Biomedical subjects

Deepak Vashishth

Publications and source records attributed to Deepak Vashishth.

9 recordsLinked to original sources

PubMed2006

Morphology, localization and accumulation of in vivo microdamage in human cortical bone.

In vivo, microdamage occurs in the form of linear microcracks and diffuse damage. However, it is unknown whether the age-related changes in bone quality predispose bone to form one type of damage morphology over the other during in vivo loading. In this study, histological and histomorphometrical analyses were conducted on transverse cross sections, obtained from the tibiae of aging human bone (age 19 to 89), to investigate the in vivo accumulation and localization of damage morphologies. The results demonstrate that old donor bone (83+/-3 years) contains more linear microcracks than younger donor bone in the cortices predominantly subjected to compressive (p<0.01) and tensile loading (p<0.01). In contrast, young donor bone (40+/-10 years) contains more diffuse damage than older donor bone in the cortex predominantly subjected to tensile loading (p<0.01). The formation of damage morphology showed no correlation with bone geometry parameters and exhibited distinct preferences with bone microstructure. Linear microcracks formed in the interstitial bone (p<0.01) and were either trapped or arrested by the microstructural interfaces (cement line and lamellar interface) (p<0.05). Areas of diffuse damage, however, were preferentially associated with secondary osteonal bone (p<0.01) and had no relationship with the microstructural interfaces (p<0.01). Based upon these findings, we conclude that age-related changes in bone microstructure, but not bone geometry, play a key role in the propensity of old donors to form linear microcrack over diffuse damage under in vivo loading conditions.

Adult↗

PubMed2006

Anisotropy of age-related toughness loss in human cortical bone: a finite element study.

A mechanistic understanding of the role of bone quality on fracture processes is essential for determining the underlying causes of age-related changes in the mechanical response of the human bone. In this study, a previously developed cohesive finite element model was used to investigate the effects of age-related changes and the orientation of crack growth on the toughening behavior of human cortical bone. The change in the anisotropy of toughening mechanisms with age was also studied. Finite element method (FEM) simulations showed that the initiation toughness decreased by 3% and 8%/decade for transverse and longitudinal crack growth, respectively. In contrast, fracture resistance curve slope for transverse and longitudinal crack growth decreased by 2% and 3%/decade, respectively. Initiation fracture toughness values were higher for the transverse than for the longitudinal for a given age. On the other hand, propagation fracture toughness values were higher for longitudinal than for transverse crack growth for a given age. With respect to age, the toughness ratio for crack initiation decreased by 6%/decade, but that for propagation showed almost no change (less than 1%). In light of these findings, an analytical model evaluating the crack arresting feature of cement lines, is proposed to explain the factors that determine crack penetration into osteons or its deflection by cement lines.

Aging↗

PubMed2006

Interactions between microstructural and geometrical adaptation in human cortical bone.

With aging and in disease, the changes in bone microstructure and geometry influence the mechanical properties of cortical bone, however, the level of interaction between the two is not known. Here, we investigate the interaction between the changes in microstructural and geometrical properties of the aging male tibia in proximal and distal middiaphysis. The microstructural measurements include variables related to the size and density of osteons and intracortical porosity. The macroscopic geometrical properties include variables related to bone surfaces (periosteal and endosteal) and cross section (area, moment of inertia). Site-specific correlations were found between the microstructural and geometrical properties along the bone length and at different bone surfaces. In contrast to the proximal middiaphysis of male tibia, where no correlation existed, significant (p<0.05) correlations were found in the distal middiaphysis of tibia. The changes in parameters partially related to bone formation in the cortex, including the osteonal area, showed positive correlations with an increase in the periosteal diameter. Similarly, parameters related to bone resorption and/or failed formation in the cortex, including porosity and pore size, showed significant correlations with cortical thinning. These findings support the concept that, with aging, anabolic and catabolic responses in the human tibia at microstructural and macrostructural levels are spatially related and site specific.

Adult↗

PubMed2005

Cohesive finite element modeling of age-related toughness loss in human cortical bone.

Although the age-related loss of bone quality has been implicated in bone fragility, a mechanistic understanding of the relationship is necessary for developing diagnostic and treatment modalities in the elderly population at risk of fracture. In this study, a finite element based cohesive zone model is developed and applied to human cortical bone in order to capture the experimentally shown rising crack growth behavior and age-related loss of bone toughness. The cohesive model developed here is based on a traction-crack opening displacement relationship representing the fracture processes in the vicinity of a propagating crack. The traction-displacement curve, defining the cohesive model, is composed of ascending and descending branches that incorporate material softening and nonlinearity. The results obtained indicate that, in contrast to initiation toughness, the finite element simulations of crack growth in compact tension (CT) specimens successfully capture the rising R-curve (propagation toughness) behavior and the age-related loss of bone toughness. In close correspondence with the experimentally observed decrease of 14-15% per decade, the finite element simulation results show a decrease of 13% in the R-curve slope per decade. The success of the simulations is a result of the ability of cohesive models to capture and predict the parameters related to bone fracture by representing the physical processes occurring in the vicinity of a propagating crack. These results illustrate that fracture mechanisms in the process zone control bone toughness and any modification to these would cause age-related toughness loss.

