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Increased reduction in bone density and skin thickness in postmenopausal women taking long-term corticosteroid therapy: a suggested role for estrogen add-back therapy.

BACKGROUND: Long-term corticosteroid therapy is complicated by osteoporosis and generalized thinning of the skin. These two complications of such therapy were routinely assessed at the Menopause Clinic of St. Luke's Hospital Medical School, University of Malta. METHODS: A cross-sectional study was performed on 64 postmenopausal women who had been taking long-term corticosteroids. Each woman had her skin thickness measured using high-resolution ultrasound (22 MHz) and her bone density measured by dual-energy X-ray absorptiometry (DEXA). These measurements were compared with those of a control group (n = 557), a group of women who had sustained osteoporotic fractures (n = 180) and a group of women taking hormone replacement therapy (HRT) (n = 399). A longitudinal study of 29 postmenopausal women taking corticosteroids was also performed. This study compared results for women who, in addition to their corticosteroids, were taking HRT and for those who were taking corticosteroids alone. RESULTS: The cross-sectional study showed that corticosteroid therapy was associated with the lowest mean skin thickness measurement (0.83 mm). Similarly, low mean bone density measurements for the lumbar spine (0.805 g/cm2) and left hip (0.715 g/cm2) were obtained for this group. The mean skin thicknesses in the control group and the HRT group were 0.93 mm and 0.935 mm, respectively, while that in the osteoporotic fracture group was 0.88 mm. The bone density of the fracture group was similar to that of the group of women taking long-term corticosteroids, with the lumbar spine having a mean density of 0.805 g/cm2 and 0.81 g/cm2, and the left hip having a density of 0.705 g/cm2 and 0.715 g/cm2, respectively. Bone densities were similar for the control group and the HRT group, and higher than that of the corticosteroid or fracture group. The lumbar spine had a mean density of 0.925 g/cm2 in the control group and 0.93 g/cm2 in the hormonally treated group. Both the treated and control groups had similar bone densities of the left hip at about 0.82 g/cm2. The small longitudinal study compared postmenopausal women on long-term corticosteroid therapy taking HRT with another group who were not taking HRT. This 4-year study revealed mean total increases in skin thickness of 6.1% and bone density of 5.5% (left hip) and 14.6% (lumbar spine) in the HRT group, since the start of the study. Conversely, the control group registered reductions over 4 years in both skin thickness (2.8%) and bone density (lumbar spine 4.5% and hip 5.0%). CONCLUSION: In postmenopausal women taking long-term corticosteroids, skin thickness and bone density were both decreased, but the addition of HRT as add-back improved the situation dramatically. Skin thickness and bone density in women taking long-term corticosteroids were comparable to those in women who had sustained osteoporotic fractures. It is therefore suggested that HRT be used as add-back therapy in postmenopausal women taking long-term corticosteroid therapy.

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Bone density effects of continuous estrone sulfate and varying doses of medroxyprogesterone acetate. Ogen/Provera Study Group.

OBJECTIVE: To establish the optimum oral daily dose of medroxyprogesterone acetate with estrone sulfate for 2 years to maintain bone density. METHODS: A multicenter, double-blind study involved 568 postmenopausal women given estrone sulfate, 1.25 mg, and randomized to receive 2.5, 5, or 10 mg of medroxyprogesterone acetate. Bone density analyses of the lumbar spine and femoral neck were done at baseline and 12 and 24 months. RESULTS: There was a significant increase from baseline to 24 months in mean lumbar spine (4.0% +/- 0.27%) and femoral neck (3.2% +/- 0.28%) bone density, with no significant differences between the treatment groups. Factors most influencing bone density changes were baseline bone density and treatment duration. Significant increases were seen in the spine over 2 years; in the hip, those occurred in the first 12 months only. In both sites, lower baseline bone density resulted in greater increases. In the spine only, no previous hormone replacement therapy, higher body mass index, more than 2 years postmenopause, and nonsmoking resulted in greater gains. Once those covariates and center-to-center variations were corrected for, in the spine, the 10-mg group had smaller increases than the other groups. Changes were unrelated to age, parity, calcium, and alcohol intakes in either site. CONCLUSION: Daily estrone sulfate, 1.25 mg, with 2.5, 5, or 10 mg medroxyprogesterone acetate was effective for preventing bone loss in postmenopausal women.

Adult↗

Effect of estrogen and calcitonin on vertebral bone density and vertebral height in osteoporotic women.

