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Bone Fragility (bone + fragility)
Selected AbstractsBone Fragility Contributes to the Risk of Fracture in Children, Even After Moderate and Severe Trauma,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 2 2008Emma M Clark Abstract We prospectively examined whether the relationship between skeletal fragility and fracture risk in children 9.9 ± 0.3 (SD) yr is affected by trauma level. Bone size relative to body size and humeral vBMD showed similar inverse relationships with fracture risk, irrespective of whether fractures followed slight or moderate/severe trauma. Introduction: Fracture risk in childhood is related to underlying skeletal fragility. However, whether this relationship is confined to low-trauma fractures or whether skeletal fragility also contributes to the risk of fracture caused by higher levels of trauma is currently unknown. Materials and Methods: Total body DXA scan results obtained at 9.9 yr of age were linked to reported fractures over the following 2 yr in children from the Avon Longitudinal Study of Parents and Children. DXA scan results that were subsequently derived included total body less head (TBLH) bone size relative to body size (calculated from TBLH area adjusted for height and weight) and humeral volumetric BMD (vBMD; derived from subregional analysis at this site). Trauma level was assigned using the Landin classification based on a questionnaire asking about precipitating causes. Results: Of the 6204 children with available data, 549 (8.9%) reported at least one fracture over the follow-up period, and trauma level was assigned in 280 as follows: slight trauma, 56.1%; moderate trauma, 41.0%; severe trauma, 2.9%. Compared with children without fractures, after adjustment for age, sex, socioeconomic status, and ethnicity, children with fractures from both slight and moderate/severe trauma had a reduced bone size relative to body size (1133 cm2 in nonfractured children versus 1112 cm2 for slight trauma fractures, p < 0.001; 1112 cm2 for moderate/severe trauma fractures, p = 0.001) and reduced humeral vBMD (0.494 g/cm3 in nonfractured children versus 0.484 g/cm3 for slight trauma fractures, p = 0.036; and 0.482g/cm3 for moderate/severe trauma fractures, p = 0.016). Conclusions: Skeletal fragility contributes to fracture risk in children, not only in fractures caused by slight trauma but also in those that result from moderate or severe trauma. [source] Bone Fragility and Collagen Cross-Links,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 12 2004Eleftherios P Paschalis Abstract Infrared imaging analysis of iliac crest biopsy specimens from patients with osteoporotic and multiple spontaneous fractures shows significant differences in the spatial variation of the nonreducible:reducible collagen cross-links at bone-forming trabecular surfaces compared with normal bone. Introduction: Although the role of BMC and bone mineral quality in determining fracture risk has been extensively studied, considerably less attention has been paid to the quality of collagen in fragile bone. Materials and Methods: In this study, the technique of Fourier transform infrared imaging (FTIRI) was used to determine the ratio of nonreducible:reducible cross-links, in 2- to 4-,m-thick sections, from human iliac crest biopsy specimens (N = 27) at bone-forming trabecular surfaces. The biopsy specimens were obtained from patients that had been diagnosed as high- or low-turnover osteoporosis, as well as premenopausal women <40 years of age, with normal BMD and biochemistry, who suffered multiple spontaneous fractures. The obtained values were compared with previously published analyses of trabecular bone from normal non-osteoporotic subjects (N = 14, 6 males and 8 females; age range, 51,70 years). Results and Conclusions: Collagen cross-links distribution within the first 50 ,m at forming trabecular surfaces in patients with fragile bone was markedly different compared with normal bone. [source] Gnathodiaphyseal Dysplasia: A Syndrome of Fibro-Osseous Lesions of Jawbones, Bone Fragility, and Long Bone BowingJOURNAL OF BONE AND MINERAL RESEARCH, Issue 9 2001Mara Riminucci Abstract We report an unusual generalized skeletal syndrome characterized by fibro-osseous lesions of the jawbones with a prominent psammomatoid body component, bone fragility, and bowing/sclerosis of tubular bones. The case fits with the emerging profile of a distinct syndrome with similarities to previously reported cases, some with an