Aging↗

PubMed2005

Age-related change in the damage morphology of human cortical bone and its role in bone fragility.

Application of cyclic loading results in the formation of distinct strain-dependent microdamage morphologies. It is still unknown; however, how the morphology of microdamage affects age-related increase in bone fragility. In this study, four-point bending fatigue tests were conducted on aging human bone (age 26 to 89) in conjunction with histological evaluation of the resultant tensile (diffuse damage) and compressive (linear microcracks) damage to identify the damage morphologies associated with an increase in age-related bone fragility. The results demonstrate that young donors (38 +/- 9 years) had a longer fatigue life (P < 0.05) and formed more diffuse damage than the older donors (82 +/- 5 years) (P < 0.05). In contrast, old donors had a shorter fatigue life and formed more linear microcracks than the younger donors (P < 0.05). Linear microcracks were longer in older than in younger donors (P < 0.05) and were associated with weak lamellar interfaces. Areas of diffuse damage were, however, larger in younger than in older donors (P < 0.05), and these showed no relationship with the lamellar arrangement of bone. These findings show, for the first time, that the propensity of bone to form a particular damage morphology is subject to change with age and that the propensity of young donors to form diffuse damage over interlamellae linear microcracks plays a critical role in the ability of bone to dissipate energy and resist a catastrophic fracture. Age-related changes in damage morphology may therefore be an important contributor to the increased bone fragility in the elderly.

Adult↗

PubMed2005

Sexual dimorphism and age dependence of osteocyte lacunar density for human vertebral cancellous bone.

The sexual dimorphism in age-related loss of human vertebral cancellous bone is not fully understood and could be related to dimorphism in the bone cell populations. The objective of this study was to investigate age- and gender-related differences in the osteocyte population and its relationship with bone volume fraction for human vertebral cancellous bone. Histomorphometric techniques were used to quantify osteocyte lacunae (a measure of osteocyte population) and bone volume fraction in male and female human T12 vertebrae, the most common site of vertebral fracture. Two measures of osteocyte population [number of osteocytes per bone area (OtLcDn) and number of osteocytes per total area (OtLcN/TA)] and their relationships with age and bone volume fraction were found to be sexually dimorphic. Dimorphism in osteocyte density may explain the dimorphic patterns of bone loss in human vertebrae due to the sensory and signal communication functions that osteocytes perform.

Adult↗

PubMed2005

Age-dependent biomechanical modifications in bone.

Age-related nontraumatic fractures are a major public health problem. Even though lower bone mass is the most commonly implicated variable for the age-related increase in fracture incidence, studies show that the resistance of bone material against fracture (toughness) diminishes with age. The mechanisms for the age-related loss of toughness are, however, unknown and may involve alterations in the quality of the bone material. The review of literature presented here identifies changes in the quality of bone material at ultrastructural, lamellar, osteonal, and tissue levels as plausible contributors to the biomechanical changes in aging human bone. The changes in bone quality at these multiple levels of organization result in a systematic breakdown of the mechanical and biological mechanisms that provide bone with its resistance against fracture. Animal studies conducted to date suggest that, similar to bone mass, bone quality may be partially regulated by genetics.

Aging↗

PubMed2004

Rising crack-growth-resistance behavior in cortical bone: implications for toughness measurements.

Fracture mechanics studies have characterized bone's resistance to fracture in terms of critical stress intensity factor and critical strain energy release rate measured at the onset of a fracture crack. This approach, although useful, provide a limited insight into fracture behavior of bone because, unlike classical brittle materials, bone is a microcracking solid that derives its resistance to fracture during the process of crack propagation from microfracture mechanisms occurring behind the advancing crack front. To address this shortfall, a crack propagation-based approach to measure bone toughness is described here and compared with crack initiation approach. Post hoc analyses of data from previously tested bovine and antler cortical bone compact specimens demonstrates that, in contrast to crack initiation approach, the crack propagation approach successfully identifies the superior toughness properties of red deer's antler cortical bone. Propagation-based slope of crack growth resistance curve is, therefore, a more useful parameter to evaluate cortical bone fracture toughness.

Animals↗

PubMed2003

Trabecular shear stresses predict in vivo linear microcrack density but not diffuse damage in human vertebral cancellous bone.

Linear microcracks and diffuse damage (staining over a broad region) are two types of microscopic damage known to occur in vivo in human vertebral trabecular bone. These damage types might be associated with vertebral failure. Using microcomputed tomography and finite element analysis for specimens of cancellous bone, we estimated the stresses in the trabeculae of human vertebral tissue for inferosuperior loading. Microdamage was quantified histologically. The density of in vivo linear microcracks was, but the diffuse damage area was not, related to the estimates of von Mises stress distribution in the tissue. In vivo linear microcrack density increased with increasing coefficient of variation of the trabecular von Mises stress and with increasing average trabecular von Mises stress generated per superoinferior apparent axial stress. Nonlinear increase in linear crack density, similar to the increase of the coefficient of variation of trabecular shear stresses, with decreasing bone stiffness and bone volume fraction suggests that damage may accumulate rather rapidly in diseases associated with low bone density due to the dramatic increase of shear stresses in the tissue.

Adult↗