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D Vashishth

Publications and source records attributed to D Vashishth.

At least 19 recordsLinked to original sources

Susceptibility of aging human bone to mixed-mode fracture increases bone fragility.

Since bone-mass-based measurements have demonstrated limited success in predicting age-related increase in fracture incidence, recent emphasis has been placed on quantification of bone quality. Specifically, material parameters such as strength, stiffness, and toughness have been quantified to characterize bone quality through mechanical testing. This study is the first one to report multiaxial failure characteristics of bone (quality) by conducting fatigue tests on human cortical bone specimens under physiologically relevant loading involving simultaneous application of axial and torsional loading to produce previously reported in vivo shear/normal stress ratios. Our results show that, compared to uniaxial tests, multiaxial fatigue tests show up to a 20-fold reduction in the fatigue life of human cortical bone. More significantly, the susceptibility of mixed-mode failure increases bone fragility in aging human bone. Furthermore, since the magnitude of mixed-mode loading varies with physiological activities, results of this study also suggest that a reduction in the activities involving significant mixed-mode loading may lower the overall fracture incidence among older individuals.

Adult↗

Damage mechanisms and failure modes of cortical bone under components of physiological loading.

Fatigue damage development in cortical bone was investigated in vitro under different mechanical components of physiological loading including tension, compression, and torsion. During each test, stress and strain data were collected continuously to monitor and statistically determine the occurrence of the primary, secondary, and tertiary stages associated with fatigue and/or creep failure of bone. The resultant microdamage and failure modes were identified by histological and fractographic analysis, respectively. The tensile group demonstrated Mode I cracking and the three classic stages of fatigue and creep suggesting a low crack initiation threshold, steady crack propagation and final failure by coalescence of microcracks. In contrast, the compressive group displayed Mode II cracking and a two-stage fatigue behavior with limited creep suggesting a high crack initiation threshold followed by a sudden fracture. The torsion group also displayed a two-stage fatigue profile but demonstrated extensive damage from mixed mode (Modes II and III) microcracking and predominant time-dependent damage. Thus, fatigue behavior of bone was found to be uniquely related to the individual mechanical components of physiological loading and the latter determined the specific damage mechanisms associated with fatigue fracture.

Animals↗

Effects of damage morphology on cortical bone fragility.

Despite a general understanding that bone microdamage has distinct strain dependent morphologies, very little information exists on how different damage morphologies develop and participate in bone fracture. In this study, cortical bone beams were subjected to the primary or tertiary phases of bending fatigue followed by either post-hoc fracture toughness tests or microdamage analysis to determine the sequence in which linear microcracks and diffuse damage form during bending fatigue and how they affect the propensity of bone to fracture. The results demonstrate that, following the primary phase, linear microcracks and diffuse damage are formed on the compressive and tensile sides, respectively (p<0.05). Furthermore, this mode of damage formation results in a greater toughness loss if a fracture crack initiates from the tensile side rather than the compressive side (p<0.05). Continued loading of bone specimens to the tertiary phase, however, leads to further accumulation of damage only on the compressive side (p<0.05), and this mode of damage formation results in a further toughness loss if a fracture crack initiates from the compressive side rather than the tensile side (p<0.05). Thus, cortical bone compartmentalizes the damage morphologies in different regions and the sequence of damage production in different phases of cyclic loading to dissipate energy and resist a catastrophic fracture.

Algorithms↗

Influence of phase angle between axial and torsional loadings on fatigue fractures of bone.

Fatigue fractures of cortical bone involve combined axial-torsional loading yet it is unknown how the relationship between axial and torsional loadings affects the fatigue behavior of bone. In this study the effect of superimposing in-phase and out-of-phase torsional on axial loading on the fatigue behavior of bone was investigated by conducting in vitro tests involving 0 degrees and 90 degrees phase shift between cyclic torsional and axial loadings. Results obtained indicate that fatigue life, patterns of moduli loss, microcracking and modes of fractures are dependent on the phase angle between axial and torsional loadings. Specimens subjected to in-phase torsional on axial loading demonstrated greater mixed mode interaction, underwent proportionate stiffness losses in tension, compression, and torsion, and consequently had a shorter fatigue life. In contrast, specimens subjected to out-of-phase loading regime displayed a smaller contribution of mixed mode failure, underwent a disproportionately large stiffness loss in torsion, and had a longer fatigue life. Furthermore, increase in phase angle provided additional planes on which damage was diffused delaying the final failure. Change in phase angle, seen in vivo during a number of physiological activities including walking, running and sprinting, will therefore affect fatigue behavior and contribute to pathogenesis of fatigue fractures.

