microdamage caused by cyclic loading. The number of large Microdamage sites was a better predictor of reductions in Young's modulus caused by cyclic loading than overall damage volume fraction (DV/BV). The majority of Microdamage volume (69.12 ± 7.04%) was located more than 30 μm (the average erosion depth) from trabecular surfaces, suggesting that Microdamage occurs primarily within interstitial regions of cancellous bone. Additionally, Microdamage was less likely to be near resorption cavities than other bone surfaces (p<0.05), challenging the idea that stress risers caused by resorption cavities influence fatigue failure of cancellous bone. Together, these findings suggest that reductions in apparent level mechanical performance during fatigue loading are the result of only a few large Microdamage sites and that Microdamage accumulation in fatigue is likely dominated by heterogeneity in tissue material properties rather than stress concentrations caused by micro-scale geometry.
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Fatigue-induced Microdamage in cancellous bone occurs distant from resorption cavities and trabecular surfaces.
Bone, 2015Co-Authors: M G Goff, Floor M Lambers, Clare M Rimnac, T M Nguyen, J Sung, Christopher J HernandezAbstract:Impaired bone toughness is increasingly recognized as a contributor to fragility fractures. At the tissue level, toughness is related to the ability of bone tissue to resist the development of microscopic cracks or other tissue damage. While most of our understanding of Microdamage is derived from studies of cortical bone, the majority of fragility fractures occur in regions of the skeleton dominated by cancellous bone. The development of tissue Microdamage in cancellous bone may differ from that in cortical bone due to differences in microstructure and tissue ultrastructure. To gain insight into how Microdamage accumulates in cancellous bone we determined the changes in number, size and location of Microdamage sites following different amounts of cyclic compressive loading. Human vertebral cancellous bone specimens (n=32, 10 male donors, 6 female donors, age 76 ± 8.8, mean ± SD) were subjected to sub-failure cyclic compressive loading and Microdamage was evaluated in three-dimensions. Only a few large Microdamage sites (the largest 10%) accounted for 70% of all Microdamage caused by cyclic loading. The number of large Microdamage sites was a better predictor of reductions in Young's modulus caused by cyclic loading than overall damage volume fraction (DV/BV). The majority of Microdamage volume (69.12 ± 7.04%) was located more than 30 μm (the average erosion depth) from trabecular surfaces, suggesting that Microdamage occurs primarily within interstitial regions of cancellous bone. Additionally, Microdamage was less likely to be near resorption cavities than other bone surfaces (p
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quantitative relationships between Microdamage and cancellous bone strength and stiffness
Bone, 2014Co-Authors: Floor M Lambers, Christopher J Hernandez, J. Widjaja, C. Chapa, Clare M RimnacAbstract:Microscopic tissue damage (Microdamage) is an aspect of bone quality associated with impaired bone mechanical performance. While it is clear that bone tissue submitted to more severe loading has greater amounts of Microdamage (as measured through staining), how Microdamage influences future mechanical performance of the bone has not been well studied, yet is necessary for understanding the mechanical consequences of the presence of Microdamage. Here we determine how stained Microdamage generated by a single compressive overload affects subsequent biomechanical performance of cancellous bone. Human vertebral cancellous bone specimens (n=47) from 23 donors (14 males, 9 females, 64-92years of age) were submitted to a compressive overload, stained for Microdamage, then reloaded in compression to determine the relationship between the amount of Microdamage caused by the initial load and reductions in mechanical performance during the reload. Damage volume fraction (DV/BV) caused by the initial overload was related to reductions in Young's modulus, yield strength, ultimate strength, and yield strain upon reloading (p<0.05, R(2)=0.18-0.34). The regression models suggest that, on average, relatively small amounts of Microdamage are associated with large reductions in reload mechanical properties: a 1.50% DV/BV caused by a compressive overload was associated with an average reduction in Young's modulus of 41.0±3.2% (mean±SE), an average reduction in yield strength of 63.1±4.5% and an average reduction in ultimate strength of 52.7±4.0%. Specimens loaded beyond 1.2% (1.2-4.0% apparent strain) demonstrated a single relationship between reload mechanical properties (Young's modulus, yield strength, and ultimate strength) and bone volume fraction despite a large range in amounts of Microdamage. Hence, estimates of future mechanical performance of cancellous bone can be achieved using the bone volume fraction and whether or not a specimen was previously loaded beyond ultimate strain. The empirical relationships provided in this study make it possible to estimate the degree of impaired mechanical performance resulting from an observed amount of stained Microdamage.
