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Carbon-fiber-reinforced polyetheretherketone (CF/PEEK) composites are widely utilized in aerospace, medical devices, and automotive industries, renowned for their superior mechanical properties and high-temperature resistance. Despite these advantages, the thermomechanical coupling behavior of CF/PEEK under dynamic loading conditions is not well understood. This study aims to explore the thermomechanical coupling effects of CF/PEEK at elevated strain rates, employing Hopkinson bar impact tests and scanning electron microscopy (SEM) for detailed characterization. Our findings indicate that an increase in temperature led to significant reductions in the yield strength, peak stress, and specific energy absorption of CF/PEEK, while fracture strain had no significant effect. For instance, at 200 °C, the yield strength, peak stress, and specific energy absorption decreased by 39%, 37%, and 38%, respectively, compared to their values at 20 °C. Furthermore, as the strain rate increased, the yield strength, peak stress, specific energy absorption, and fracture strain all exhibited strain-hardening effects. However, as the strain rate further increased, above 4000 s-1, the enhancing effect of the strain rate on the yield strength and peak stress gradually diminished. The interaction of the temperature and strain rate significantly affected the mechanical performance of CF/PEEK under high-speed impact conditions. While the strain rate generally enhanced these properties, the strain-hardening effect on the yield strength weakened as the temperature increased, and both the temperature and strain rate contributed to the increase in specific energy absorption. Microdamage mechanism analysis revealed that interface debonding and sliding between the fibers and the matrix were more pronounced under static compression than under dynamic compression, thereby diminishing the efficiency of stress transfer. Additionally, higher temperatures caused the PEEK matrix to soften and exhibit increased viscoelastic behavior, which in turn affected the material's toughness and the mechanisms of stress transfer. These insights hold substantial engineering significance, particularly for the optimization of CF/PEEK composite design and applications in extreme environments.

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Prediction of bone fracture risk is clinically challenging. Computational modeling plays a vital role in understanding bone structure and diagnosing bone diseases, leading to novel therapies. The research objectives were to demonstrate the anisotropic structure of the bone at the micro-level taking into consideration the density and subject demography, such as age, gender, body mass index (BMI), height, weight, and their roles in damage accumulation. Out of 438 developed 3D bone models at the micro-level, 46.12% were female. The age distribution ranged from 23 to 95 years. The research unfolds in two phases: micro-morphological features examination and stress distribution investigation. Models were developed using Mimics 22.0 and SolidWorks. The anisotropic material properties were defined before importing into Ansys for simulation. Computational simulations further uncovered variations in maximum von-Misses stress, highlighting that young Black males experienced the highest stress at 127.852 ± 10.035 MPa, while elderly Caucasian females exhibited the least stress at 97.224 ± 14.504 MPa. Furthermore, age-related variations in stress levels for both normal and osteoporotic bone micro models were elucidated, emphasizing the intricate interplay of demographic factors in bone biomechanics. Additionally, a prediction equation for bone density incorporating demographic variables was proposed, offering a personalized modeling approach. In general, this study, which carefully examines the complexities of how bones behave at the micro-level, emphasizes the need for an enhanced approach in orthopedics. We suggest taking individual characteristics into account to make therapeutic interventions more precise and effective.

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Hydrogel-based devices commonly have a high demand for material durability when subjected to prolonged or cyclic loads. To extend their service life, it is crucial to have a deep understanding of the fatigue mechanisms of hydrogels. It is well-known that double-network (DN) hydrogels are characterized by high strength and toughness and are thus recognized as a promising candidate under load-bearing conditions. However, the existing studies in the literature mainly focus on their resistant capability to fatigue crack growth, while the underlying mechanisms of fatigue crack nucleation are still inconclusive. This work aims to bridge this knowledge gap by formulating a fatigue life predictor for DN hydrogels within the framework of configurational mechanics to elucidate the underlying mechanisms governing fatigue crack nucleation. The fatigue life predictor for DN hydrogels is derived from the configurational stress by incorporating the corresponding constitutive models and the thermodynamic evolution laws for microdamage mechanisms and material viscoelasticity. With the developed fatigue predictor, the effect of the microdamage mechanism on fatigue is elucidated, i.e., the internal damage of the sacrificial network can improve the fatigue life of DN hydrogels. The fatigue life predictor is also adopted to evaluate the effects of some other factors on the fatigue crack nucleation, such as the loading rate, pre-stretching treatment, and water diffusion, identifying feasible loading profiles that could improve material durability. Overall, the theoretical framework and the modeling results in this work are expected to shed light on unveiling the fatigue mechanisms of DN hydrogels and advance the design of hydrogel-based devices.