Animals↗

Experimental validation of a microcracking-based toughening mechanism for cortical bone.

It has been proposed that cortical bone derives its toughness by forming microcracks during the process of crack propagation (J. Biomech. 30 (1997) 763; J. Biomech. 33 (2000) 1169). The purpose of this study was to experimentally validate the previously proposed microcrack-based toughening mechanism in cortical bone. Crack initiation and propagation tests were conducted on cortical bone compact tension specimens obtained from the antlers of red deer. For these tests, the main fracture crack was either propagated to a predetermined crack length or was stopped immediately after initiating from the notch. The microcracks produced in both groups of specimens were counted in the same surface area of interest around and below the notch, and crack growth resistance and crack propagation velocity were analyzed. There were more microcracks in the surface area of interest in the propagation than in initiation specimens showing that the formation of microcracks continued after the initiation of a fracture crack. Crack growth resistance increased with crack extension, and crack propagation velocity vs. crack extension curves demonstrated the characteristic jump increase and decrease pattern associated with the formation of microcracks. The scanning electron micrographs of crack initiation and propagation displayed the formation of a frontal process zone and a wake, respectively. These results support the microcrack-based toughening mechanism in cortical bone. Bone toughness is, therefore, determined by its ability to form microcracks during fracture.

Animals↗

Determination of bone volume by osteocyte population.

During development and growth, biological tissues and organisms can control their size and mass by regulating cell number (Raff, 1992; Conlon and Raff, 1999). Later in life both cell number and organ mass decrease (Buetow, 1985). We demonstrate that the number density of bone cells buried in the calcified matrix (osteocyte lacunar density) predicts extracellular matrix volume for both cancellous and cortical bone in a broad cross-section of the population (males and females, age range 23-91 years, r(2) = 0.98). Our hypothesis is that bone mass is determined by the control of osteocyte number, and that this is a particular instance of the control of organ size through the social controls on cell survival and death (Raff, 1992; Conlon and Raff, 1999).

Adolescent↗

Trabecular shear stress in human vertebral cancellous bone: intra- and inter-individual variations.

Correlation of the mean and standard deviation of trabecular stresses has been proposed as a mechanism by which a strong relationship between the apparent strength and stiffness of cancellous bone can be achieved. The current study examined whether the relationship between the mean and standard deviation of trabecular von Mises stresses can be generalized for any group of cancellous bone. Cylindrical human vertebral cancellous bone specimens were cut in the infero-superior direction from T12 of 23 individuals (inter-individual group). Thirty nine additional specimens were prepared similarly from the T4-T12 and L2-L5 vertebrae of a 63 year old male (intra-individual group). The specimens were scanned by micro-computed tomography (microCT) and trabecular von Mises stresses were calculated using finite element modeling. The expected value, standard deviation and coefficient of variation of the von Mises stress were calculated form a three-parameter Weibull function fitted to von Mises stress data from each specimen. It was found that the average and standard deviation of trabecular von Mises shear stress were: (i) correlated with each other, supporting the idea that high correlation between the apparent strength and stiffness of cancellous bone can be achieved through controlling the trabecular level shear stress variations, (ii) dependent on anatomical site and sample group, suggesting that the variation of stresses are correlated to the mean stress to different degrees between vertebrae and individuals, and (iii) dependent on bone volume fraction, consistent with the idea that shear stress is less well controlled in bones with low BV/TV. The conversion of infero-superior loading into trabecular von Mises stresses was maximum for the tissue at the junction of the thoracic and lumbar spine (T12-L1) consistent with this junction being a common site of vertebral fracture.

Adult↗

Fatigue of cortical bone under combined axial-torsional loading.

