Bone Microdamage Research Articles

Preservation of Bone Tissue Integrity with Temperature Control for In Situ SR-MicroCT Experiments.

Digital volume correlation (DVC), combined with in situ synchrotron microcomputed tomography (SR-microCT) mechanics, allows for 3D full-field strain measurement in bone at the tissue level. However, long exposures to SR radiation are known to induce bone damage, and reliable experimental protocols able to preserve tissue properties are still lacking. This study aims to propose a proof-of-concept methodology to retain bone tissue integrity, based on residual strain determination using DVC, by decreasing the environmental temperature during in situ SR-microCT testing. Compact and trabecular bone specimens underwent five consecutive full tomographic data collections either at room temperature or 0 °C. Lowering the temperature seemed to reduce microdamage in trabecular bone but had minimal effect on compact bone. A consistent temperature gradient was measured at each exposure period, and its prolonged effect over time may induce localised collagen denaturation and subsequent damage. DVC provided useful information on irradiation-induced microcrack initiation and propagation. Future work is necessary to apply these findings to in situ SR-microCT mechanical tests, and to establish protocols aiming to minimise the SR irradiation-induced damage of bone.

Assessing bone quality through mechanical properties in postmenopausal trabecular bone

BackgroundThe inner structure of trabecular bone is a result of structural optimization provided by remodeling processes. Changes in hormonal status related to menopause cause bone tissue loss and micro-architectural deterioration with a consequent susceptibility to fracture. Accumulation of micro-damage in bone, as a function of the rate of production and rate of repair, underlies the development of stress fractures, increasing fragility associated to age and osteoporosis, especially in transmenopausal women. Patients and MethodsQuasi-static and nano-dynamic mechanical characterization were undertaken in trabecular bone from femoral neck biopsies of postmenopausal women. AFM (Atomic Force Microscopy) complementary studies were performed to determine nano-roughness (SRa) and the fibrils width of collagen. Nanoindentations were used to quantify transmenopausal changes in intrinsic mechanical properties of trabecular bone: hardness (Hi), modulus of Young (Ei), complex modulus (E*), tan delta (δ), storage modulus (E') and loss modulus (E"). ResultsAs result of the quasi-static measurements, 0.149 (0.036) GPa and 2.95 (0.73) GPa of Hi and Ei were obtained, respectively. As result of the nano-dynamic measurements, 17.94 (3.15), 0.62 (0.10), 13.79 (3.21 and 6.39 (1.28) GPa of E*, tan (δ), E' and E" were achieved, respectively. 101.07 SRa and 831.28 nm of fibrils width were additionally obtained. ConclusionsThis study poses a first approach to the measurement of bone quality in postmenopausal trabecular bone by combining quasi-static, nano-DMA analysis and tribology of dentin surface through AFM characterization.

Prolonged high force high repetition pulling induces trabecular bone loss and microcracks, while low force high repetition pulling induces bone anabolism

We have an operant rat model of upper extremity reaching and grasping in which we examined the impact of performing a high force high repetition (High-ForceHR) versus a low force low repetition (Low-ForceHR) task for 18 weeks on the radius, compared to age-matched controls. High-ForceHR rats performed at 4 reaches/min and 50% of their maximum voluntary pulling force for 2 hrs/day, 3 days/wk. Low-ForceHR rats performed at 6% maximum voluntary pulling force. High-ForceHR rats showed decreased trabecular bone volume in the distal radius and increased catabolic indices (microcracks and increased osteocyte apoptosis), compared to controls. In contrast, Low-ForceHR rats showed increased trabecular bone volume, and no microcracks or osteocyte apoptosis. Thus, prolonged performance of an upper extremity reaching and grasping task is loading-dependent with high force loading leading to accumulation of bone microdamage. The target grasp force (1.27N) of the High-ForceHR rats was 50% of their mean maximum voluntary force of 2.45N, easily below the predicted maximum acceptable force (MAF) of 1.64N (predicted from published equations). The presence of microcracks and bone loss leads us to suggest that the published equations over-estimated the MAF on these tissues by 1.3 fold.