autosomal dominant inheritance and others sporadic. We suggest that the syndrome be named gnathodiaphyseal dysplasia. The patient had been diagnosed previously with polyostotic fibrous dysplasia (PFD) elsewhere, but further clinical evaluation, histopathological study, and mutation analysis excluded this diagnosis. In addition to providing a novel observation of an as yet poorly characterized syndrome, the case illustrates the need for stringent diagnostic criteria for FD. The jaw lesions showed fibro-osseous features with the histopathological characteristics of cemento-ossifying fibroma, psammomatoid variant. This case emphasizes that the boundaries between genuine GNAS1 mutation-positive FD and other fibro-osseous lesions occurring in the jawbones should be kept sharply defined, contrary to a prevailing tendency in the literature. A detailed pathological study revealed previously unreported features of cemento-ossifying fibroma, including the participation of myofibroblasts and the occurrence of psammomatoid bodies and aberrant mineralization, within the walls of blood vessels. Transplantation of stromal cells grown from the lesion into immunocompromised mice resulted in a close mimicry of the native lesion, including the sporadic formation of psammomatoid bodies, suggesting an intrinsic abnormality of bone-forming cells. [source] Inaccuracies Inherent in Dual-Energy X-Ray Absorptiometry In Vivo Bone Mineral Density Can Seriously Mislead Diagnostic/Prognostic Interpretations of Patient-Specific Bone FragilityJOURNAL OF BONE AND MINERAL RESEARCH, Issue 5 2001H. H. Bolotin First page of article [source] Heterogeneity in the Growth of the Axial and Appendicular Skeleton in Boys: Implications for the Pathogenesis of Bone Fragility in MenJOURNAL OF BONE AND MINERAL RESEARCH, Issue 10 2000Michelle Bradney Abstract Men with spine fractures have reduced vertebral body (VB) volume and volumetric bone mineral density (vBMD). Men with hip fractures have reduced femoral neck (FN) volume and vBMD, site-specific deficits that may have their origins in growth. To describe the tempo of growth in regional bone size, bone mineral content (BMC), and vBMD, we measured bone length, periosteal and endocortical diameters, BMC, and vBMD using dual-energy X-ray absorptiometry in 184 boys aged between 7 and 17 years. Before puberty, growth was more rapid in the legs than in the trunk. During puberty, leg growth slowed while trunk length accelerated. Bone size was more advanced than BMC in all regions, being ,70% and ,35% of their predicted peaks at 7 years of age, respectively. At 16 years of age, bone size had reached its adult peak while BMC was still 10% below its predicted peak. The legs accounted for 48%, whereas the spine accounted for 10%, of the 1878 g BMC accrued between 7 and 17 years. Peripubertal growth contributed (i) 55% of the increase in leg length but 78% of the mineral accrued and (ii) 69% of the increase in spine length but 87% of the mineral accrued. Increased metacarpal and midfemoral cortical thickness was caused by respective periosteal expansion with minimal change in the endocortical diameter. Total femur and VB vBMD increased by 30,40% while size and BMC increased by 200,300%. Thus, growth builds a bigger but only slightly denser skeleton. We speculate that effect of disease or a risk factor during growth depends on the regions maturational stage at the time of exposure. The earlier growth of a regions size than mass, and the differing growth patterns from region to region, predispose to site-specific deficits in bone size, vBMD, or both. Regions further from their peak may be more severely affected by illness than those nearer completion of growth. Bone fragility in old age is likely to have its foundations partly established during growth. [source] Construction of the Femoral Neck During Growth Determines Its Strength in Old Age,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 7 2007Roger M D Zebaze Abstract Study of the design of the FN in vivo in 697 women and in vitro in 200 cross-sections of different sizes and shapes along each of 13 FN specimens revealed that strength in old age was largely achieved during growth by differences in the distribution rather than the amount of bone material in a given FN cross-section from individual to individual. Introduction: We studied the design of the femoral neck (FN) to gain insight into the structural basis of FN strength in adulthood and FN fragility in old age. Materials and Methods: Studies in vivo