Risk Of Fracture In Old Age Research Articles

Hip load capacity and yield load in men and women of all ages.

Quantitative computed tomography (QCT) based finite element (FE) models can compute subject-specific proximal femoral strengths, or fracture loads, that are associated with hip fracture risk. These fracture loads are more strongly associated with measured fracture loads than are DXA and QCT measures and are predictive of hip fracture independently of DXA bone mineral density (BMD). However, interpreting FE-computed fracture loads of younger subjects for the purpose of evaluating hip fracture risk in old age is challenging due to limited reference data. The goal of this study was to address this issue by providing reference data for male and female adult subjects of all ages. QCT-based FE models of the left proximal femur of 216 women and 181 men, age 27 to 90years, from a cohort of Rochester, MN residents were used to compute proximal femoral load capacities, i.e. the maximum loads that can be supported, in single-limb stance and posterolateral fall loading (Stance_LC and Fall_LC, respectively) [US Patent No. 9,245,069] and yield load under fall loading (Fall_yield). To relate these measures to information about hip fracture, the CT scanner and calibration phantom were cross-calibrated with those from our previous prospective study of hip fracture in older fracture and control subjects, the Age Gene/Environment Susceptibility (AGES) Reykjavik cohort. We then plotted Stance_LC, Fall_LC and Fall_yield versus age for the two cohorts on the same graphs. Thus, proximal femoral strengths in individuals above 70years of age can be assessed through direct comparison with the FE data from the AGES cohort which were analyzed using identical methods. To evaluate younger individuals, reductions in Stance_LC, Fall_LC and Fall_yield from the time of evaluation to age 70years can be cautiously estimated from the average yearly cross-sectional decreases found in this study (108N, 19.4N and 14.4N, respectively, in men and 120N, 19.4N and 21.6N, respectively, in women), and the projected fracture loads can be compared with data from the AGES cohort. Although we did not set specific thresholds for identifying individuals at risk of hip fracture, these data provide some guidance and may be used to help establish diagnostic criteria in future. Additionally, given that these data were nearly entirely from Caucasian subjects, future research involving subjects of other races/ethnicities is necessary.

Exercise in youth: High bone mass, large bone size, and low fracture risk in old age.

Physical activity is favorable for peak bone mass but if the skeletal benefits remain and influence fracture risk in old age is debated. In a cross-sectional controlled mixed model design, we compared dual X-ray absorptiometry-derived bone mineral density (BMD) and bone size in 193 active and retired male elite soccer players and 280 controls, with duplicate measurements of the same individual done a mean 5 years apart. To evaluate lifetime fractures, we used a retrospective controlled study design in 397 retired male elite soccer players and 1368 controls. Differences in bone traits were evaluated by Student's t-test and fracture risk assessments by Poisson regression and Cox regression. More than 30 years after retirement from sports, the soccer players had a Z-score for total body BMD of 0.4 (0.1 to 0.6), leg BMD of 0.5 (0.2 to 0.8), and femoral neck area of 0.3 (0.0 to 0.5). The rate ratio for fracture after career end was 0.6 (0.4 to 0.9) and for any fragility fracture 0.4 (0.2 to 0.9). Exercise-associated bone trait benefits are found long term after retirement from sports together with a lower fracture risk. This indicates that physical activity in youth could reduce the burden of fragility fractures.

Impacts of Body Mass Index, Physical Activity, and Smoking on Femoral Bone Loss: The Tromsø Study

Bone mineral density (BMD) is a reflection of bone strength and lifestyles that preserve bone mass and may reduce fracture risk in old age. This study examined the effect of combined profiles of smoking, physical activity, and body mass index (BMI) on lifetime bone loss. Data were collected from the population-based Tromsø Study. BMD was measured as g/cm(2) by dual-energy X-ray absorptiometry (DXA) at the total hip and femoral neck in 2580 women and 2084 men aged 30 to 80 years in the 2001-02 survey, and repeated in 1401 women and 1113 men in the 2007-08 survey. Height and weight were measured and lifestyle information was collected through questionnaires. Data were analyzed using linear mixed models with second-degree fractional polynomials. From the peak at the age around 40 years to 80 years of age, loss rates varied between 4% at the total hip and 14% at femoral neck in nonsmoking, physically active men with a BMI of 30 kg/m(2) to approximately 30% at both femoral sites in heavy smoking, physically inactive men with a BMI value of 18 kg/m(2) . In women also, loss rates of more than 30% were estimated in the lifestyle groups with a BMI value of 18 kg/m(2) . BMI had the strongest effect on BMD, especially in the oldest age groups, but a BMI above 30 kg/m(2) did not exert any additional effect compared with the population average BMI of 27 kg/m(2) . At the age of 80 years, a lifestyle of moderate BMI to light overweight, smoking avoidance, and physical activity of 4 hours of vigorous activity per week through adult life may result in 1 to 2 standard deviations higher BMD levels compared with a lifestyle marked by heavy smoking, inactivity, and low weight. In the prevention of osteoporosis and fracture risk, the effect of combined lifestyles through adult life should be highlighted. © 2014 American Society for Bone and Mineral Research.