An Automated Step-Wise Micro-Compression Device for 3D Dynamic Image-Guided Failure Assessment of Bone Tissue on a Microstructural Level Using Time-Lapsed Tomography

Microstructural bone phenotypes, such as the intracortical canal network, could be directly linked to the mechanical failure behavior of cortical bone tissue. In addition, high accumulation of microdamage can significantly increase bone brittleness and thus, is a precursor of mechanical failure. Here, we discuss the development and validation of an automated step-wise micro-compression device (MCD) for dynamic image-guided failure assessment (DIGFA) of intracortical bone microstructure and bone microdamage. The device was found to be highly accurate and precise with positioning errors of less than 1 µm and force errors of less than 1.25 N. In addition, the results of a first biological study using DIGFA and time-lapsed computed tomography are presented. In short, whole mouse femora from mature C57BL/6 (B6) and C3H/He (C3H) mice with mid-diaphyseal notches were tested in step-wise compression and concomitantly imaged until failure. DIGFA was performed at the TOMCAT beamline of the Swiss Light Source using synchrotron radiation-based computed tomography (SR CT). Following the experiment, intracortical porosity was separated into the canal network, osteocyte lacunae, and microcracks for subsequent morphometric evaluation. The thicker cortex of C3H was penetrated by a dense canal network, whereas in B6 only a few scattered canals were observed. For B6, the first occurrence of crack was noted at 1.45% local strain, while for C3H, crack initiation took place only at 2.66% local strain. In addition, we were able to relate whole bone mechanics to local failure events by deriving correlations between microstructural porosity and microdamage propagation. In conclusion, initiation and accumulation of microcracks were investigated for two mouse phenotypes demonstrating that DIGFA in combination with SR CT is a suitable technique for time-lapsed three-dimensional assessment of bone morphology and bone fracture behavior down to the cellular level.

Subchondral bone microdamage accumulation in distal metacarpus of Thoroughbred racehorses

Microdamage accumulation leads to subchondral bone injury and/or fracture in racehorses. An understanding of this process is essential for developing strategies for injury prevention. To quantify subchondral bone microdamage in the third metacarpal bone of Thoroughbred racehorses at different stages of the training cycle. Cross-sectional. Bone blocks from the palmar aspect of the medial condyles of third metacarpal bones from 46 racing Thoroughbred horses undergoing post-mortem were examined with micro computed tomography (microCT) to detect calcified microcracks, and light microscopy to quantify bulk stained microcracks. Racing and training histories were obtained for comparison with microdamage data using regression modelling. Subchondral bone microcracks were observed in all bones with at least one method. Microdamage grade was greater in older horses, levelling-off for horses 5 years and older (quadratic term P = 0.01), and with lower bone material density in the parasagittal groove (P = 0.02). Microcrack density was higher in older horses (P = 0.004), and with higher bone volume fraction (BV/TV) in the parasagittal groove in horses in training (interaction effect, P = 0.01) and lower in horses resting from training (P = 0.02). Cross-sectional data only. Incomplete detection of microdamage due to the limits of resolution of microCT and lack of three-dimensional imaging with microscopy. Multicollinearity between variables that indicated career progression (e.g. age, number of career starts, duration of training period) was detected. Fatigue damage in the distal metacarpal subchondral bone is common in Thoroughbred racehorses undergoing post-mortem and appears to accumulate throughout a racing career. Reduced intensity or duration of training and racing and/or increased duration of rest periods may limit microdamage accumulation. Focal subchondral bone sclerosis indicates the presence of microdamage.

Bone matrix microdamage and vascular changes characterize bone marrow lesions in the subchondral bone of knee osteoarthritis.

Bone marrow lesions (BMLs) in the subchondral bone in osteoarthritis (OA) are suggested to be multifactorial, although the pathogenic mechanisms are unknown. Bone metabolism and cardiovascular risk factors associate with BML in epidemiologic studies. However, there are no studies at the tissue level investigating the relationship between these processes and BML. The aim of this study was to investigate the relationship between BMLs in the tibial plateau (TP) of knee OA and bone matrix microdamage, osteocyte density and vascular changes. TP were obtained from 73 patients at total knee replacement surgery and BMLs were identified ex vivo in TP tissue using MRI. Comparator 'No BML' tissue was from matched anatomical sites to the BMLs. Quantitative assessment was made of subchondral bone microdamage, bone resorption indices, osteocyte cellularity, and vascular features. Several key parameters were different between BML and No BML tissue. These included increased microcrack burden (p = .01, p = .0001), which associated positively with bone resorption and negatively with cartilage volume, and greater osteocyte numerical density (p = .02, p = .01), in the subchondral bone plate and subchondral trabeculae, respectively. The marrow tissue within BML zones contained increased arteriolar density (p = .04, p = .0006), and altered vascular characteristics, in particular increased wall thickness (p = .007) and wall:lumen ratio (wall thickness over internal lumen area) (p = .001), compared with No BML bone. Increased bone matrix microdamage and altered vasculature in the subchondral bone of BMLs is consistent with overloading and vascular contributions to the formation of these lesions. Given the important role of BMLs in knee OA, these contributing factors offer potential targets for the treatment and prevention of knee OA.