were performed using densitometry in 697 women and in vitro using high-resolution ,CT and direct measurements in 13 pairs of postmortem specimens. Results: The contradictory needs of strength for loading yet lightness for mobility were met by varying FN size, shape, spatial distribution, and proportions of its trabecular and cortical bone in a cross-section, not its mass. Wider and narrower FNs were constructed with similar amounts of bone material. Wider FNs were relatively lighter: a 1 SD higher FN volume had a 0.67 (95% CI, 0.61,0.72) SD lower volumetric BMD (vBMD). A 1 SD increment in height was achieved by increasing FN volume by 0.32 (95% CI, 0.25,0.39) SD with only 0.15 (95% CI, 0.08,0.22) SD more bone, so taller individuals had a relatively lighter FN (vBMD was 0.13 [95% CI, 0.05,0.20 SD] SD lower). Greater periosteal apposition constructing a wider FN was offset by even greater endocortical resorption so that the same net amount of bone was distributed as a thinner cortex further from the neutral axis, increasing resistance to bending and lowering vBMD. This was recapitulated at each point along the FN; varying absolute and relative degrees of periosteal apposition and endocortical resorption focally used the same amount of material to fashion an elliptical FN of mainly cortical bone near the femoral shaft to offset bending but a more circular FN of proportionally more trabecular and less cortical bone to accommodate compressive loads adjacent to the pelvis. This structural heterogeneity was largely achieved by adaptive modeling and remodeling during growth,most of the variance in FN volume, BMC, and vBMD was growth related. Conclusions: Altering structural design while minimizing mass achieves FN strength and lightness. Bone fragility may be the result of failure to adapt bone's architecture to loading, not just low bone mass. [source] Heterogeneity in the Growth of the Axial and Appendicular Skeleton in Boys: Implications for the Pathogenesis of Bone Fragility in MenJOURNAL OF BONE AND MINERAL RESEARCH, Issue 10 2000Michelle Bradney Abstract Men with spine fractures have reduced vertebral body (VB) volume and volumetric bone mineral density (vBMD). Men with hip fractures have reduced femoral neck (FN) volume and vBMD, site-specific deficits that may have their origins in growth. To describe the tempo of growth in regional bone size, bone mineral content (BMC), and vBMD, we measured bone length, periosteal and endocortical diameters, BMC, and vBMD using dual-energy X-ray absorptiometry in 184 boys aged between 7 and 17 years. Before puberty, growth was more rapid in the legs than in the trunk. During puberty, leg growth slowed while trunk length accelerated. Bone size was more advanced than BMC in all regions, being ,70% and ,35% of their predicted peaks at 7 years of age, respectively. At 16 years of age, bone size had reached its adult peak while BMC was still 10% below its predicted peak. The legs accounted for 48%, whereas the spine accounted for 10%, of the 1878 g BMC accrued between 7 and 17 years. Peripubertal growth contributed (i) 55% of the increase in leg length but 78% of the mineral accrued and (ii) 69% of the increase in spine length but 87% of the mineral accrued. Increased metacarpal and midfemoral cortical thickness was caused by respective periosteal expansion with minimal change in the endocortical diameter. Total femur and VB vBMD increased by 30,40% while size and BMC increased by 200,300%. Thus, growth builds a bigger but only slightly denser skeleton. We speculate that effect of disease or a risk factor during growth depends on the regions maturational stage at the time of exposure. The earlier growth of a regions size than mass, and the differing growth patterns from region to region, predispose to site-specific deficits in bone size, vBMD, or both. Regions further from their peak may be more severely affected by illness than those nearer completion of growth. Bone fragility in old age is likely to have its foundations partly established during growth. [source] Hip Fractures and the Contribution of Cortical Versus Trabecular Bone to Femoral Neck Strength,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 3 2009Gerold Holzer Abstract Osteoporotic fractures are caused by both cortical thinning and trabecular bone loss. Both are seen to be important for bone fragility. The relative contributions of cortical versus trabecular bone have not been established. The aim of this study was to test the contribution of cortical versus