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Bone microdamage is common at subchondral bone (SCB) sites subjected to repeated high rate and magnitude of loading in the limbs of athletic animals and humans. Microdamage can affect the biomechanical behaviour of bone under physiological loading conditions. To understand the effects of microdamage on the mechanical properties of SCB, it is important to be able to quantify it. The extent of SCB microdamage had been previously estimated qualitatively using plain microcomputed tomography (µCT) and a radiocontrast quantification method has been used for trabecular bone but this method may not be directly applicable to SCB due to differences in bone structure. In the current study, SCB microdamage detection using lead uranyl acetate (LUA) and quantification by contrast-enhanced µCT and backscattered scanning electron microscopy (SEM) imaging techniques were assessed to determine the specificity of the labels to microdamage and the accuracy of damaged bone volume metrices. SCB specimens from the metacarpus of racehorses, with the hyaline articular cartilage (HAC) removed, were grouped into two with one group subjected to ex vivo uniaxial compression loading to create experimental bone damage. The other group was not loaded to preserve the pre-existing in vivo propagated bone microdamage. A subset of each group was stained with LUA using an established or a modified protocol to determine label penetration into SCB. The µCT and SEM images of stained specimens showed that penetration of LUA into the SCB was better using the modified protocol, and this protocol was repeated in SCB specimens with intact hyaline articular cartilage. The percentage of total label localised to bone microdamage was determined on SEM images, and the estimated labelled bone volume determined by µCT in SCB groups was compared. Label was present around diffuse and linear microdamage as well as oblique linear microcracks present at the articular surface, except in microcracks with high-density mineral infills. Bone surfaces lining pores with recent mineralisation were also labelled. Labelled bone volume fraction (LV/BV) estimated by µCT was higher in the absence of HAC. At least 50% of total labels were localised to bone microdamage when the bone area fraction (B.Ar/T.Ar) of the SCB was greater than 0.85 but less than 30% when B.Ar/T.Ar of the SCB was less than 0.85. To adjust for LUA labels on bone surfaces, a measure of the LV/BV corrected for bone surface area (LV/BV BS-1) was used to quantify damaged SCB. In conclusion, removal of HAC and using a modified labelling protocol effectively stained damaged SCB of the metacarpus of racehorses and represents a technique useful for quantifying microdamage in SCB. This method can facilitate future investigations of the effects of microdamage on joint physiology.