Osteoporosis and osteoporotic fracture occurrence and prevention in the elderly: a geriatric perspective

Age is a major determinant of osteoporosis, but the elderly are rarely assessed and often remain untreated for this condition. Falls, co-morbidities and co-medications compound the risk of fracture in senile osteoporosis. The prevalence of osteoporosis is expected to increase with increasing life expectancy, and the associated fractures - particularly hip fractures - will lead to significant demands on health resources. Treatment of senile osteoporosis can include pharmacological and non-pharmacological intervention. Calcium and vitamin D dietary supplementation is a relatively low-cost way of reducing the risk of fracture. Pharmacological interventions with risedronate, zoledronic acid, or teriparatide have been shown to reduce vertebral fracture risk in osteoporosis patients over the age of 75. Zoledronic acid has been shown to reduce fracture risk in frail patients with recent hip fracture. In the oldest old (patients over 80), strontium ranelate is the first agent with documented anti-fracture efficacy for both non-vertebral and vertebral fracture and documented sustained efficacy over 5 years. Falls prevention is an essential component of any strategy for decreasing fracture risk in old age. Currently, senile osteoporosis is under-diagnosed and under-treated, but age should not be a barrier to intervention.

Lifetime high calcium intake increases osteoporotic fracture risk in old age

Caloric restriction prolongs life span. Calcium restriction may preserve bone health. In osteoporosis, bone mineral density (BMD) has significantly decreased, due to a lack of osteoblast bone formation. Traditional osteoporosis prevention is aimed at maximizing BMD, but the lifetime effects of continuously maintaining a high BMD on eventual bone health in old age, have not been studied. Strikingly, in countries with a high mean BMD, fracture rates in the elderly are significantly higher than in countries with a low mean BMD. Studies show that this is not based on genetic differences. Also, in primary hyperparathyroidism, on the brink of osteoporosis, BMD levels may be significantly higher than normal. Maybe, BMD does not represent long term bone health, but merely momentary bone strength. And maybe, maintaining a high BMD might actually wear out bone health. Since osteoporosis particularly occurs in the elderly, and because in osteoporotic bone less osteoblasts are available, the underlying process may have to do with ageing of osteoblastic cells. In healthy subjects, osteoblastic bone cells respond to the influx of calcium by composing a matrix upon which calcium precipitates. In the process of creating this matrix, 50-70% of the involved osteoblasts die. The greater the influx of calcium, the greater osteoblast activity, and the greater osteoblast apoptosis rate. An increased osteoblast apoptosis rate leads to a decrease in the age-related osteoblast replicative capacity (ARORC). In comparison to healthy bone, in osteoporotic bone the decrease in the replicative capacity of osteoblastic cells is greater. Due to the eventual resulting lack of osteoblast activity, micro-fractures cannot be repaired. Continuously maintaining a high BMD comes with continuously high bone remodeling rates, which regionally exhaust the ARORC, eventually leading to irreparable microfractures. Regarding long time influences on bone health, adequate estrogen levels are known to be protective against osteoporosis. This is generally attributed to its inhibiting influence on osteoclast activity. Instead, its net effects on osteoblast metabolism may be the key to osteoporosis prevention. Adequate estrogen levels inhibit osteoblast activity, calcium apposition and osteoblast apoptosis rate, preserving the ARORC. Regarding osteoporosis prevention, ARORC better than BMD represents bone health. Regarding ARORC, adequate estrogen levels are protective, opposing the similar effects of hyperparathyroidism and a high calcium diet. Tests need to be performed in mice to assess the lifetime effects of a high versus a low calcium diet, on eventual bone fracture toughness.

Structural and biomechanical basis of sexual dimorphism in femoral neck fragility has its origins in growth and aging.

