Muscle strength is a determinant of bone mineral content in the hemiparetic upper extremity: implications for stroke rehabilitation.

Individuals with stroke have a high incidence of bone fractures and approximately 30% of these fractures occur in the upper extremity. The high risk of falls and the decline in bone and muscle health make the chronic stroke population particularly prone to upper extremity fractures. This was the first study to investigate the bone mineral content (BMC), bone mineral density (BMD), and soft tissue composition of the upper extremities and their relationship to stroke-related impairments in ambulatory individuals with chronic stroke (onset >1 year). Dual-energy X-ray absorptiometry (DXA) was used to acquire total body scans on 56 (22 women) community-dwelling individuals (>or=50 years of age) with chronic stroke. BMC (g) and BMD (g/cm2), lean mass (g), and fat mass (g) for each arm were derived from the total body scans. The paretic upper extremity was evaluated for muscle strength (hand-held dynamometry), impairment of motor function (Fugl-Meyer motor assessment), spasticity (Modified Ashworth Scale), and amount of use of the paretic arm in daily activities (Motor Activity Log). Results showed that the paretic arm had significantly lower BMC (13.8%, P<0.001), BMD (4.5%, P<0.001), and lean mass (9.0%, P<0.001) but higher fat mass (6.3%, P=0.028) than the non-paretic arm. Multiple regression analysis showed that lean mass in the paretic arm, height, and muscle strength were significant predictors (R2=0.810, P<0.001) of the paretic arm BMC. Height, muscle strength, and gender were significant predictors (R2=0.822, P<0.001) of lean mass in the paretic arm. These results highlight the potential of muscle strengthening to promote bone health of the paretic arm in individuals with chronic stroke.

Predictive value of low BMD for 1-year fracture outcomes is similar for postmenopausal women ages 50-64 and 65 and Older: results from the National Osteoporosis Risk Assessment (NORA).

UNLABELLED: The relationship of low bone mass and fracture in younger postmenopausal women has not been extensively studied. In a large cohort of postmenopausal women > or =50 years of age, we found the relationship of BMD measured at peripheral sites and subsequent 1-year fracture risk to be similar between women <65 and those > or =65 years of age. INTRODUCTION: Low bone mass and fractures are prevalent in older postmenopausal women. However, the frequency of low bone mass and fracture in younger postmenopausal women has not been studied extensively. There are very limited data regarding the association between BMD measurements and fractures in postmenopausal women who are between the ages of 50 and 64. MATERIALS AND METHODS: In the National Osteoporosis Risk Assessment (NORA) we studied the frequency of low bone mass and its association with fracture in women 50-64 years of age in comparison with women > or =65 of age. NORA enrolled 200,160 postmenopausal women > or =50 years of age who had no prior diagnosis of osteoporosis. Baseline BMD was measured at the heel, forearm, or finger. A 1-year follow-up survey requesting incident fractures since baseline was completed by 163,935 women, 87,594 (53%) of whom were 50-64 years of age. The association between BMD and fracture was assessed using logistic regression, adjusted for important covariates. RESULTS: Thirty-one percent of women 50-64 years of age had low bone mass (T scores < or = -1.0) compared to 62% of women > or =65 years of age. During the first year of follow-up, 2440 women reported fractures of wrist/forearm, rib, spine, or hip, including 440 hip fractures. Nine hundred four women 50-64 years of age reported fractures, including 86 hip fractures, accounting for 37% of fractures and 20% of hip fractures reported in the entire NORA cohort. Relative risk for osteoporotic fracture was 1.5 for each SD decrease in BMD for both the younger and older groups of women. CONCLUSION: Low BMD in younger postmenopausal women 50-64 years of age showed a 1-year relative risk of fracture similar to that found in women > or =65 years of age.

Randomized trial of effect of alendronate continuation versus discontinuation in women with low BMD: results from the Fracture Intervention Trial long-term extension.