Estrogen and calcitonin increase bone density of osteoporotic women, particularly on the axial skeleton. To verify whether the effect of these drugs might in part be biased by spurious increases in bone density due to radiologically irrelevant microfractures, and consequent subtle decreases in vertebral height, we followed the changes in vertebral bone density (VBD), assessed by quantitative computed tomography, in relation to vertebral height (VH) in 60 osteoporotic women. VH was measured as the sum of anterior, central and posterior heights of L1-L3 vertebral bodies on lateral radiographs. Patients received either salmon calcitonin (sCT: 50 IU subcutaneously three times per week, n = 18), hormonal replacement therapy (HRT: conjugated estrogen 0.625 mg/day, days 1-25, plus medroxyprogesterone acetate 10 mg/day, days 16-25 of each month; n = 21) or calcium alone (Ca: 1000 mg/day, n = 21). After 1 year, VBD increased in the HRT group (+5.0 +/- 1.9%, p = 0.010), did not change significantly in the sCT group (+3.3 +/- 2.3%, p = 0.167), and decreased by 6.1 +/- 1.0% (p less than 0.001) in the Ca group. By analysis of variance, the changes induced by HRT and sCT were significantly different from those observed in the Ca group (F = 7.982, p less than 0.001). VH decreased slightly in all three subsets of patients (-0.9 +/- 0.5% in sCT, -1.5 +/- 0.3% in HRT, -0.1 +/- 0.5% in Ca), but these changes were not significantly different between groups (F = 2.545, p = 0.081).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Bone density and hemoglobin levels in older persons: results from the InCHIANTI study.

Hypoxemia has been recognized as a risk factor for bone loss. The aim of the present study is to investigate the relationship of bone mass and density measures with anemia and hemoglobin levels in a large sample of older community-dwelling persons. The study is based on data from 950 participants enrolled in the "Invecchiare in Chianti" (Aging in the Chianti area, InCHIANTI) study. All the analyses were performed considering continuous hemoglobin levels as well as the dichotomous anemia variable (defined according to WHO criteria as hemoglobin < 12 g/dl in women and < 13 g/dl in men). A peripheral quantitative computerized tomography (pQCT) scan of the right calf was performed in all participants to evaluate total bone density, trabecular bone density, cortical bone density, and the ratio between cortical and total bone area. Linear regression analyses were used to assess the multivariate relationship of pQCT bone measures with anemia and hemoglobin levels after adjustment for demographics, chronic conditions, muscle strength and biological variables. Participants were 75.0 (SD 6.9) years old. In our sample, 101 participants (10.6%) were anemic. In women, coefficients from adjusted linear regression analyses evaluating the association between pQCT bone measures (per SD increase) and hemoglobin levels/anemia showed significant associations of anemia with total bone density (beta = -0.335, SE = 0.163; P = 0.04) and cortical bone density (beta = -0.428, SE = 0.160; P = 0.008). Relationships with borderline significance were found for the associations of anemia with trabecular bone density and the ratio between cortical and total bone area. Significant associations were found between hemoglobin levels and trabecular bone density (beta = 0.112, SE = 0.049; P = 0.02), total bone density (beta = 0.101, SE = 0.046; P = 0.03), cortical bone density (beta = 0.100, SE = 0.046; P = 0.03) and the ratio between cortical bone and total area (beta = 0.092, SE = 0.045; P = 0.04). In men, significant associations were found for hemoglobin levels with total bone density (beta = 0.076, SE = 0.036; P = 0.03) and cortical bone density (beta = 0.095, SE = 0.41; P = 0.02). A borderline significance was reported for the association between anemia and cortical bone density. We concluded that anemia and low hemoglobin levels are negatively and independently associated with bone mass and density. The bone loss associated with hemoglobin levels mainly occurs in the cortical bone. Women with lower hemoglobin levels demonstrate a higher bone loss than male counterparts.

Aged↗

Bone density in young males with recently diagnosed inflammatory bowel disease.

OBJECTIVES: Patients with inflammatory bowel disease are at increased risk of developing osteopenia and osteoporosis. Our study was designed to determine the degree of decreased bone density in steroid naïve young male patients with inflammatory bowel disease and to unmask possible risk factors. METHODS: Before the initiation of any treatment in young male patients aged 26 +/- 4.8 years with inflammatory bowel disease, ultrasound bone density measurement at the right calcaneous was performed using a Lunar Achilles plus device. Stiffness Index and T-score were measured. We also performed an ultrasound bone density measurement at right calcaneous in healthy age- and sex-matched controls. RESULTS: Nine out of 32 patients with inflammatory bowel disease had osteopenia or osteoporosis (approximately 28%). Of controls, two individuals had osteopenia (approximately 7%). There was a positive correlation between T-score and body mass index, but not between T-score and age in patients with inflammatory bowel disease. There was a statistically significant difference in T-score between patients with disease duration>6 months and those with disease duration<6 months (P=0.032), but not between the patients with Crohn's disease compared with the patients with ulcerative colitis. CONCLUSION: Steroid naïve young male patients with inflammatory bowel disease have lower bone density values than healthy controls. According to our findings, duration of disease above 6 months and low body mass index are major risk factors for low bone density in these patients. Bone density measurement should be performed in all patients with inflammatory bowel disease in an early stage of the disease.