The influence of torsional loading on the fatigue life of cortical bone was investigated by conducting in vitro testing. Fatigue tests were conducted on cylindrical dumbbell bovine cortical bone specimens in an environmental chamber under axial loading, torsional loading and various combinations of axial-torsional loading where the phase relationship and relative magnitudes of axial and torsional loadings were systematically varied. It was found that the superposition of torque on axial loading reduced the fatigue life of cortical bone. The reduction in fatigue life was significant when the maximum shear stress was greater than 59% of the maximum normal stress. The magnitude of reduction in the fatigue life of bone at low as well as high levels of axial loading depended on the magnitude of torsional loading, but was independent of the phase angle by which the torsional loading lagged the axial loading. Furthermore, oblique fracture profiles, characteristic of torsion-induced failure, were observed for combined axial-torsional load cases. Based on these results, it is suggested that torsional loading plays a significant role in determining the fatigue life of cortical bone.

Animals↗

Influence of nonenzymatic glycation on biomechanical properties of cortical bone.

In this study, the influence of nonenzymatic glycation (NEG) on the mechanical properties of bone and bone collagen were investigated. Bovine cortical bone specimens were incubated in ribose to cause collagen cross-links in vitro, and nondestructive mechanical testing was used to determine tensile and compressive elastic modulus as a function of incubation time. Mechanical properties associated with yield, postyield, and final fracture of bone were determined at the end of the incubation period. The stiffness of the collagen network was measured using stress relaxation tests of demineralized bone cylinders extracted periodically throughout the incubation period. It was found that accumulation of nonenzymatic glycation end-products in cortical bone caused stiffening of the type I collagen network in bone (r2 = 0.92; p < 0.001) but did not significantly affect the overall stiffness of the mineralized bone (p = 0.98). The ribosylated group had significantly more NEG products and higher yield stress and strain than the control group (p < 0.05). Postyield properties including postyield strain and strain energy were lower in the ribosylated group but were not significantly different from the control group (p = 0.24). Compared with the control group, the ribosylated group was characterized by significantly higher secant modulus and lower damage fraction (p < 0.05). Taken together, the results of this study suggest that collagen in bone is susceptible to the same NEG-mediated changes as collagen in other connective tissues and that an increased stiffness of the collagen network in bone due to NEG may explain some of the age-related increase in skeletal fragility and fracture risk.

Animals↗

Estimation of bone matrix apparent stiffness variation caused by osteocyte lacunar size and density.

The role of osteocyte lacunar size and density on the apparent stiffness of bone matrix was predicted using a mechanical model from the literature. Lacunar size and lacunar density for different bones from different gender and age groups were used to predict the range of matrix apparent stiffness values for human cortical and cancellous tissue. The results suggest that bone matrix apparent stiffness depends on tissue type (cortical versus cancellous), age, and gender, the magnitudes of the effects being significant but small in all cases. Males had a higher predicted matrix apparent stiffness than females for vertebral cancellous bone (p< I0(-7)) and the difference increased with age (p =0.0007). In contrast, matrix apparent stiffness was not different between males and females forfemoral cortical bone and increased with age in both males (p < 0.0001) and females (p < 0.0364). Osteocyte lacunar density and size may cause significant gender and age-related variations in bone matrix apparent stiffness. The magnitude of variations in matrix apparent stiffness was small within the physiological range of lacunar size and density for healthy bone, whereas the variations can be profound in certain pathological cases. It was proposed that the mechanical effects of osteocyte density be uncoupled from their biological effects by controlling lacunar size in normal bone.

Adolescent↗

Contribution, development and morphology of microcracking in cortical bone during crack propagation.

A fracture mechanics study of cortical bone is presented to investigate the contribution, development morphology of microcracking in cortical bone during crack propagation. Post-hoc analyses of microcrack orientation, crack propagation velocity and fracture surface roughness were conducted on previously tested human and bovine bone compact tension specimens. It was found that, consistent with its higher toughness, bovine bone formed significantly more longitudinal, transverse and inclined microcracks than human bone. However, in human bone more of the microcracks that formed were longitudinal than transverse or inclined, a feature that would optimise bone's toughness. Crack propagation velocity in human and bovine bone displayed the same characteristic pattern with crack extension, where an increase in velocity is followed by a consequent decrease and vice versa. On the basis of this pattern, a model or crack propagation has been proposed. It provides a detailed account of mocrocrack formation and contribution towards the propagation of a fracture crack. Analyses of fracture surfaces indicated that, consistent with its higher toughness, bovine bone displays a rougher surface than human bone but they both have the same basic fractured element, i.e. a mineralised collagen fibril.