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Quantitative relationships between Microdamage and cancellous bone strength and stiffness
Bone, 2014Co-Authors: Christopher J Hernandez, Floor M Lambers, J. Widjaja, C. Chapa, Clare M RimnacAbstract:Microscopic tissue damage (Microdamage) is an aspect of bone quality associated with impaired bone mechanical performance. While it is clear that bone tissue submitted to more severe loading has greater amounts of Microdamage (as measured through staining), how Microdamage influences future mechanical performance of the bone has not been well studied, yet is necessary for understanding the mechanical consequences of the presence of Microdamage. Here we determine how stained Microdamage generated by a single compressive overload affects subsequent biomechanical performance of cancellous bone. Human vertebral cancellous bone specimens (n=47) from 23 donors (14 males, 9 females, 64-92years of age) were submitted to a compressive overload, stained for Microdamage, then reloaded in compression to determine the relationship between the amount of Microdamage caused by the initial load and reductions in mechanical performance during the reload. Damage volume fraction (DV/BV) caused by the initial overload was related to reductions in Young's modulus, yield strength, ultimate strength, and yield strain upon reloading (p
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Microdamage caused by fatigue loading in human cancellous bone relationship to reductions in bone biomechanical performance
PLOS ONE, 2013Co-Authors: Floor M Lambers, Amanda R Bouman, Clare M Rimnac, Christopher J HernandezAbstract:Vertebral fractures associated with osteoporosis are often the result of tissue damage accumulated over time. Microscopic tissue damage (Microdamage) generated in vivo is believed to be a mechanically relevant aspect of bone quality that may contribute to fracture risk. Although the presence of Microdamage in bone tissue has been documented, the relationship between loading, Microdamage accumulation and mechanical failure is not well understood. The aim of the current study was to determine how Microdamage accumulates in human vertebral cancellous bone subjected to cyclic fatigue loading. Cancellous bone cores (n = 32) from the third lumbar vertebra of 16 donors (10 male, 6 female, age 76±8.8, mean ± SD) were subjected to compressive cyclic loading at σ/E0 = 0.0035 (where σ is stress and E0 is the initial Young’s modulus). Cyclic loading was suspended before failure at one of seven different amounts of loading and specimens were stained for Microdamage using lead uranyl acetate. Damage volume fraction (DV/BV) varied from 0.8±0.5% (no loading) to 3.4±2.1% (fatigue-loaded to complete failure) and was linearly related to the reductions in Young’s modulus caused by fatigue loading (r2 = 0.60, p<0.01). The relationship between reductions in Young’s modulus and proportion of fatigue life was nonlinear and suggests that most Microdamage generation occurs late in fatigue loading, during the tertiary phase. Our results indicate that human vertebral cancellous bone tissue with a DV/BV of 1.5% is expected to have, on average, a Young’s modulus 31% lower than the same tissue without Microdamage and is able to withstand 92% fewer cycles before failure than the same tissue without Microdamage. Hence, even small amounts of microscopic tissue damage in human vertebral cancellous bone may have large effects on subsequent biomechanical performance.
Amanda R Bouman - One of the best experts on this subject based on the ideXlab platform.
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the effects of tensile compressive loading mode and microarchitecture on Microdamage in human vertebral cancellous bone
Journal of Biomechanics, 2014Co-Authors: Floor M Lambers, Amanda R Bouman, Christopher J Hernandez, Tony M Keaveny, Evgeniy V TkachenkoAbstract:The amount of Microdamage in bone tissue impairs mechanical performance and may act as a stimulus for bone remodeling. Here we determine how loading mode (tension vs. compression) and microstructure (trabecular microarchitecture, local trabecular thickness, and presence of resorption cavities) influence the number and volume of Microdamage sites generated in cancellous bone following a single overload. Twenty paired cylindrical specimens of human vertebral cancellous bone from 10 donors (47–78 years) were mechanically loaded to apparent yield in either compression or tension, and imaged in three dimensions for microarchitecture and Microdamage (voxel size 0.7×0.7×5.0 μm3). We found that the overall proportion of damaged tissue was greater (p=0.01) for apparent tension loading (3.9±2.4%, mean±SD) than for apparent compression loading (1.9±1.3%). Individual Microdamage sites generated in tension were larger in volume (p<0.001) but not more numerous (p=0.64) than sites in compression. For both loading modes, the proportion of damaged tissue varied more across donors than with bone volume fraction, traditional measures of microarchitecture (trabecular thickness, trabecular separation, etc.), apparent Young׳s modulus, or strength. Microdamage tended to occur in regions of greater trabecular thickness but not near observable resorption cavities. Taken together, these findings indicate that, regardless of loading mode, accumulation of Microdamage in cancellous bone after monotonic loading to yield is influenced by donor characteristics other than traditional measures of microarchitecture, suggesting a possible role for tissue material properties.
