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Bone Geometry (bone + geometry)
Selected AbstractsThe Influence of an Insulin-Like Growth Factor I Gene Promoter Polymorphism on Hip Bone Geometry and the Risk of Nonvertebral Fracture in the Elderly: The Rotterdam Study,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2004Fernando Rivadeneira Abstract The absence of the wildtype allele of a promoter polymorphism of the IGF-I gene is associated with increased risk (1.5; 95% CI, 1.1-2.0) of fragility fracture in women (n = 4212) but not in men (n = 2799). An approximation of hip bone geometry (from DXA) suggested the polymorphism is associated with bone strength and stability in gender-specific ways. Introduction: Previously, we found a CA-repeat promoter polymorphism in the insulin-like growth factor I (IGF-I) gene associated with IGF-I levels and BMD in postmenopausal women, but the relationship with fractures is unclear. In this large population-based study of elderly men and women, we examined the association between this IGF-I promoter polymorphism with parameters of bone geometry and the occurrence of fractures. Material and Methods: Within the Rotterdam Study, a prospective population-based cohort, the IGF-I polymorphism was analyzed in relation to incident nonvertebral fractures in 2799 men and 4212 women followed on average for 8.6 years. Furthermore, we estimated structural parameters of hip bone geometry indirectly from DXA outputs of the femoral neck in 2372 men and 3114 women. We studied neck width, cortical thickness, and the cortical buckling ratio and the section modulus as indexes of bone stability and bending strength. Results: Women heterozygotes and noncarriers of the allele had, respectively, 1.2 (95% CI, 1.0-1.5) and 1.5 (95% CI, 1.1-2.0) increased risk of having a fragility fracture at older age compared with homozygotes for the 192-bp allele (p trend = 0.0007). In men, fracture risk was not influenced by the polymorphism. Compared with homozygotes for the 192-bp allele, noncarrier males had ,1% narrower femoral necks and 2.2% lower section moduli (p trend < 0.05). Noncarrier females had 1.7% thinner cortices and 1.6% higher buckling ratios (p trend < 0.05) but no significant differences in femoral neck widths and section moduli. In women with low body mass index, genotype differences in bone strength (section modulus) and fracture risk were accentuated (p interaction = 0.05). The genotype-dependent differences in hip bone geometry did not fully explain the genotype-dependent differences in fracture risk. Conclusions: The CA-repeat promoter polymorphism in the IGF-I gene is associated with the risk for fragility fracture at old age in women and with bone structure in both genders. [source] Association of Geometric Factors and Failure Load Level With the Distribution of Cervical vs.JOURNAL OF BONE AND MINERAL RESEARCH, Issue 6 2006Trochanteric Hip Fractures Abstract We experimentally studied the distribution of hip fracture types at different structural mechanical strength. Femoral neck fractures were dominant at the lowest structural strength levels, whereas trochanteric fractures were more common at high failure loads. The best predictor of fracture type across all failure loads and in both sexes was the neck-shaft angle. Introduction: Bone geometry has been shown to be a potential risk factor for osteoporotic fractures. Risk factors have been shown to differ between cervical and trochanteric hip fractures. However, the determinants of cervical and trochanteric fractures at different levels of structural mechanical strength are currently unknown. In addition, it is not known if the distribution of fracture types differs between sexes. The aim of this experimental study on excised femora was to investigate whether there exist differences in the distribution of cervical and trochanteric fractures between different structural mechanical strength levels and different sexes and to identify the geometric determinants that predict a fracture type. Materials and Methods: The sample was comprised of 140 cadavers (77 females: mean age, 81.7 years; 63 males: mean age, 79.1 years) from whom the left femora were excised for analysis. The bones were radiographed, and geometrical parameters were determined from the digitized X-rays. The femora were mechanically tested in a side impact configuration, simulating a sideways fall. After the mechanical test, the fracture patterns were classified into cervical and trochanteric. Results: The overall proportion of cervical fractures was higher in females (74%) than in males (49%) (p = 0.002). The fracture type distribution differed significantly across