The structural basis for sex differences in femoral neck (FN) fragility was studied in 1196 subjects and 307 patients with hip fracture. The absolute and relative patterns of modeling and remodeling on the periosteal and endocortical envelopes during growth and aging produce changes in FN geometry and structure that results in FN fragility in both sexes and sexual dimorphism in hip fracture risk in old age. Femoral neck (FN) fragility in old age is usually attributed to age-related bone loss, while the sex differences in hip fracture rate are attributed to less bone loss in men than in women. The purpose of this study was to define the structural and biomechanical basis underlying the increase in FN fragility in elderly men and women and the structural basis of sex differences in hip fracture incidence in old age. We measured FN dimensions and areal bone mineral density in 1196 healthy subjects (801 females) 18-92 years of age and 307 patients (180 females) with hip fracture using DXA. We then used the DXA-derived FN areal bone mineral density (BMD) and measured periosteal diameter to estimate endocortical diameter, cortical thickness, section modulus (a measure of bending strength), and buckling ratio (indices for structural stability). Neither FN cortical thickness nor volumetric density differed in young adult women and men after height and weight adjustment. The sex differences in geometry were confined to the further displacement of the cortex from the FN neutral axis in young men, which produced 13.4% greater bending strength than in young women. Aging amplified this geometric difference; widening of the periosteal and endocortical diameters continued in both sexes but was greater in men, shifting the cortex even further from the neutral axis maintaining bending strength in men, not in women. In both sexes, less age-related periosteal than endocortical widening produced cortical thinning increasing the risk for structural failure by local buckling of the enlarged thin walled FN. Relative to age-matched controls, women and men with hip fractures had reduced cortical thickness, but FN periosteal diameter was increased in women and reduced in men, differences are likely to be originated in growth. The absolute and relative patterns of modeling and remodeling on the periosteal and endocortical envelopes during growth and aging produce changes in FN diameters, cortical thickness, and geometry that results in FN fragility in both sexes and sexual dimorphism in hip fracture risk in old age.

Altered loading patterns and femoral bone mineral density in children with unilateral Legg-Calvé-Perthes disease.

Maximization of bone accrual during the growing years is thought to be an important factor in minimizing fracture risk in old age. Mechanical loading through physical activity has been recommended as a modality for the conservation of bone mineral in adults; however, few studies have evaluated the impact of different loading regimes in growing children. The purpose of this study was to compare bone mineral density (BMD) in weight-bearing and non-weight-bearing limbs in 17 children with unilateral Legg Calvé Perthes Disease (LCPD). Children with this condition have an altered weight-bearing pattern whereby there is increased mechanical loading on the noninvolved normal hip and reduced loading on the involved painful hip. Thus, these children provide a unique opportunity to study the impact of differential mechanical loading on BMD during the growing years while controlling for genetic disposition. BMD at four regions of the proximal femur (trochanter, intertrochanter, femoral neck, total of the regions) was measured using dual energy x-ray absorptiometry (DXA), and the values were compared between the involved and noninvolved sides of the children with LCPD. The BMD of the both sides also were compared with normative values based on both chronological and skeletal age data. A significantly higher BMD was found on the noninvolved side over the involved side for all regions (P < 0.01 and percentage differences of 12-15%) except at the femoral neck (percentage difference of 3.9%). The BMD (at all regions) of the noninvolved side also was significantly greater (P < 0.01) than either the chronological or skeletal age based norms for all sites except the trochanter. The results support the concept that mechanical loading of the skeleton during the growing years is an important factor in BMD accrual.

The two faces of growth: benefits and risks to bone integrity.

Bones grow by two processes: cortical bone is made by periosteal apposition (growth in width), and cancellous bone is made by endochondral ossification (growth in length). In both the axial and appendicular skeleton, about half of peak adult bone mass is accumulated during the adolescent growth spurt, which occurs two years earlier in girls than in boys, and is under pituitary control via interactions between growth hormone and sex hormones. Throughout growth, but particularly during adolescence, the ability of bone to adapt to mechanical loading is much greater than after maturity. This is the main reason why the effects of physical activity on bone are greater in cross-sectional studies in young athletes than in longitudinal studies in previously sedentary adults. In wild animals, by the time growth has ceased, the bones must be as strong as they will ever need to be, and attainment of further strength after cessation of growth would serve no biologic purpose. Adaptation of growing bone to mechanical loading is the purpose of the mechanostat, which enables physiologic adaptation in individuals to establish and maintain a species-specific property of the bones that is determined by evolutionary adaptation in populations. But growth confers risks as well as benefits to the skeleton. The large increase in incidence of upper extremity (particularly lower forearm) fractures, coincident with the adolescent growth spurt in both sexes, is due to an increase in cortical porosity as a consequence of an increase in intracortical bone turnover, which supplies some of the calcium needed by the growing ends of the long bones. This enables an increased demand for calcium to be spread over a longer time, analogous to the cyclic physiologic osteoporosis which occurs during the antler growth cycle in deer. The subsequent decline in cortical porosity is responsible for the continued increase in radial bone density after cessation of growth, referred to as consolidation. In the present state of knowledge, an increased incidence of fracture during the adolescent growth spurt is the inescapable consequence of an appropriate level of physical activity, and is the price that has to be paid in order to maximize bone accumulation during growth and minimize fracture risk in old age.