Animals↗

Decline in osteocyte lacunar density in human cortical bone is associated with accumulation of microcracks with age.

Despite osteocytes' ideal position to sense the local environment and thereby influence bone remodeling, the function of osteocytes in bone remains controversial. In this study, histomorphometric examination of male and female femoral middiaphyseal cortical bone was conducted to determine if bone's remodeling response, indicated by tissue porosity and accumulation of damage, is associated with osteocyte lacunar density (number of osteocyte lacunae per bone area). The results support the sensory role of the osteocyte network as the decline in osteocyte lacunar density in human cortical bone is associated with the accumulation of microcracks and increase in porosity with age. Porosity and microcrack density increased exponentially with a decline in osteocyte lacunar density indicating that a certain minimum number of osteocytes is essential for an "operational" network. No gender-related differences were found in the relationship of osteocyte lacunar density to age, porosity, or microcrack density. The coefficient of variation of osteocyte lacunar density increased linearly with age, indicating that aging bone tissue is characterized by increased heterogeneity in the spatial organization of osteocytes. Osteocyte lacunar density, porosity, and microcrack density exhibited the same exponential probability density distribution in the donor population, indicating their regulation by similar biological phenomena.

Adolescent↗

Bone stiffness predicts strength similarly for human vertebral cancellous bone in compression and for cortical bone in tension.

The yield strength and ultimate strength of cortical and cancellous bone tissue are very highly correlated to bone stiffness. For samples of human vertebral cancellous bone in compression and for bovine cortical bone in tension, the coefficient of determination (r2) for regression between ultimate strength and stiffness was 0.89 and 0.92, and between yield strength and stiffness it was 0.94 and 0.93, respectively. The slope of the regression for human vertebral cancellous bone ultimate strength predicted by stiffness was not statistically different from similar regressions for cortical bone in tension in either a bovine sample or in published data from multiple species. We believe that the observed correlation results from the evolutionary need to build sufficiently strong bones using cells that are sensitive to deformation and that directly control bone stiffness, but not strength. The practical significance of this work is that an in vivo estimate of bone stiffness (e.g., from ultrasound measurement) may be a surrogate for bone strength.

Adaptation, Physiological↗

In vivo diffuse damage in human vertebral trabecular bone.

Accumulation of microdamage in vivo may lead to loss of bone quality. Until recently, linear microcracks were the only known form of in vivo microdamage, but through the use of confocal microscopy an additional level of damage (diffuse damage) has been identified. In this study, in vivo diffuse damage was characterized and quantified in human vertebral trabecular bone as a function of tissue morphology, age, race, gender, and previously quantified in vivo linear microcracks. Presence of diffuse damage in human vertebral tissue was confirmed and validated by simultaneous use of polarized, ultraviolet, and laser confocal microscopy. Diffuse damage was found to occur preferentially within trabecular packets rather than in interstitial bone (p < 0.05). It was consistently higher in men compared with women (p < 0.05), but was not different by race or age group. Diffuse damage did not correlate with linear microcracks, but both exhibited the same probability distribution in which the percentage of individuals having a particular amount of damage decreased exponentially as damage content increased. These findings suggest that diffuse damage accumulation and repair are governed by the same biological phenomena as microcracks, but diffuse damage contributes independently to the microdamage content of bone.

Adult↗

Crack growth resistance in cortical bone: concept of microcrack toughening.