load quartiles in females (p = 0.025), but not in males (p = 0.205). At the lowest load quartiles, 94.7% of fractures in female and 62.5% in males were femoral neck fractures. At the highest quartiles, in contrast, only 52.6% of fractures in females and 33.3% in males were cervical fractures. Among geometric variables, the neck-shaft angle was the best predictor of fracture type, with higher values in subjects with cervical fractures. This finding was made in females (p < 0.001) and males (p = 0.02) and was consistent across all failure load quartiles. Conclusions: Femoral neck fractures predominate at the lowest structural mechanical strength levels, whereas trochanteric fractures are more common at high failure loads. Females are more susceptible to femoral neck fractures than males. The best predictor of fracture type across all structural strength levels and both sexes was the neck-shaft angle. [source] Compensatory bone remodelling in moose: a study of age, sex, and cross-sectional cortical bone dimensions in moose at Isle Royale National ParkINTERNATIONAL JOURNAL OF OSTEOARCHAEOLOGY, Issue 5 2002Mary Hindelang Abstract We studied interrelationships among age, sex, and cross-sectional cortical bone dimensions using quantitative computed tomography (QCT) scans of metatarsal bones of 180 moose (Alces alces) that died in Isle Royale National Park, Michigan. As a large-bodied quadruped with demanding ecological constraints on movement and behaviour, a moose experiences different weight-bearing and mechanical stressors than humans, to whom most existing studies of mechanical adaptations of bone pertain. In moose, both sexes showed significant subperiosteal expansion and an increase in medullary area, with an overall increase in cortical bone area over time. Female moose did not exhibit cortical thinning or reduction in cross-sectional area with age, rather they showed an increase in cortical bone area with periosteal apposition exceeding endosteal resorption, similar to the males. We also found that moose undergo changes in bone geometry through remodelling of bone similar to humans, suggesting a compensatory mechanism for increasing bone strength under conditions of decline in bone mineral density with age. Copyright © 2002 John Wiley & Sons, Ltd. [source] Hip geometry variation is associated with bone mineralization pathway gene variants: The framingham studyJOURNAL OF BONE AND MINERAL RESEARCH, Issue 7 2010Ching-Lung Cheung Abstract Mineralization of bone matrix is an important process in bone formation; thus defects in mineralization have been implicated in bone mineral density (BMD) and bone structure alterations. Three central regulators of phosphate balance, ALPL, ANKH, and ENPP1, are central in the matrix mineralization process; therefore, the genes encoding them are considered important candidates genes for BMD and bone geometry. To test for an association between these three candidate genes and BMD and bone geometry traits, 124 informative single-nucleotide polymorphisms (SNPs) were selected and genotyped in 1513 unrelated subjects from the Framingham offspring cohort. Initial results showed that SNP rs1974201 in the gene ENPP1 was a susceptibility variant associated with several hip geometric indices, with the strongest p value of 3.8,×,10,7 being observed for femoral neck width. A few modest associations were observed between SNPs in or near ALPL and several bone traits, but no association was observed with ANKH. The association signals observed for SNPs around rs1974201 were attenuated after conditional analysis on rs1974201. Transcription factor binding-site prediction revealed that the HOXA7 binding site was present in the reference sequence with the major allele, whereas this potential binding site is lost in the sequence with the minor allele of rs1974201. In conclusion, we found evidence for association of bone geometry variation with an SNP in ENPP1, a gene in the mineralization pathway. The alteration of a binding site of the deregulator of extracellular matrix HOXA7 warrants further investigation. © 2010 American Society for Bone and Mineral Research [source] Peak Bone Mass After Exposure to Antenatal Betamethasone and Prematurity: Follow-up of a Randomized Controlled Trial,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2006Stuart R Dalziel Abstract Small birth size is associated with reduced adult bone mass. We determined if antenatal betamethasone exposure, birth weight, or prematurity affects peak bone mass in 174 adults. Antenatal betamethasone exposure did not. Lower birth weight and prematurity predicted reduced adult height. Slower fetal growth rather than prematurity predicted