UNLABELLED: To determine the effects of continuation versus discontinuation of alendronate on BMD and markers of bone turnover, we conducted an extension trial in which 1099 older women who received alendronate in the FIT were re-randomized to alendronate or placebo. Compared with women who stopped alendronate, those continuing alendronate for 3 years maintained a higher BMD and greater reduction of bone turnover, showing benefit of continued treatment. However, among women who discontinued alendronate and took placebo in the extension, BMD remained higher, and reduction in bone turnover was greater than values at FIT baseline, showing persistence of alendronate's effects on bone. INTRODUCTION: Prior trials including the Fracture Intervention Trial (FIT) have found that therapy with alendronate increases BMD and decreases fracture risk for up to 4 years in postmenopausal women with low BMD. However, it is uncertain whether further therapy with alendronate results in preservation or further gains in BMD and if skeletal effects of alendronate continue after treatment is stopped. MATERIALS AND METHODS: We conducted a follow-up placebo-controlled extension trial to FIT (FIT long-term extension [FLEX]) in which 1099 women 60-86 years of age who were assigned to alendronate in FIT with an average duration of use of 5 years were re-randomized for an additional 5 years to alendronate or placebo. The results of a preplanned interim analysis at 3 years are reported herein. Participants were re-randomized to alendronate 10 mg/day (30%), alendronate 5 mg/day (30%), or placebo (40%). All participants were encouraged to take a calcium (500 mg/day) and vitamin D (250 IU/day) supplement. The primary outcome was change in total hip BMD. Secondary endpoints included change in lumbar spine BMD and change in markers of bone turnover (bone-specific alkaline phosphatase and urinary type I collagen cross-linked N-telopeptide). RESULTS: Among the women who had prior alendronate therapy in FIT, further therapy with alendronate (5 and 10 mg groups combined) for 3 years compared with placebo maintained BMD at the hip (2.0% difference; 95% CI, 1.6-2.5%) and further increased BMD at the spine (2.5% difference; 95% CI, 1.9-3. 1%). Markers of bone turnover increased among women discontinuing alendronate, whereas they remained stable in women continuing alendronate. Cumulative increases in BMD at the hip and spine and reductions in bone turnover from 8.6 years earlier at FIT baseline were greater for women continuing alendronate compared with those discontinuing alendronate. However, among women discontinuing alendronate and taking placebo in the extension, BMD remained higher and reduction in bone turnover was greater than values at FIT baseline. CONCLUSIONS: Compared with women who stopped alendronate after an average of 5 years, those continuing alendronate maintained a higher BMD and greater reduction of bone turnover, showing benefit of continued alendronate treatment on BMD and bone turnover. On discontinuation of alendronate therapy, rates of change in BMD at the hip and spine resumed at the background rate, but discontinuation did not result in either accelerated bone loss or a marked increase in bone turnover, showing persistence of alendronate's effects on bone. Data on the effect of continuation versus discontinuation on fracture risk are needed before making definitive recommendations regarding the optimal length of alendronate treatment.

Beta-adrenergic blockers reduce the risk of fracture partly by increasing bone mineral density: Geelong Osteoporosis Study.

UNLABELLED: This population-based study documented beta-blocker use in 59/569 cases with incident fracture and 112/775 controls. OR for fracture associated with beta-blocker use was 0.68 (95%CI, 0.49-0.96). Beta-blockers were associated with higher BMD at the total hip (2.5%) and UD forearm (3.6%) after adjusting for age, anthropometry, and thiazide use. Beta-blocker use is associated with reduced fracture risk and higher BMD. INTRODUCTION: Animal data suggests that bone formation is under beta-adrenergic control and that beta-blockers stimulate bone formation and/or inhibit bone resorption. MATERIALS AND METHODS: We evaluated the association between beta-blocker use, bone mineral density (BMD), and fracture risk in a population-based study in Geelong, a southeastern Australian city with a single teaching hospital and two radiological centers providing complete fracture ascertainment for the region. Beta-blocker use was documented for 569 women with radiologically confirmed incident fractures and 775 controls without incident fracture. Medication use and lifestyle factors were documented by questionnaire. RESULTS: Odds ratio for fracture associated with beta-blocker use was 0.68 (95% CI, 0.49-0.96) for any fracture. Adjusting for age, weight, medications, and lifestyle factors had little effect on the odds ratio. Beta-blocker use was associated with a higher BMD at the total hip (2.5%, p = 0.03) and ultradistal forearm (3.6%, p = 0.04) after adjustment for age, anthropometry, and thiazide use. CONCLUSION: Beta-blockers are associated with a reduction in fracture risk and higher BMD.