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Bone turnover and microdamage are impacted by the presence of skeletal metastases which can contribute to increased fracture risk. Treatments for metastatic disease may further impact bone quality. This exploratory study aimed to establish an initial understanding of microdamage accumulation and load to failure in healthy and osteolytic rat vertebrae following focal and systemic cancer treatment (docetaxel (DTX), stereotactic body radiotherapy (SBRT), or zoledronic acid (ZA)). Osteolytic spine metastases were developed in 6-week-old athymic female rats via intracardiac injection of HeLa human cervical cancer cells (day 0). Additional rats served as healthy controls. Rats were either untreated, received SBRT to the T10-L6 vertebrae on day 14 (15 Gy, two fractions), DTX on day 7 or 14, or ZA on day 7. Rats were euthanized on day 21. Tumor burden was assessed with bioluminescence images acquired on day 14 and 21, histology of the excised T11 and L5 vertebrae, and ex-vivo µCT images of the T13-L4. Microstructural parameters (bone volume/total volume, trabecular number, spacing, thickness, and bone mineral density) were measured from L2 vertebrae. Load to failure was measured with axial compressive loading of the L1-L3 motion segments. Microdamage accumulation was labeled in T13 vertebrae with BaSO4 staining and was visualized with high resolution µCT imaging. Microdamage volume fraction was defined as the ratio of BaSO4 to bone volume. DTX administered on day 7 reduced tumor growth significantly (p < 0.05). Microdamage accumulation was found to be increased by the presence of metastases but was reduced by all treatments with ZA showing the largest improvement in HeLa cell injected rats. Load to failure was decreased in untreated and SBRT HeLa cell injected rats compared to healthy controls (p < 0.01). There was a moderate negative correlation between load to failure and microdamage volume fraction in vertebrae from rats injected with HeLa cells (R = -0.35, p = 0.031). Strong correlations were also found between microstructural parameters and load to failure and microdamage accumulation. Several factors, including the presence of osteolytic lesions and use of cancer therapies, influence microdamage accumulation and load to failure in rat vertebrae. Understanding the impact of these treatments on fracture risk of metastatic vertebrae is important to improve management of patients with spinal metastases.

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As a daily physiological mechanism in bone, microdamage accumulation dissipates energy and helps to prevent fractures. However, excessive damage accumulation might bring adverse effects to bone mechanical properties, which is especially problematic among the osteoporotic and osteopenic patients treated by bisphosphonates. Some pre-clinical studies in the literature applied forelimb loading models to produce well-controlled microdamage in cortical bone. Ovariectomized animals were also extensively studied to assimilate human conditions of estrogen-related bone loss. In the present study, we combined both experimental models to investigate microdamage accumulation in the context of osteopenia and zoledronate treatment. Three-month-old normal and ovariectomized rats treated by saline or zoledronate underwent controlled compressive loading on their right forelimb to create in vivo microdamage, which was then quantified by barium sulfate contrast-enhanced micro-CT imaging. Weekly in vivo micro-CT scans were taken to evaluate bone (re)modeling and to capture microstructural changes over time. After sacrifice, three-point-bending tests were performed to assess bone mechanical properties. Results show that the zoledronate treatment can reduce cortical microdamage accumulation in ovariectomized rats, which might be explained by the enhancement of several bone structural properties such as ultimate force, yield force, cortical bone area and volume. The rats showed increased bone formation volume and surface after the generation of microdamage, especially for the normal and the ovariectomized groups. Woven bone formation was also observed in loaded ulnae, which was most significant in ovariectomized rats. Although all the rats showed strong correlations between periosteal bone formation and microdamage accumulation, the correlation levels were lower for the zoledronate-treated groups, potentially because of their lower levels of microdamage. The present study provides insights to further investigations of pharmaceutical treatments for osteoporosis and osteopenia. The same experimental concept can be applied in future studies on microdamage and drug testing.

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In this study, the role of inelastic deformation of bone on its strain rate-dependent mechanical behaviour was investigated. For this, human cortical bone samples were cyclically loaded to accumulate inelastic strain and subsequently, mechanical response was investigated under compressive loading at different strain rates. The strain rate behaviour of fatigued samples was compared with non-loaded control samples. Furthermore, cyclic loading-induced microdamage was quantified through histological analysis. The compression test results show that the strength of fatigue-loaded bone reduced significantly at low strain rates but not at high strain rates. The difference in microcrack density was not significant between fatigued and control groups. The results indicate that the mechanism of load transfer varies between low strain rate and high strain rate regimes. The inelastic deformation mechanisms are more prominent at low strain rates but not at high strain rates. This study shed light on the role of inelastic deformation on the rate-dependent behaviour of cortical bone.