lower bone mass, but this lower bone mass was appropriate for reduced adult height. Introduction: Small size at birth is reported to be associated with lower bone mass in adulthood. However, previous studies have not distinguished the relative contributions of length of gestation and fetal growth to size at birth. Fetal exposure to excess glucocorticoids has been proposed as a core mechanism underlying the associations between birth size and later disease risk. Antenatal glucocorticoids are given to pregnant women at risk for preterm delivery for the prevention of neonatal respiratory distress syndrome in their infants. We determined the relationship of antenatal exposure to betamethasone, birth weight, and prematurity to peak bone mass and femoral geometry in the adult survivors of the first randomized trial of antenatal glucocorticoids. Materials and Methods: We studied 174 young adults (mean age, 31 years) whose mothers participated in a randomized trial of antenatal betamethasone. Mothers received two doses of intramuscular betamethasone or placebo 24 h apart. Two thirds of participants were born preterm (<37 weeks gestation). We measured indices of bone mass and size and derived estimates of volumetric density and bone geometry from DXA assessments of the lumbar spine, femur, and total body. Results: There were no differences between betamethasone-exposed and placebo-exposed groups in any of the lumbar spine, femur, or total body DXA measures. There was no effect of antenatal betamethasone on adult height, although leg length was increased relative to trunk length (p = 0.002). A lighter birth weight (p , 0.001) and lower gestational age (p = 0.013) were associated with shorter stature (height Z scores) at age 31 years. Prematurity had no effect on peak bone mass or femoral geometry. However, lower birth weight, independent of gestational age, was associated with lower later bone mass (p < 0.001 for lumbar spine and total body, p = 0.003 for femoral neck BMC). These effects on bone mass were related to bone size and not to estimates of volumetric density. In the femur, lower birth weight, independent of gestational age, was associated with narrowing of the upper shaft and narrow neck regions. Conclusions: Antenatal betamethasone exposure does not affect peak bone mass or femoral geometry in adulthood. Birth weight and prematurity predict adult height, but it is slower fetal growth, rather than prematurity, that predicts lower peak bone mass. The lower peak bone mass in those born small is appropriate for their adult height. [source] The Influence of an Insulin-Like Growth Factor I Gene Promoter Polymorphism on Hip Bone Geometry and the Risk of Nonvertebral Fracture in the Elderly: The Rotterdam Study,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2004Fernando Rivadeneira Abstract The absence of the wildtype allele of a promoter polymorphism of the IGF-I gene is associated with increased risk (1.5; 95% CI, 1.1-2.0) of fragility fracture in women (n = 4212) but not in men (n = 2799). An approximation of hip bone geometry (from DXA) suggested the polymorphism is associated with bone strength and stability in gender-specific ways. Introduction: Previously, we found a CA-repeat promoter polymorphism in the insulin-like growth factor I (IGF-I) gene associated with IGF-I levels and BMD in postmenopausal women, but the relationship with fractures is unclear. In this large population-based study of elderly men and women, we examined the association between this IGF-I promoter polymorphism with parameters of bone geometry and the occurrence of fractures. Material and Methods: Within the Rotterdam Study, a prospective population-based cohort, the IGF-I polymorphism was analyzed in relation to incident nonvertebral fractures in 2799 men and 4212 women followed on average for 8.6 years. Furthermore, we estimated structural parameters of hip bone geometry indirectly from DXA outputs of the femoral neck in 2372 men and 3114 women. We studied neck width, cortical thickness, and the cortical buckling ratio and the section modulus as indexes of bone stability and bending strength. Results: Women heterozygotes and noncarriers of the allele had, respectively, 1.2 (95% CI, 1.0-1.5) and 1.5 (95% CI, 1.1-2.0) increased risk of having a fragility fracture at older age compared with homozygotes for the 192-bp allele (p trend = 0.0007). In men, fracture risk was not influenced by the polymorphism. Compared with homozygotes for the 192-bp allele, noncarrier males had ,1% narrower femoral necks and 2.2% lower section moduli (p trend < 0.05). Noncarrier females had 1.7% thinner cortices and 1.6% higher buckling ratios (p trend < 0.05) but no significant differences in femoral neck widths and section moduli. In women with low body mass index, genotype differences in bone strength (section modulus) and fracture risk were accentuated (p interaction = 0.05). The genotype-dependent differences in hip bone geometry did not fully explain the genotype-dependent differences in fracture risk. Conclusions: The CA-repeat promoter polymorphism in the IGF-I gene is associated with the risk for fragility fracture at old age in women and with bone structure in both genders. [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] Changes in proximal femoral mineral geometry precede the onset of radiographic hip osteoarthritis: The study of osteoporotic fracturesARTHRITIS & RHEUMATISM, Issue 7 2009M. K. Javaid Objective Radiographic hip osteoarthritis (RHOA) is associated with increased hip areal bone mineral density (aBMD). This study was undertaken to examine whether femoral geometry is associated with RHOA independent of aBMD. Methods Participants in the Study of Osteoporotic Fractures in whom pelvic radiographs had been obtained at visits 1 and 5 (mean 8.3 years apart) and hip dual x-ray absorptiometry (DXA) had been performed (2 years after baseline) were included. Prevalent and incident RHOA phenotypes were defined as composite (osteophytes and joint space narrowing [JSN]), atrophic (JSN without osteophytes), or osteophytic (femoral osteophytes without JSN). Analogous definitions of progression were based on minimum joint space and total osteophyte score. Hip DXA scans were assessed using the Hip Structural Analysis program to derive geometric measures, including femoral neck length, width, and centroid position. Relative risks and 95% confidence intervals for prevalent, incident, and progressive RHOA per SD increase in geometric measure were estimated in a hip-based analysis using multinomial logistic regression with adjustment for age, body mass index, knee height, and total hip aBMD. Results In 5,245 women (mean age 72.6 years), a wider femoral neck with a more medial centroid position was associated with prevalent and incident osteophytic and composite RHOA phenotypes (P < 0.05). Increased neck width and centroid position were associated with osteophyte progression (both P < 0.05). No significant geometric associations with atrophic RHOA were found. Conclusion Differences in proximal femoral bone geometry and spatial distribution of bone mass occur early in hip OA and predict prevalent, incident, and progressive osteophytic and composite phenotypes, but not the atrophic phenotype. These bone differences may reflect responses to loading occurring early in the natural history of RHOA. [source] Musculoskeletal abnormalities of the tibia in juvenile rheumatoid arthritisARTHRITIS & RHEUMATISM, Issue 3 2007Elena M. O. Felin Objective To characterize local bone geometry, density, and strength, using peripheral quantitative computed tomography (pQCT), compared with general bone characteristics as measured using dual x-ray absorptiometry (DXA), and to assess their relationship to disease-related factors in children with juvenile rheumatoid arthritis (JRA). Methods Forty-eight children ages 4,18 years with JRA (17 pauciarticular, 23 polyarticular, 8 systemic) were compared with age-matched healthy controls (n = 266). Measurements included cortical and trabecular bone geometry, density, and strength at the distal and midshaft tibia determined by pQCT, and whole-body, lumbar spine, and femoral neck measurements by DXA. Results Methotrexate (MTX) was prescribed to 23 of 48 patients (47.9%) and glucocorticoids and MTX were prescribed to 15 of 48 patients (31.3%), with the greatest use in children with systemic JRA. All JRA patients had decreased tibia trabecular bone density, cortical bone size and strength, and muscle mass. Children with systemic JRA had lower femoral neck densities. Systemic JRA was associated with a shorter, less mineralized skeleton, while a narrower, less mineralized skeleton was observed in polyarticular JRA. The tibia diaphysis was narrower with decreased muscle mass, but normal, size-adjusted bone mineral in all subtypes indicated a localized effect of JRA on bone. Patients exposed to glucocorticoids and MTX or to glucocorticoids or MTX alone had greatly reduced trabecular density, cortical bone geometry properties, and bone mineral content, muscle mass, and bone strength. Conclusion Children with JRA have decreased skeletal size, muscle mass, trabecular bone density, cortical bone geometry, and strength. Not surprisingly, these bone abnormalities are more pronounced in children with greater disease severity. [source] | ||||||||||