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The effects of tensile-compressive loading mode and microarchitecture on Microdamage in human vertebral cancellous bone.
Journal of biomechanics, 2014Co-Authors: Floor M Lambers, Amanda R Bouman, Tony M Keaveny, Evgeniy V Tkachenko, Christopher J HernandezAbstract:The amount of Microdamage in bone tissue impairs mechanical performance and may act as a stimulus for bone remodeling. Here we determine how loading mode (tension vs. compression) and microstructure (trabecular microarchitecture, local trabecular thickness, and presence of resorption cavities) influence the number and volume of Microdamage sites generated in cancellous bone following a single overload. Twenty paired cylindrical specimens of human vertebral cancellous bone from 10 donors (47–78 years) were mechanically loaded to apparent yield in either compression or tension, and imaged in three dimensions for microarchitecture and Microdamage (voxel size 0.7×0.7×5.0 μm3). We found that the overall proportion of damaged tissue was greater (p=0.01) for apparent tension loading (3.9±2.4%, mean±SD) than for apparent compression loading (1.9±1.3%). Individual Microdamage sites generated in tension were larger in volume (p
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Microdamage caused by fatigue loading in human cancellous bone relationship to reductions in bone biomechanical performance
PLOS ONE, 2013Co-Authors: Floor M Lambers, Amanda R Bouman, Clare M Rimnac, Christopher J HernandezAbstract:Vertebral fractures associated with osteoporosis are often the result of tissue damage accumulated over time. Microscopic tissue damage (Microdamage) generated in vivo is believed to be a mechanically relevant aspect of bone quality that may contribute to fracture risk. Although the presence of Microdamage in bone tissue has been documented, the relationship between loading, Microdamage accumulation and mechanical failure is not well understood. The aim of the current study was to determine how Microdamage accumulates in human vertebral cancellous bone subjected to cyclic fatigue loading. Cancellous bone cores (n = 32) from the third lumbar vertebra of 16 donors (10 male, 6 female, age 76±8.8, mean ± SD) were subjected to compressive cyclic loading at σ/E0 = 0.0035 (where σ is stress and E0 is the initial Young’s modulus). Cyclic loading was suspended before failure at one of seven different amounts of loading and specimens were stained for Microdamage using lead uranyl acetate. Damage volume fraction (DV/BV) varied from 0.8±0.5% (no loading) to 3.4±2.1% (fatigue-loaded to complete failure) and was linearly related to the reductions in Young’s modulus caused by fatigue loading (r2 = 0.60, p<0.01). The relationship between reductions in Young’s modulus and proportion of fatigue life was nonlinear and suggests that most Microdamage generation occurs late in fatigue loading, during the tertiary phase. Our results indicate that human vertebral cancellous bone tissue with a DV/BV of 1.5% is expected to have, on average, a Young’s modulus 31% lower than the same tissue without Microdamage and is able to withstand 92% fewer cycles before failure than the same tissue without Microdamage. Hence, even small amounts of microscopic tissue damage in human vertebral cancellous bone may have large effects on subsequent biomechanical performance.
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Microdamage Caused by Fatigue Loading in Human Cancellous Bone: Relationship to Reductions in Bone Biomechanical Performance
PLoS ONE, 2013Co-Authors: Floor M Lambers, Amanda R Bouman, Clare M Rimnac, Christopher J HernandezAbstract:Vertebral fractures associated with osteoporosis are often the result of tissue damage accumulated over time. Microscopic tissue damage (Microdamage) generated in vivo is believed to be a mechanically relevant aspect of bone quality that may contribute to fracture risk. Although the presence of Microdamage in bone tissue has been documented, the relationship between loading, Microdamage accumulation and mechanical failure is not well understood. The aim of the current study was to determine how Microdamage accumulates in human vertebral cancellous bone subjected to cyclic fatigue loading. Cancellous bone cores (n = 32) from the third lumbar vertebra of 16 donors (10 male, 6 female, age 76±8.8, mean ± SD) were subjected to compressive cyclic loading at σ/E0 = 0.0035 (where σ is stress and E0 is the initial Young’s modulus). Cyclic loading was suspended before failure at one of seven different amounts of loading and specimens were stained for Microdamage using lead uranyl acetate. Damage volume fraction (DV/BV) varied from 0.8±0.5% (no loading) to 3.4±2.1% (fatigue-loaded to complete failure) and was linearly related to the reductions in Young’s modulus caused by fatigue loading (r2 = 0.60, p