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Microdamage accumulated through sustained periods of cyclic loading or single overloading events contributes to bone fragility through a reduction in stiffness and strength. Monitoring microdamage in vivo remains unattainable by clinical imaging modalities. As such, there are no established computational methods for clinical fracture risk assessment that account for microdamage that exists in vivo at any specific timepoint. We propose a method that combines multiple clinical imaging modalities to identify an indicative surrogate, which we term 'hidden porosity', that incorporates pre-existing bone microdamage in vivo. To do so, we use the third metacarpal bone of the equine athlete as an exemplary model for fatigue induced microdamage, which coalesces in the subchondral bone. N = 10 metacarpals were scanned by clinical quantitative computed tomography (QCT) and magnetic resonance imaging (MRI). We used a patch-based similarity method to quantify the signal intensity of a fluid sensitive MRI sequence in bone regions where microdamage coalesces. The method generated MRI-derived pseudoCT images which were then used to determine a pre-existing damage (Dpex) variable to quantify the proposed surrogate and which we incorporate into a nonlinear constitutive model for bone tissue. The minimum, median, and maximum detected Dpex of 0.059, 0.209, and 0.353 reduced material stiffness by 5.9%, 20.9%, and 35.3% as well as yield stress by 5.9%, 20.3%, and 35.3%. Limb-specific voxel-based finite element meshes were equipped with the updated material model. Lateral and medial condyles of each metacarpal were loaded to simulate physiological joint loading during gallop. The degree of detected Dpex correlated with a relative reduction in both condylar stiffness (p = 0.001, R2 > 0.74) and strength (p < 0.001, R2 > 0.80). Our results illustrate the complementary value of looking beyond clinical CT, which neglects the inclusion of microdamage due to partial volume effects. As we use clinically available imaging techniques, our results may aid research beyond the equine model on fracture risk assessment in human diseases such as osteoarthritis, bone cancer, or osteoporosis.

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Bone adaptation to mechanical loading happens predominantly via modeling and remodeling, but the latter is poorly understood. Haversian remodeling (cortical bone replacement resulting in secondary osteons) is thought to occur in regions of low strain as part of bone maintenance or high strain in response to microdamage. However, analyses of remodeling in primates have revealed an unappreciated association with the number of daily load cycles. We tested this relationship by raising 30 male domestic rabbits (Oryctolagus cuniculus) on disparate diets from weaning to adulthood (48 weeks), facilitating a naturalistic perspective on mandibular bone adaptation. A control group consumed only rabbit pellets and an 'overuse' group ate hay in addition to pellets. To process hay, which is tougher and stiffer, rabbits increase chewing investment and duration without increasing bite force (i.e. corpus mean peak strain is similar for the two foods). Corpus remodeling in overuse rabbits was ∼1.5 times that of controls, measured as osteon population density and percentage Haversian bone. In the same subjects, there was a significant increase in overuse corpus bone formation (ratio of cortical area to cranial length), consistent with previous reports on the same dietary manipulation and bone formation in rabbits. This is the first evidence that both modeling and remodeling are simultaneously driven by the number of load cycles, independent of strain magnitude. This novel finding provides unique data on the feeding apparatus, challenges traditional thought on Haversian remodeling, and highlights the need for experimental studies of skeletal adaptation that examine mechanical factors beyond strain magnitude.