Increased sclerostin associated with stress fracture of the third metacarpal bone in the Thoroughbred racehorse.

ObjectivesThe exact aetiology and pathogenesis of microdamage-induced long bone fractures remain unknown. These fractures are likely to be the result of inadequate bone remodelling in response to damage. This study aims to identify an association of osteocyte apoptosis, the presence of osteocytic osteolysis, and any alterations in sclerostin expression with a fracture of the third metacarpal (Mc-III) bone of Thoroughbred racehorses.MethodsA total of 30 Mc-III bones were obtained; ten bones were fractured during racing, ten were from the contralateral limb, and ten were from control horses. Each Mc-III bone was divided into a fracture site, condyle, condylar groove, and sagittal ridge. Microcracks and diffuse microdamage were quantified. Apoptotic osteocytes were measured using TUNEL staining. Cathepsin K, matrix metalloproteinase-13 (MMP-13), HtrA1, and sclerostin expression were analyzed.ResultsIn the fracture group, microdamage was elevated 38.9% (sd 2.6) compared with controls. There was no difference in the osteocyte number and the percentage of apoptotic cells between contralateral limb and unraced control; however, there were significantly fewer apoptotic cells in fractured samples (p < 0.02). Immunohistochemistry showed that in deep zones of the fractured samples, sclerostin expression was significantly higher (p < 0.03) than the total number of osteocytes. No increase in cathepsin K, MMP-13, or HtrA1 was present.ConclusionThere is increased microdamage in Mc-III bones that have fractured during racing. In this study, this is not associated with osteocyte apoptosis or osteocytic osteolysis. The finding of increased sclerostin in the region of the fracture suggests that this protein may be playing a key role in the regulation of bone microdamage during stress adaptation.Cite this article: N. Hopper, E. Singer, F. Henson. Increased sclerostin associated with stress fracture of the third metacarpal bone in the Thoroughbred racehorse. Bone Joint Res 2018;7:94–102. DOI: 10.1302/2046-3758.71.BJR-2016-0202.R4.

An in vivo model of a mechanically-induced bone marrow lesion

Bone marrow lesions (BMLs) are radiologic abnormalities in magnetic resonance images of subchondral bone that are correlated with osteoarthritis. Little is known about the physiologic processes within a BML, although BMLs are associated with mechanical stress, bone tissue microdamage and increased bone remodeling. Here we establish a rabbit model to study the pathophysiology of BMLs. We hypothesized that in vivo loads that generate microdamage in cancellous bone would also create BMLs and increase bone remodeling. In vivo cyclic loading (0.2–2.0 MPa in compression for 10,000 cycles at 2 Hz) was applied to epiphyseal cancellous bone in the distal femurs of New Zealand white rabbits (n=3, right limb loaded, left limb controls experienced surgery but no loading). Magnetic resonance images were collected using short tau inversion recovery (STIR) and T1 weighted sequences at 1 and 2 weeks after surgery/loading and histological analysis of the BML was performed after euthanasia to examine tissue microdamage and remodeling. Loaded limbs displayed BMLs while control limbs showed only a small BML-like signal caused by surgery. Histological analysis of the BML at 2 weeks after loading showed increased tissue microdamage (p=0.03) and bone resorption (p=0.01) as compared to controls. The model described here displays the hallmarks of load-induced BMLs, supporting the use of the model to examine changes in bone during the development, progression and treatment of BMLs.