trabecular bone to femoral neck stability in bone strength. In one femur from each pair of 18 human cadaver femurs (5 female; 4 male), trabecular bone was completely removed from the femoral neck, providing one bone with intact and the other without any trabecular structure in the femoral neck. Geometrical, X-ray, and DXA measurements were carried out before biomechanical testing (forces to fracture). Femoral necks were osteotomized, slices were analyzed for cross-sectional area (CSA) and cross-sectional moment of inertia (CSMI), and results were compared with biomechanical testing data. Differences between forces needed to fracture excavated and intact femurs (,F/F mean) was 7.0% on the average (range, 4.6,17.3%). CSA of removed spongiosa did not correlate with difference of fracture load (,F/F mean), nor did BMD. The relative contribution of trabecular versus cortical bone in respect to bone strength in the femoral neck seems to be marginal and seems to explain the subordinate role of trabecular bone and its changes in fracture risk and the effects of treatment options in preventing fractures. [source] Childhood Fractures Are Associated With Decreased Bone Mass Gain During Puberty: An Early Marker of Persistent Bone Fragility?,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 4 2006Serge L Ferrari MD Abstract Whether peak bone mass is low among children with fractures remains uncertain. In a cohort of 125 girls followed over 8.5 years, 42 subjects reported 58 fractures. Among those, BMC gain at multiple sites and vertebral bone size at pubertal maturity were significantly decreased. Hence, childhood fractures may be markers of low peak bone mass acquisition and persistent skeletal fragility. Introduction: Fractures in childhood may result from a deficit in bone mass accrual during rapid longitudinal growth. Whether low bone mass persists beyond this period however remains unknown. Materials and Methods: BMC at the spine, radius, hip, and femur diaphysis was prospectively measured over 8.5 years in 125 girls using DXA. Differences in bone mass and size between girls with and without fractures were analyzed using nonparametric tests. The contribution of genetic factors was evaluated by mother-daughter correlations and that of calcium intake by Cox proportional hazard models. Results: Fifty-eight fractures occurred in 42 among 125 girls (cumulative incidence, 46.4%), one-half of all fractures affecting the forearm and wrist. Girls with and without fractures had similar age, height, weight. and calcium intake at all time-points. Before and during early puberty, BMC and width of the radius diaphysis was lower in the fracture compared with no-fracture group (p < 0.05), whereas aBMD and BMAD were similar in the two groups. At pubertal maturity (Tanner's stage 5, mean age ± SD, 16.4 ± 0.5 years), BMC at the ultradistal radius (UD Rad.), femur trochanter, and lumbar spine (LS), and LS projected bone area were all significantly lower in girls with fractures. Throughout puberty, BMC gain at these sites was also decreased in the fracture group (LS, ,8.0%, p = 0.015; UD Rad., ,12.0%, p = 0.004; trochanter, ,8.4%, p = 0.05 versus no fractures). BMC was highly correlated between prepuberty and pubertal maturity (R = 0.54,0.81) and between mature daughters and their mothers (R = 0.32,0.46). Calcium intake was not related to fracture risk. Conclusions: Girls with fractures have decreased bone mass gain in the axial and appendicular skeleton and reduced vertebral bone size when reaching pubertal maturity. Taken together with the evidence of tracking and heritability for BMC, these observations indicate that childhood fractures may be markers for low peak bone mass and persistent bone fragility. [source] Female Premenopausal Fracture Risk Is Associated With Gc Phenotype,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 6 2004Anna Lis Lauridsen Abstract The phenotype of the vitamin D binding and macrophage activating protein, Gc, is a predictor of premenopausal bone fracture risk, possibly mediated through activation of osteoclasts. This was concluded from a study on 595 Danish perimenopausal women 45-58 years of age (30,040 person years). Introduction: The multifunctional plasma protein Gc, also known as group-specific component, Gc globulin, or vitamin D binding protein (DBP), has two functions with relation to bone tissue: it is the major carrier protein of vitamin D in the circulation, and deglycosylation converts it into a very potent macrophage- and osteoclast-activating