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BACKGROUND: The aim of this study was to investigate the effects of orthodontic miniscrew pitch and thread shape on microdamage in cortical bone. The relationship between the microdamage and primary stability was also examined. METHODS: Ti6Al4V orthodontic miniscrews and 1.0-mm-thick cortical bone pieces from fresh porcine tibia were prepared. The orthodontic miniscrews had custom-made thread height (H) and pitch (P) size geometries, and were classified into three groups: control geometry; HCPC (HC; thread height = 0.12 mm, PC; pitch size = 0.60 mm), geometry with a narrower pitch; HCPN (HC; thread height = 0.12 mm, PN; pitch size = 0.30 mm), and geometry with a taller thread height; HTPC (HT; thread height = 0.36 mm, PC; pitch size = 0.60 mm). The orthodontic miniscrews were inserted into a pilot hole in the cortical bone, and maximum insertion torque and Periotest value were measured. After insertion, the samples were stained with basic fuchsin. Histological thin sections were obtained and the bone microdamage parameters, i.e., total crack length and total damage area, and insertion state parameters, i.e., orthodontic miniscrew surface length and bone compression area were calculated. RESULTS: The orthodontic miniscrews with the taller thread height resulted in lower primary stability with minimal bone compression and microdamage; however, the narrower thread pitch led to maximum bone compression and extensive bone microdamage. CONCLUSIONS: A wider thread pitch reduced microdamage, and decreased thread height resulted in increased bone compression, ultimately resulting in increased primary stability.

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Bone is a dynamic tissue capable of adapting to its loading environment, allowing the skeleton to remain structurally sound throughout life. One way adaptation occurs in mammals is via Haversian remodeling: the site-specific, coupled resorption and formation of cortical bone that results in secondary osteons. Remodeling occurs at a baseline rate in most mammals, but it also occurs in relation to strain by repairing deleterious microdamage. Yet, not all animals with bony skeletons remodel. Among mammals, there is inconsistent or absent evidence for Haversian remodeling among monotremes, insectivores, chiropterans, cingulates, and rodents. Three possible explanations for this disparity are discussed: the capacity for Haversian remodeling, body size as a constraint, and age and lifespan as constraints. It is generally accepted, although not thoroughly documented, that rats (a common model used in bone research) do not typically exhibit Haversian remodeling. The present aim is to more specifically test the hypothesis that rats of advanced age do remodel intracortically because of the longer lifespan over which baseline remodeling could occur. Most published histological descriptions of rat bone only include young (3-6 months) rats. Excluding aged rats possibly overlooks a transition from modeling (i.e., bone growth) to Haversian remodeling as the primary mode of bone adaptation. Here, midshaft and distal femora (typical sites for remodeling in other mammals) of 24-month-old rats were examined for presence of secondary osteons. None were found, suggesting that Haversian remodeling does not occur in rats under normal physiological conditions at any age. A likely explanation is that modeling of cortical bone continues throughout most of the short rat lifespan, negating the stimulus for Haversian remodeling. Thorough sampling of key rodent taxa of varying body sizes and lifespans is key to elucidating the reasons why (i.e., body size, age/lifespan, phylogenetic factors) Haversian remodeling might not occur in all mammals.

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Introduction: Recent evidence has emerged suggesting that a non-contact anterior cruciate ligament (ACL) tear can result from repetitive submaximal loading of the ligament. In other words, when the intensity of ACL-straining athletic activities is increased too rapidly, microdamage can accumulate in the ligament beyond the rate at which it can be repaired, thereby leading to material fatigue in the ligament and its eventual failure. The objective of this survey-based exploratory study was to retrospectively determine whether the levels of various athletic activities performed by ACL-injured patients significantly changed during the 6 months before injury. Methods: Forty-eight ACL-injured patients completed a survey to characterize their participation in various activities (weightlifting, sport-specific drills, running, jumping, cutting, pivoting/twisting, and decelerating) at three timepoints (1 week, 3 months, 6 months) prior to ACL injury. Activity scores, which summarized the frequency and intensity of each activity, were calculated for each patient at each time interval. A series of linear mixed-effects regression models was used to test whether there was a significant change in levels of the various activities in the 6-month period leading up to ACL injury. Results: Patients who sustained a non-contact ACL injury markedly increased their sport-specific drills activity levels in the time leading up to injury (p = 0.098), while those patients who sustained a contact ACL injury exhibited no change in this activity during the same time period (p = 0.829). Levels of running, jumping, cutting, pivoting/twisting, and decelerating increased for non-contact ACL-injured patients but decreased for contact ACL-injured patients, though not significantly (p values > 0.10). Weightlifting activity significantly decreased leading up to injury among contact ACL-injured patients (p = 0.002). Discussion: We conclude that levels of ACL-straining athletic activities or maneuvers in non-contact ACL-injured patients markedly increased in the 6 months leading up to their injury, providing evidence that changing levels of certain activities or maneuvers may play a role in ACL injury risk. This warrants further investigation of the hypothesis that too rapid an increase in activities or maneuvers known to place large loads on the ACL can cause microdamage to accumulate in the ligament, thereby leading to failure.