A rate-independent continuum model for bone tissue with interaction of compressive and tensile micro-damage

Low bone strength is a major risk factor for osteoporotic fractures and is only partially determined by clinical densitometry. Accumulated micro-damage induces residual strains, degrades elastic modulus and reduces bone strength independently of bone mineral density. Histologically, overloading of bone in compression and tension leads to distinct crack size, distribution and orientation which interact during combined loading scenarios. Statistics of rheological models can describe this process and reproduce experimental stress-strain curves with an unprecedented realism, but are computationally expensive and therefore difficult to generalize to 3D. Accordingly, the aim of this work is to formulate a continuum damage model that describes the key features of bone micro-damage, namely the accumulation of residual strains, the degradation of elastic modulus and the reduction of strength in compression, tension and especially in their sequential application. The promising qualitative agreement of the model with the experiments will motivate a generalization to 3D and allow the biomechanical investigation of bones and bone-implant systems subjected to cyclic overloading in tension and/or compression.

Bisphosphonates and atypical subtrochanteric fractures of the femur.

ObjectivesBisphosphonates are widely used as first-line treatment for primary and secondary prevention of fragility fractures. Whilst they have proved effective in this role, there is growing concern over their long-term use, with much evidence linking bisphosphonate-related suppression of bone remodelling to an increased risk of atypical subtrochanteric fractures of the femur (AFFs). The objective of this article is to review this evidence, while presenting the current available strategies for the management of AFFs.MethodsWe present an evaluation of current literature relating to the pathogenesis and treatment of AFFs in the context of bisphosphonate use.ResultsSix broad themes relating to the pathogenesis and management of bisphosphonate-related AFFs are presented. The key themes in fracture pathogenesis are: bone microdamage accumulation; altered bone mineralisation and altered collagen formation. The key themes in fracture management are: medical therapy and surgical therapy. In addition, primary prevention strategies for AFFs are discussed.ConclusionsThis article presents current knowledge about the relationship between bisphosphonates and the development of AFFs, and highlights key areas for future research. In particular, studies aimed at identifying at-risk subpopulations and organising surveillance for those on long-term therapy will be crucial in both increasing our understanding of the condition, and improving population outcomes.Cite this article: N. Kharwadkar, B. Mayne, J. E. Lawrence, V. Khanduja. Bisphosphonates and atypical subtrochanteric fractures of the femur. Bone Joint Res 2017;6:144–153. DOI: 10.1302/2046-3758.63.BJR-2016-0125.R1.

Subchondral bone microarchitecture and failure mechanism under compression: A finite element study

Subchondral bone (SCB) microdamage is commonly observed in traumatic joint injuries and has been strongly associated with post-traumatic osteoarthritis (PTOA). Knowledge of the three-dimensional stress and strain distribution within the SCB tissue helps to understand the mechanism of SCB failure, and may lead to an improved understanding of mechanisms of PTOA initiation, prevention and treatment. In this study, we used high-resolution micro-computed tomography (µCT)-based finite element (FE) modelling of cartilage-bone to evaluate the failure mechanism and the locations of SCB tissue at high-risk of initial failure under compression. The µCT images of five cartilage-bone specimens with an average SCB thickness of 1.23±0.20mm were used to develop five µCT-based FE models. The FE models were analysed under axial compressions of approximately 30MPa applied to the cartilage surface while the bone edges were constrained. Strain and stress-based failure criteria were then applied to evaluate the failure mechanism of the SCB tissue under excessive compression through articular cartilage. µCT-based FE models predicted two locations in the SCB at high-risk of initial failure: (1) the interface of the calcified-uncalcified cartilage due to excessive tension, and (2) the trabecular bone beneath the subchondral plate due to excessive compression. µCT-based FE models of cartilage-bone enabled us to quantify the distribution of the applied compression which was transferred through the articular cartilage to its underlying SCB, and to investigate the mechanism and the mode of SCB tissue failure. Ultimately, the results will help to understand the mechanism of injury formation in relation to PTOA.

Calcium and bone metabolism across women's life stages. Stress fracture in female athletes.

Stress fractures are common overuse injuries in athletes, especially in long-distance runner, jumping sports and gymnastics in female athletes. The pathology of stress fracture mainly includes repeated biomechanical loading, which leads to bone micro-damage and failure of bone structure. Female athlete triad(FAT), which includes low energy availability with or without an eating disorder, functional hypothalamic amenorrhea, and osteoporosis, is a serious healthcare concern in female athletes. For prevention and treatment of stress fracture, management of biomechanical factors modifying the load applied to a bone is important, and especially in female athletes, management for FAT is one of the important factors. This report outlines the current knowledge on the epidemiology, diagnosis, treatment and prevention of stress fracture, relating to FAT in female athletes.