factor (Gc-MAF). There are several phenotypes of Gc, and in this study, we examined the relation between Gc phenotype and bone fragility. Materials and Methods: By isoelectric focusing we identified the Gc phenotype of 595 white recent postmenopausal women enrolled into the Danish Osteoporosis Prevention Study (DOPS) and identified three groups: Gc1-1 (n = 323), Gc1-2 (n = 230), and Gc2-2 (n = 42). Differences between the three groups were examined with respect to number of fractures before enrollment, BMC and BMD, and various biochemical and clinical parameters, including the concentration of Gc measured by immunonephelometry and the concentration of the macrophage marker soluble CD163 measured by ELISA. Results and Conclusions: The risk of having at least one premenopausal bone fracture (total number of women with fracture = 179) differed significantly (p = 0.017) in women with phenotype Gc1-1 (110/323 = 0.34), Gc1-2 (63/230 = 0.27), and Gc2-2 (6/42 = 0.14). The differences were even more striking (p = 0.005) for fractures caused by low-energy traumas. Using logistic regression, we found the relative risk of premenopausal fracture to be 0.32 (0.13-0.80) in Gc2-2 compared with Gc1-1. We propose that the Gc phenotypes cause differences in osteoclast activity, a theory supported by our finding of lower levels of Gc and of soluble CD163 in women with Gc2-2 compared with Gc1-1. [source] The Structural and Hormonal Basis of Sex Differences in Peak Appendicular Bone Strength in Rats,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 1 2003Bom-Taeck Kim Abstract To identify the structural and hormonal basis for the lower incidence of fractures in males than females, sex differences in femoral mid-shaft geometry and breaking strength were studied in growth hormone (GH)-replete and -deficient male and female rats. Sexual dimorphism appeared during growth. Cortical thickening occurred almost entirely by acquisition of bone on the outer (periosteal) surface in males and mainly on the inner (endocortical) surface in females. By 8 months of age, males had 22% greater bone width and 33% greater breaking strength than females. Gonadectomy (Gx) at 6 weeks reduced sex differences in bone width to 7% and strength to 21% by halving periosteal bone formation in males and doubling it in females. Gx had no net effect on the endocortical surface in males but abolished endocortical bone acquisition in females. GH deficiency halved periosteal bone formation and had no net effect on the endocortical surface in males, but abolished bone acquisition on both surfaces in females, leaving males with 17% greater bone width and 44% greater breaking strength than females. Sex hormone deficiency produces greater bone fragility in males than females by removing a stimulator of periosteal growth in males and removing an inhibitor of periosteal growth in females. GH deficiency produces less bone fragility in males than females because males retain androgen-dependent periosteal bone formation while bone acquisition on both surfaces is abolished in females. Thus, periosteal growth is independently and additively stimulated by androgens and GH in males, inhibited by estrogen, and stimulated by GH in females. The hormonal regulation of bone surfaces establishes the amount and spatial distribution of bone and so the sexual dimorphism in its strength. [source] Perspective: Reconsidering the Effects of Antiresorptive Therapies in Reducing Osteoporotic FractureJOURNAL OF BONE AND MINERAL RESEARCH, Issue 12 2001C. H. Chesnut III Abstract Concepts of what constitutes osteoporosis have evolved from the single criterion of low bone mass to a more inclusive consideration of bone strength, based on both quantity and quality. The evidence driving this shift is drawn from many sources. For example, recent studies of bone geometry have shown what engineers have always known: material properties and structural strength are inseparable. Genetic factors also argue against a one-dimensional (1D) view of osteoporosis. Large-scale family studies present a strong case for genetic influences on bone mass and predisposition to fracture. The contribution of aging to fracture risk has long been known, but we are only now beginning to understand what happens to bone remodeling and microstructure in an aging skeleton. The recognition that osteoporosis is far more complex than previously thought suggests that factors in addition to bone mineral density (BMD) may be useful for evaluating bone fragility and therapeutic