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This paper studies the drawing-induced intercolonial microdamage (ICMD) in pearlitic microstructures. The analysis was performed from the direct observation of the microstructure of the progressively cold-drawn pearlitic steel wires associated with the distinct steps (cold-drawing passes) of a real cold-drawing manufacturing scheme, constituted by seven cold-drawing passes. Three types of ICMD were found in the pearlitic steel microstructures, all affecting two or more pearlite colonies, namely: (i) intercolonial tearing; (ii) multi-colonial tearing; and (iii) micro-decolonization. The ICMD evolution is quite relevant to the subsequent fracture process of cold-drawn pearlitic steel wires, since the drawing-induced intercolonial micro-defects act as weakest links or fracture promoters/initiators, thereby affecting the microstructural integrity of the wires.

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Bone fragility is a profound complication of type 1 diabetes mellitus (T1DM), increasing patient morbidity. Within the mineralized bone matrix, osteocytes build a mechanosensitive network that orchestrates bone remodeling; thus, osteocyte viability is crucial for maintaining bone homeostasis. In human cortical bone specimens from individuals with T1DM, we found signs of accelerated osteocyte apoptosis and local mineralization of osteocyte lacunae (micropetrosis) compared with samples from age-matched controls. Such morphological changes were seen in the relatively young osteonal bone matrix on the periosteal side, and micropetrosis coincided with microdamage accumulation, implying that T1DM drives local skeletal aging and thereby impairs the biomechanical competence of the bone tissue. The consequent dysfunction of the osteocyte network hampers bone remodeling and decreases bone repair mechanisms, potentially contributing to the enhanced fracture risk seen in individuals with T1DM. STATEMENT OF SIGNIFICANCE: Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disease that causes hyperglycemia. Increased bone fragility is one of the complications associated with T1DM. Our latest study on T1DM-affected human cortical bone identified the viability of osteocytes, the primary bone cells, as a potentially critical factor in T1DM-bone disease. We linked T1DM with increased osteocyte apoptosis and local accumulation of mineralized lacunar spaces and microdamage. Such structural changes in bone tissue suggest that T1DM speeds up the adverse effects of aging, leading to the premature death of osteocytes and potentially contributing to diabetes-related bone fragility.

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Fatigue can cause cracks to propagate from the micro- to the macroscale, which results in a decrease of Young's modulus of the bone. Non-destructive measurements of bone fatigue damage are of great importance for bone quality assessment and fracture prevention. Unfortunately, there is still a lack of effective nondestructive methods sensitive to the initial deterioration during damage accumulation, particularly in the field of orthopedics and biomechanics. In this study, terahertz spectroscopy was adopted to evaluate microscale bone damage. Specifically, the refractive index and Young's modulus of bone samples subjected to different degrees of fatigue damage were tested at a fixed area. Both parameters are found to decrease in two stages under cycled fatigue loading, which is attributed to the initial onset and subsequent development of microdamage during fatigue loading. The change in refractive index reflects the accumulation of fatigue damage as well as the decrease in Young's modulus.