Trabecular bone microarchitecture is deteriorated in men with spinal cord injury.

UNLABELLED: Using magnetic resonance imaging, men with spinal cord injury (n = 10) were found to have fewer trabeculae that were spaced further apart in the knee than able-bodied controls of similar age, height, and weight (n = 8). The deteriorated trabecular bone microarchitecture may contribute to the increased fracture incidence after injury. INTRODUCTION: Spinal cord injury results in a dramatic decline in areal bone mineral density (aBMD) and a marked increase in lower extremity fracture; however, its effect on trabecular bone microarchitecture is unknown. The purpose of this study was to determine if trabecular bone microarchitecture is deteriorated in the knee of men with long-term, complete spinal cord injury. MATERIALS AND METHODS: Apparent bone volume to total volume (appBV/TV), trabecular number, (appTb.N), trabecular thickness (appTb.Th), and trabecular separation (appTb.Sp), measures of trabecular bone microarchitecture, were assessed in the distal femur and proximal tibia of men with long-term (>2 years) complete spinal cord injury (SCI; n = 10) and able-bodied controls (CON; n = 8) using high-resolution magnetic resonance imaging. Proximal tibia and arm aBMD were determined using DXA. Independent t-tests were used to assess group differences in anthropometrics and bone parameters. Pearson correlation analysis was used to assess the relationships among trabecular bone microarchitecture, aBMD, and time since injury. RESULTS: There were no group differences in age, height, or weight; however, the distal femur and proximal tibia of SCI had 27% and 20% lower appBV/TV, 21% and 20% lower appTb.N, and 44% and 33% higher appTb.Sp, respectively (p < 0.05). The distal femur of SCI also had 8% lower appTb.Th (p < 0.05). Whereas arm aBMD was not different in the two groups, proximal tibia aBMD was 43% lower in SCI. In SCI and CON combined, aBMD was correlated with appBV/TV (r = 0.62), appTb.N (r = 0.78), and appTb.Sp (r = -0.82) in the proximal tibia (p < 0.05). Time since injury was more strongly correlated with appTb.N (r = -0.54) and appTb.Sp (r = 0.56) than aBMD (r = -0.36) in the distal tibia, although none of the relationships were statistically significant (p > 0.05). CONCLUSION: Men with complete spinal cord injury have markedly deteriorated trabecular bone microarchitecture in the knee, which may contribute to their increased fracture incidence.

Evaluation of a high dose to a finger from a 60Co accident.

Electron spin resonance and fluorescence in situ hybridization were used to evaluate the dose to the finger of a worker who accidentally touched a radiotherapy 60Co therapy source in November 1995. In September 1999, the middle finger was amputated. We estimated the dose to the bone of the finger to be 6.4 +/- 0.5 Gy using the electron spin resonance additive dose method and a corrected dose of about 20 +/- 3 Gy could be inferred by translocation analysis in peripheral lymphocytes using the fluorescence in situ hybridization method. This retrospective dosimetry was performed for the victim 4 y after the accident, but the compatibility of the results obtained by physical and biological methods reinforce their validity, although in the case of partial-body exposure the biological method has limitations and demonstrates the need to find appropriate correction factors.