effectiveness. Although assessment of BMD is noninvasive and widely available, the degree of increase in BMD alone fails to account for the broader effectiveness of antiresorptive agents in reducing the risk of fractures related to osteoporosis. Indeed, the very multiplicity of factors that determine fracture risk implies that response to therapy may be equally complex. Studies of response to antiresorptive agents and the cellular processes they induce are at best preliminary at this time. Although new technologies have been applied to studying bone microarchitecture, their invasive nature limits wide use. New methods are needed to provide insight into the causes and effects of bone fragility. The definition of osteoporosis, meanwhile, must still be considered a work in progress. [source] Gnathodiaphyseal Dysplasia: A Syndrome of Fibro-Osseous Lesions of Jawbones, Bone Fragility, and Long Bone BowingJOURNAL OF BONE AND MINERAL RESEARCH, Issue 9 2001Mara Riminucci Abstract We report an unusual generalized skeletal syndrome characterized by fibro-osseous lesions of the jawbones with a prominent psammomatoid body component, bone fragility, and bowing/sclerosis of tubular bones. The case fits with the emerging profile of a distinct syndrome with similarities to previously reported cases, some with an autosomal dominant inheritance and others sporadic. We suggest that the syndrome be named gnathodiaphyseal dysplasia. The patient had been diagnosed previously with polyostotic fibrous dysplasia (PFD) elsewhere, but further clinical evaluation, histopathological study, and mutation analysis excluded this diagnosis. In addition to providing a novel observation of an as yet poorly characterized syndrome, the case illustrates the need for stringent diagnostic criteria for FD. The jaw lesions showed fibro-osseous features with the histopathological characteristics of cemento-ossifying fibroma, psammomatoid variant. This case emphasizes that the boundaries between genuine GNAS1 mutation-positive FD and other fibro-osseous lesions occurring in the jawbones should be kept sharply defined, contrary to a prevailing tendency in the literature. A detailed pathological study revealed previously unreported features of cemento-ossifying fibroma, including the participation of myofibroblasts and the occurrence of psammomatoid bodies and aberrant mineralization, within the walls of blood vessels. Transplantation of stromal cells grown from the lesion into immunocompromised mice resulted in a close mimicry of the native lesion, including the sporadic formation of psammomatoid bodies, suggesting an intrinsic abnormality of bone-forming cells. [source] Quantitative Ultrasound Does Not Reflect Mechanically Induced Damage in Human Cancellous BoneJOURNAL OF BONE AND MINERAL RESEARCH, Issue 12 2000P. H. F. Nicholson Abstract This study investigated the ability of quantitative ultrasound (QUS) to detect reductions in the elastic modulus of cancellous bone caused by mechanical damage. Ultrasonic velocity and attenuation were measured using an in-house parametric imaging system in 46 cancellous bone cores from the human calcaneus. Each core was subjected to a mechanical testing regime to (a) determine the predamage elastic modulus, (b) induce damage by applying specified strains in excess of the yield strain, and (c) measure the postdamage elastic modulus. The specimens were divided into four groups: a control group subjected to a nominally nondestructive 0.7% maximum strain (,m) and three damage groups subjected to increasing strain levels (,m = 1.5, 3.0, and 4.5%). QUS measurements before and after the mechanical testing showed no significant differences between the control group and damage groups, despite highly significant (p < 0.001) reductions in the elastic modulus of up to 72%. These results indicate that current QUS techniques do not intrinsically reflect the elastic properties of cancellous bone. This is consistent with ultrasonic properties being determined by other factors (apparent density and/or architecture), which normally are associated strongly with elastic properties, but only when bone is mechanically intact. Clinically, this implies that ultrasound cannot be expected to detect bone fragility in the absence of major changes in bone density and/or trabecular architecture. [source] Suppressed Bone Turnover by Bisphosphonates Increases Microdamage Accumulation and Reduces Some Biomechanical Properties in Dog RibJOURNAL OF BONE AND MINERAL RESEARCH, Issue 4 2000Tasuku Mashiba