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The growing health and economic burden of bone fractures, their intricate multiscale features and the existing knowledge gaps in the comprehension of micro-scale bone damage occurrence make fracture diagnosis a challenging issue. In this scenario, deep-learning and artificial intelligence embody the new frontier of healthcare system, by overcoming the subjectivity of clinicians in the analysis of medical images. However, the preliminary attempts in exploiting the power of machine learning algorithms such as neural networks are still limited to bone macro-scale, while there is an evident lack in their application to smaller scales, where damage starts nucleating. Currently, speculations at the micro-scale are only feasible with the aid of high-resolution imaging techniques, that are particularly time consuming in terms of output images analysis. In this context, this works aims at combining the visualization of the micro-crack propagation mechanism with the promising application of convolutional neural networks. The implemented artificial intelligence tool is based for the first time on a large number of human synchrotron images coming from healthy and osteoporotic femoral heads tested under micro-compression. The designed convolutional neural networks are able to automatically detect lacunae and micro-cracks at different compression levels with high accuracy levels; indeed, with the baseline setup, networks achieve more than 0.99 level of accuracy for both cracks and lacunae, and more than 0.87 of the meanIoU adopted as validation metric. This approach is particularly encouraging for the development of powerful recognition system to comprehend bone micro-damage initiation and propagation, paving the way to the application of machine learning studies to bone micromechanics. This could be additionally crucial for future patient specific micro-scale observations to be related to the clinical practice.

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INTRODUCTION: One of the current approaches to improve our understanding of osteoporosis is to study the development of bone microdamage under mechanical loading. The current practice for evaluating bone microdamage is to quantify damage volume from images of bone samples stained with a contrast agent, often composed of toxic heavy metals and requiring long tissue preparation. This work aims to evaluate the potential of linear microcracks detection and segmentation in trabecular bone samples using well-known deep learning models, namely YOLOv4 and Unet, applied on microCT images. METHODS: Six trabecular bovine bone cylinders underwent compression until ultimate stress and were subsequently imaged with a microCT at a resolution of 1.95 µm. Two of these samples (samples 1 and 2) were then stained using barium sulfate (BaSO4) and imaged again. The unstained samples (samples 3-6) were used to train two neural networks YOLOv4 to detect regions with microdamage further combined with Unet to segment the microdamage at the pixel level in the detected regions. Four different model versions of YOLOv4 were compared using the average Intersection over Union (IoU) and the mean average precision (mAP). The performance of Unet was also measured using two segmentation metrics, the Dice Score and the Intersection over Union (IoU). A qualitative comparison was finally done between the deep learning and the contrast agent approaches. RESULTS: Among the four versions of YOLOv4, the YOLOv4p5 model resulted in the best performance with an average IoU of 45,32% and 51,12% and a mAP of 28.79% and 46.22%, respectively for samples 1 and 2. The segmentation performance of Unet provided better IoU and DICE score on sample 2 compared to sample 1. The poorer performance of the test on sample 1 could be explained by its poorer contrast to noise ratio (CNR). Indeed, sample 1 resulted in a CNR of 7,96, which was worse than the average CNR in the training samples, while sample 2 resulted in a CNR of 10,08. The qualitative comparison between the contrast agent and the deep learning segmentation showed that two different regions were segmented by the two techniques. Deep learning is segmenting the region inside the cracks while the contrast agent segments the region around it or even regions with no visible damage. CONCLUSION: The combination of YOLOv4 for microdamage detection with Unet for damage segmentation showed a potential for the detection and segmentation of microdamage in trabecular bone. The accuracy of both neural networks achieved in this work is acceptable considering it is their first application in this specific field and the amount of data was limited. Even if the errors from both neural networks are accumulated, the two-steps approach is faster than the semantic segmentation of the whole volume.