Achieving ultrasensitive invivo detection of bone crack with polydopamine-capsulated surface-enhanced Raman nanoparticle.

The timely diagnosis and intervention of bone microdamage are essential for preventing its accumulation and further diminishing the risk of skeletal fracture. Although staining methods have been adopted to better depict the microdamage on bone, their clinical impacts are still limited because they are based on histological sections which are inherently destructive. Here, highly sensitive and non-invasive invivo detection of bone crack can be achieved by surface-enhanced Raman scattering (SERS) technique using a carefully chosen polydopamine (PDA)-SERS nanoparticle tag. The bone crack can be specifically labeled by PDA-SERS tags taking advantage of high affinity of PDA towards calcium exposed on the damaged bone, and identified by an intense featured Raman signal both invitro and invivo benefiting from the surface-enhanced resonance Raman scattering effect. As a preliminary invivo application, it is found that PDA-SERS tags present no serious adverse effect in mouse model and hold good biocompatibility. This work may help the development of SERS technique for ultrasensitive invivo detection of bone crack in clinic.

Characterizing microcrack orientation distribution functions in osteonal bone samples.

Prefailure microdamage in bone tissue is considered to be the most detrimental factor in defining its strength and toughness with respect to age and disease. To understand the influence of microcracks on bone mechanics it is necessary to assess their morphology and three-dimensional distribution. This requirement reaches beyond classic histology and stereology, and methods to obtain such information are currently missing. Therefore, the aim of the study was to develop a methodology that allows to characterize three-dimensional microcrack distributions in bulk bone samples. Four dumbbell-shaped specimens of human cortical bone of a 77-year-old female donor were loaded beyond yield in either tension, compression or torsion (one control). Subsequently, synchrotron radiation micro-computed tomography (SRμCT) was used to obtain phase-contrast images of the damaged samples. A microcrack segmentation algorithm was developed and used to segment microcrack families for which microcrack orientation distribution functions were determined. Distinct microcrack families were observed for each load case that resulted in distinct orientation distribution functions. Microcracks had median areas of approximately 4.7 μm2 , 33.3 μm2 and 64.0 μm2 for tension, compression and torsion. Verifying the segmentation algorithm against a manually segmented ground truth showed good results when comparing the microcrack orientation distribution functions. A size dependence was noted when investigating the orientation distribution functions with respect to the size of the volume of interest used for their determination. Furthermore, a scale separation between tensile, compressive and torsional microcracks was noticeable. Visual comparison to classic histology indicated that microcrack families were successfully distinguished. We propose a methodology to analyse three-dimensional microcrack distributions in overloaded cortical bone. Such information could improve our understanding of bone microdamage and its impact on bone failure in relation to tissue age and disease.

Equine subchondral bone failure threshold under impact compression applied through articular cartilage

Subchondral bone microdamage due to high-impact loading is a key factor leading to post-traumatic knee osteoarthritis. A quantified assessment of the mechanical characteristics of subchondral bone at the tissue-level is essential to study the mechanism of impact-induced microdamage. We combined mechanical impact testing of equine cartilage-bone with µCT image-based finite element models (μFEM) of each specimen to determine subchondral bone (including calcified cartilage: CCSB) elastic tissue modulus and local stresses and strains associated with micro-fractures within the CCSB tissue. The material properties of each specimen-specific μFEM were iteratively adjusted to match the FE-predicted stress-strain curves with experimental results. Isotropic homogeneous material properties for both uncalcified cartilage (UC) and CCSB were assumed. UC large-deformation was simulated using hyperelastic material properties. Final UC shear and CCSB tissue elastic modulus of G=38±20MPa and Et=3.3±0.7GPa were achieved after fit procedure. The results suggested that initial failure in CCSB occurred at local tensile and compressive stresses of 29.47±5.34 MPa and 64.3±21.3MPa, and tensile and compressive strains of 1.12±0.06% and 1.99±0.41%, respectively. Tissue-level material properties can be used in finite element modeling of diarthrodial joints under impact loading, and also in designing artificial cartilage-bone to replace the damaged tissue in the joint. Results can provide an estimate for the threshold of initial failure in subchondral bone tissue due to an impact compression transmitted through the overlying articular cartilage.