Abstract It has been hypothesized that suppression of bone remodeling allows microdamage to accumulate, leading to increased bone fragility. This study evaluated the effects of reduced bone turnover produced by bisphosphonates on microdamage accumulation and biomechanical properties of cortical bone in the dog rib. Thirty-six female beagles, 1,2 years old, were divided into three groups. The control group (CNT) was treated daily for 12 months with saline vehicle. The remaining two groups were treated daily with risedronate (RIS) at a dose of 0.5 mg/kg per day or alendronate (ALN) at 1.0 mg/kg per day orally. After sacrifice, the right ninth rib was assigned to cortical histomorphometry or microdamage analysis. The left ninth rib was tested to failure in three-point bending. Total cross-sectional bone area was significantly increased in both RIS and ALN compared with CNT, whereas cortical area did not differ significantly among groups. One-year treatment with RIS or ALN significantly suppressed intracortical remodeling (RIS, 53%; ALN, 68%) without impairment of mineralization and significantly increased microdamage accumulation in both RIS (155%) and ALN (322%) compared with CNT. Although bone strength and stiffness were not significantly affected by the treatments, bone toughness declined significantly in ALN (20%). Regression analysis showed a significant nonlinear relationship between suppressed intracortical bone remodeling and microdamage accumulation as well as a significant linear relationship between microdamage accumulation and reduced toughness. This study showed that suppression of bone turnover by high doses of bisphosphonates is associated with microdamage accumulation and reduced some mechanical properties of bone. [source] Fractal analysis of lumbar vertebral cancellous bone architectureCLINICAL ANATOMY, Issue 6 2001G.P. Feltrin Abstract Osteoporosis is characterized by bone mineral density (BMD) decreasing and spongy bone rearrangement with consequent loss of elasticity and increased bone fragility. Quantitative computed tomography (QCT) quantifies bone mineral content but does not describe spongy architecture. Analysis of trabecular pattern may provide additional information to evaluate osteoporosis. The aim of this study was to determine whether the fractal analysis of the microradiography of lumbar vertebrae provides a reliable assessment of bone texture, which correlates with the BMD. The lumbar segment of the spine was removed from 22 cadavers with no history of back pain and examined with standard x-ray, traditional tomography, and quantitative computed tomography to measure BMD. The fractal dimension, which quantifies the image fractal complexity, was calculated on microradiographs of axial sections of the fourth lumbar vertebra to determine its characteristic spongy network. The relationship between the values of the BMD and those of the fractal dimension was evaluated by linear regression and a statistically significant correlation (R = 0.96) was found. These findings suggest that the application of fractal analysis to radiological analyses can provide valuable information on the trabecular pattern of vertebrae. Thus, fractal dimensions of trabecular bone structure should be considered as a supplement to BMD evaluation in the assessment of osteoporosis. Clin. Anat. 6:414,417, 2001. © 2001 Wiley-Liss, Inc. [source] MECHANICAL BONE PROPERTIES OF OBESE MODEL SHR/NDmcr-cp RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2007Naomi Nishii SUMMARY 1High-blood pressure or diabetes may be related to the loss of bone mass or the development of osteoporosis. We examined the mechanical bone properties of the SHR/NDmcr-cp (SHR-cp) rat, an obese strain that develops hypertension, hyperlipidaemia and insulin-independent diabetes. 2The mechanical properties of the femur of 22-week-old Wistar-Kyoto (WKY) and SHR-cp rats were measured by Peng's three-point bending procedure modified by Shintani. Femurs were then defatted and dried. After weighing, the dried bones were ashed and the ash was weighed. The values of the dry weight, ash weight and ash weight/dry weight (%) were used as a description of the physical parameters of the bone. 3All values of stiffness, strength, toughness and ductility in SHR-cp were significantly lower than those of WKY rats (P < 0.05). The value of ash weight/dry weight (%) was lower in SHR-cp rats (P < 0.01). These results showed that bone fragility was greater in SHR-cp rats, indicative of osteopenia. [source] | ||||||||||