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A better understanding of the mechanisms of mechanical fatigue in bone could help improve understanding of the etiology of stress fractures. Investigations of small material samples of bone have identified a nonlinear relationship between strain magnitude, strained volume, and fatigue life, but it is non-trivial to extend these principles to predict the fatigue-life of whole bones which experience complex loading and non-uniform strain distribution. The purpose of this investigation was to experimentally validate a specimen-specific finite element (FE) model that predicts whole-bone fatigue failure using a stochastic model based on strain magnitude and volume. Thirty-four rabbit tibiae were previously tested to failure under cyclic compression, torsion, or both. Strain distribution during the test was estimated from computed-tomography based specimen-specific FE models, and a stochastic failure model based on strain magnitude and volume was used to predict the probability of failure as a function of loading cycles. Model predicted fracture risk matched experimental observations. Respectively, for the 25%, 50%, 75%, and 95% probabilistic predictions, we observed experimental failure ≤ model predicted values in 41%, 53%, 76%, and 80% of the tested specimens. A Brier scoring rule further demonstrated that this model, using strain magnitude and volume, more accurately predicted failure probability compared to two reference models that considered strain magnitude only. In conclusion, the stochastic model may be a powerful tool in future studies to assess mechanical factors that influence stress fracture risk.

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The quest for better predictive tools as well as new preventative and therapeutic measures for bone fragility and fracture has highlighted the need for greater mechanistic understanding of the bone fracture process. Cortical bone, the major load bearing part of the bone, employs different toughening mechanisms to either inhibit or slow down crack growth which leads to fracture. Among these toughening mechanisms, is the formation of a micro-damage process zone (MDPZ) around the region of the propagating crack. Investigations into the MDPZ to date have primarily been based on quasi-static or cyclic loading rate experiments which do not necessarily replicate physiological fracture rates. Consequently, the impact of fall-related loading rates on the formation of the micro-damage process zone was investigated comparing these to quasi-static loading rate equivalents. The size of MDPZ was found to be 42% smaller in the high-rate group compared to the quasi-static rate group. The smaller MDPZ size was associated with a brittle, unstable fracture behaviour and an overall smaller fracture resistance measure (Jmax). This result points to the possibility of a strain rate hardening mechanism at the heart of micro-damage formation, which is hampered under high loading rates, resulting in lower overall fracture resistance.

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Fatigue-induced subchondral bone (SCB) injury is common in racehorses. Understanding how subchondral microstructure and microdamage influence mechanical properties is important for developing injury prevention strategies. Mechanical properties of the disto-palmar third metacarpal condyle (MCIII) correlate poorly with microstructure, and it is unknown whether the properties of other sites within the metacarpophalangeal (fetlock) joint are similarly complex. We aimed to investigate the mechanical and structural properties of equine SCB from specimens with minimal evidence of macroscopic disease. Three sites within the metacarpophalangeal joint were examined: the disto-palmar MCIII, disto-dorsal MCIII, and proximal sesamoid bone. Two regions of interest within the SCB were compared, a 2 mm superficial and an underlying 2 mm deep layer. Cartilage-bone specimens underwent micro-computed tomography, then cyclic compression for 100 cycles at 2 Hz. Disto-dorsal MCIII specimens were loaded to 30 MPa (n = 10), while disto-palmar MCIII (n = 10) and proximal sesamoid (n = 10) specimens were loaded to 40 MPa. Digital image correlation determined local strains. Specimens were stained with lead-uranyl acetate for volumetric microdamage quantification. The dorsal MCIII SCB had lower bone volume fraction (BVTV), bone mineral density (BMD), and stiffness compared to the palmar MCIII and sesamoid bone (p < 0.05). Superficial SCB had higher BVTV and lower BMD than deeper SCB (p < 0.05), except at the palmar MCIII site where there was no difference in BVTV between depths (p = 0.419). At all sites, the deep bone was stiffer (p < 0.001), although the superficial to deep gradient was smaller in the dorsal MCIII. Hysteresis (energy loss) was greater superficially in palmar MCIII and sesamoid (p < 0.001), but not dorsal MCIII specimens (p = 0.118). The stiffness increased with cyclic loading in total cartilage-bone specimens (p < 0.001), but not in superficial and deep layers of the bone, whereas hysteresis decreased with the cycle for all sites and layers (p < 0.001). Superficial equine SCB is uniformly less stiff than deeper bone despite non-uniform differences in bone density and damage levels. The more compliant superficial layer has an important role in energy dissipation, but whether this is a specific adaptation or a result of microdamage accumulation is not clear.