Implant-induced microdamage in osteoporotic bone

AbstractWith the increase of elderly population,more and more implant operations need to be performed in osteoporotic bone, while different forms of microdamage will be produced in peri-implant bone intraoperatively, including high- and low-density diffuse damages, as well as linear cracks. The length and location of the microcracks are the main factors in affecting the biomechanical performance of bone. Suppression of bone remodeling by bisphosphonates may lead to microdamage accumulation, which is often accompanied with the decrease of bone strength and the increase of bone fragility. Microdamage can be repaired by bone remodeling or mineralization to maintain the strength and structural integrity. Both remodeling and mineralization can affect the bone quality and long-term implant stability. In this paper, we make a brief summary of some important issues and research progresses in this field.

Effects of antiresorptive therapy on the structural and material properties of bone strength

Bone strength depends on its structural and material properties. Structural properties are determined by the size and shape of bone and also the microarchitecture. Material properties are determined by mineral crystallinity, collagen structure and microdamage in bone. The strength of bone is adapted to the needs of physical activities by biologic mechanisms, bone modeling and remodeling. The deterioration of bone strength in postmenopausal women is characterized by a trabecular bone deficit with poor trabecular connectivity and followed by a cortical bone deficit with trabeculation of endocortical bone and intracortical porosity due to accelerated bone remodeling. In high turnover osteoporosis antiresorptive therapy is effective in preventing the structural deficit and in increasing the stiffness and the toughness(bone strength)by increasing the mean degree of mineralization of bone tissue through the prolongation of secondary mineralization. But the long-term use of strong antiresorber, i.e. bisphosphonate or denosumab, would result in highly mineralized bone and disturbed repair of microcracks by inhibition of bone remodeling. Intermittent use or discontinuation of strong antiresorber after about 3-5 years of administration could be recommended to avoid the deterioration of bone strength.

Finite element models predict the location of microdamage in cancellous bone following uniaxial loading

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 (≥1,000,000μm3 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.

The effect of low fluoride concentrations on microdamage accumulation in mouse tibias under impact loading

Microdamage accumulation in bone is one of the mechanisms for energy dissipation during the fracture process. Changes in the ultrastructure and composition of bone constituents due to aging or diseases could affect microdamage accumulation. Low concentration (1 mM) of sodium fluoride (NaF) has been used in this study to investigate the effect of ultrastructural changes on microdamage accumulation in mouse tibias following free-fall impact loadings. Twenty-two tibias were divided randomly into control and NaF-treated groups. Free-fall impact loading was conducted twice on each tibia to produce microdamage. The elastic modulus of NaF-treated tibias decreased significantly after the impact loadings, while there was no significant difference in the modulus of untreated samples between pre- and post-damage loadings. Microdamage morphology analysis showed that less and shorter microcracks existed in NaF-treated tibias compared with control bones. Meanwhile, more and longer microcracks were observed in tensile regions in untreated samples compared with that in compressive regions, whereas no significant difference was observed between tensile and compressive regions in NaF-treated bones. The results of this study indicate that more energy is required to generate microcracks in NaF-treated bone than in normal bone. A low concentration of fluoride treatment may increase the toughness of bone under impact loading. This study focused on the effect of ultrastructural changes on microdamage in bones under impact loadings. The elastic modulus of the NaF-treated tibias decreased significantly after impact loadings. Less and shorter microcracks existed in NaF-treated tibia bones. More energy is required to generate microdamage in NaF-treated bones. A low concentration of fluoride treatment may increase the toughness of bone.

A THREE-DIMENSIONAL COMPUTER MODEL TO SIMULATE SPONGY BONE REMODELING UNDER OVERLOAD USING A SEMI-MECHANISTIC BONE REMODELING THEORY

Overload has been suggested as a contributing factor for bone loss, for instance at the bone implant interface. The objective of this study is to investigate spongy bone resorption under overload using a semi-mechanistic bone remodeling theory. Since overload can cause the accumulation of microdamage in bone, in this study, it is assumed that overload will increase the osteoclastic activity, and also will reduce the osteocyte influence distance. First, a previously proposed semi-mechanistic bone remodeling theory was extended by defining a new form for the resorption probability function, which is based on experimental evidence. Then, in order to investigate the validity of our hypothesis, a three-dimensional finite element model of spongy bone was developed. The simulation results show that, first, trabeculae adapt with the mechanical stimuli placed on them. Secondly, a sharp reduction in spongy bone density will be resulted, in agreement with experimental evidence, when bone is under overload.