The role of microcracking in cortical bone as a toughening mechanism has been investigated in conjunction with the variation in fracture toughness with crack length. Fracture toughness tests were conducted on miniaturised compact tension specimens made from human and bovine cortical bone and the resultant microstructural damage, present in the form of microcracking on the surface, was analysed around the main propagating crack. It was found that the fracture toughness (Kc) and the cumulative number of microcracks increased linearly with crack extension in human and bovine cortical bone, although both Kc and number of microcracks were considerably higher in the latter case. Based on these results, a mechanism, derived from the resistance (R) curve concept developed for microcracking brittle solids, is proposed to explain the fracture of cortical bone, with microcracking distributed between a frontal process zone and a significant process zone wake. Evidence to support this mechanism is given from the existing bone literature, detailed scanning electron microscopical observations and the distribution of microcracks in the process zone wake.

Adult↗

Fracture toughness of human bone under tension.

The longitudinal fracture toughnesses of human cortical bone were compared to those of bovine cortical bone to test the hypothesis that although human osteonal bone is significantly weaker and more compliant than primary (plexiform) bone, it is not less tough than primary bone. The fracture toughness indices, critical strain energy release rate (Gc) and critical stress intensity factor (Kc), were determined for human Haversian bone and bovine bone under tension (Mode I) loading using the compact tension method. The effects of thickness, crack growth range and anisotropy on fracture indices for slow stable crack growth in cortical bone were determined. Plane strain assumptions required for application of linear elastic fracture mechanics (LEFM) to bone were investigated. Longitudinal oriented fracture toughness tests were used to assess the crack inhibiting effect of human bone microstructure on fracture resistance. Human bone Kc calculated from the stress concentration formula for 2 and 3 mm thick specimens equaled 4.32 and 4.05 MN m-3/2, respectively. Human bone Gc calculated from the compliance method equaled 827 N m-1 for 2 mm thick specimens and 595 N m-1 for 3 mm thick specimens. It was found that crack growth range, thickness and material assumptions affect fracture toughness. Kc calculated from Gc using an anisotropic relation provided the lowest estimate of Kc and equaled 3.31 MN m-3/2 for 2 mm thick specimens and 2.81 MN m-3/2 for 3 mm thick specimens. Both Kc and Gc were significantly reduced after being adjusted to ASTM standard thickness using ratios determined from bovine bone. The fracture toughness of bovine bone relative to human bone ranged from 1.08 to 1.66. This was compared to the longitudinal strength of bovine bone relative to the longitudinal strength of human bone which is approximately equal to 1.5. We found that even though human bone is significantly weaker than bovine bone, relative to its strength, the toughness of human and bovine bone are roughly similar, but the data were not sufficiently definitive to answer the question of which is tougher.

Aged↗

Effect of groove on bone fracture toughness.

When testing for the effects of bone orientation on mode I fracture toughness, compact tension specimens are grooved with a V-notch to provide a crack guide. The effect of grooving on the expressions for the critical stress intensity factor (Kc) and the critical strain energy release rate (Gc) for mode I fracture toughness was investigated. Experiments were performed using grooved and ungrooved bovine compact tension specimens. The results indicate that the standard expression used to determine Kc for a compact tension specimen requires modification. The thickness (B) must be modified to account for the thickness between the grooves (Bn). The thickness used in the standard expression is replaced by an effective thickness written as (BBn)0.5. It was also found that the thickness between the grooves should be used in the standard formula for Gc.

Animals↗

Age-dependent fatigue behaviour of human cortical bone.

Despite a general understanding that bone quality contributes to skeletal fragility, very little information exits on the age-dependent fatigue behavior of human bone. In this study four-point bending fatigue tests were conducted on aging bone in conjunction with the analysis of stiffness loss and preliminary investigation of nanoindentation based measurements of local tissue stiffness and histological evaluation of resultant tensile and compressive damage to identify the damage mechanism responsible for the increase in age-related bone fragility. The results obtained show that there is an exponential decrease in fatigue life with age, and old bone exhibits different modulus degradation profiles than young bone. In addition, this study provides preliminary evidence indicating that during fatigue loading, younger bone formed diffuse damage, lost local tissue stiffness on the tensile side. Older bone, in contrast, formed linear microcracks lost local tissue stiffness on the compressive side. Thus, the propensity of aging human bone to form more linear microcracks than diffuse damage may be a significant contributor to bone quality, and age related fragility in bone.

Age Factors↗