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Differential effects on bone density of progestogen-only methods for contraception in premenopausal women.

The question of differential effects on bone density by two different types of progestogen-only methods for contraception in premenopausal women was addressed. Data from a prospective randomized clinical trial among 22 premenopausal women, age 32.6 (range 20-45 years), who were randomly assigned to either of two treatments with continuous progestogens for contraception were analyzed; depot-medroxyprogesterone acetate (DMPA) or continuous levonorgestrel treatment with subdermal implants (Norplant), respectively. Forearm bone density (BMDprox) increased with 2.94% (p = 0.006) in women who were prescribed levonorgestrel, which was in contrast to stable values in those prescribed depot-medroxy-progesterone acetate; group difference at 6 months for BMDprox 3.4% (95% CI 1.3, 5.5; p = 0.025) and BMDdist 4.1% (95% CI - 1.3, 9.6; p = 0.077). The changes in bone density were consistent with the changes in biochemical indices for bone metabolism; DMPA users showed signs of increased bone turnover and users of levonorgestrel showed increased bone formation with increased levels of both alkaline phosphatase (p = 0.004) and osteocalcin (p = 0.007). The findings suggest an increase in bone density during treatment with levonorgestrel and stable values during short-term administration of DMPA, in standard clinical doses for contraception.

Adult↗

A randomized, placebo-controlled trial of calcium supplementation for decreased bone density in corticosteroid-using patients with inflammatory bowel disease: a pilot study.

BACKGROUND: Patients with inflammatory bowel disease (IBD) have a high prevalence of osteoporosis. A number of studies have found that corticosteroid use is associated with the development of osteoporosis in these patients. Calcium supplementation may be of benefit in corticosteroid-induced osteoporosis and calcium may be a nutrient that patients with IBD lack. AIM: To test the benefit of calcium supplementation on bone density in a pilot study over a 1-year period, in a group of corticosteroid-using patients with IBD, in a randomized, double-blind, placebo-controlled treatment study. METHODS: Corticosteroid-using patients with IBD including males over the age of 18 years and premenopausal females, were randomized to receive either calcium carbonate 1000 mg plus vitamin D 250 IU (Oscal) or an identically matched placebo. Dual energy X-ray absorptiometry measurements of bone density were obtained at entry and at 1 year. At entry, and every 3 months thereafter, serum was collected for the measurement of haemoglobin, biochemistry and bone hormones. Simultaneously a 24-h urine collection was analysed for calcium excretion and creatinine clearance, and a 4-day food record was collected to document dietary calcium and vitamin D ingestion. RESULTS: We found a high prevalence of moderately severe decreased bone density in corticosteroid-using patients with IBD. The dose of prednisone in the year prior to study entry was inversely correlated with bone density at the hip (R = -0.67, P = 0.004). At study entry serum osteocalcin was inversely correlated with corticosteroid dose in the year prior to the study (R = -0.64, P = 0.02) and at study end, directly correlated with the percentage change in spine bone density (R = 0.59, P = 0.01). The dietary calcium intake of these patients was close to the current RDA (recommended daily intake) for premenopausal, post-adolescent adults. Calcium supplementation with small extra doses of vitamin D conferred no obvious benefit to bone density at the end of 1 year. There was no correlation between oral calcium ingestion and bone mass measurements. Both the treatment and placebo groups' bone density remained relatively stable at 1 year, suggesting that bone loss in corticosteroid-using patients may peak early into the use of the corticosteroids. CONCLUSIONS: Calcium supplementation (1000 mg/day) conferred no significant benefit to bone density at 1 year in patients with corticosteroid-using IBD patients with osteoporosis. Future investigations should explore other therapeutic avenues that may have greater effects on increasing bone density in patients who already have considerable osteoporosis.

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Does bracing affect bone density in adolescent scoliosis?

STUDY DESIGN: This is a case-control, cross-sectional analysis of bone density. OBJECTIVES: To determine if bracing during growth affects bone density in adolescent idiopathic scoliosis and whether the effect is local or systemic. SUMMARY OF BACKGROUND DATA: Data concerning the effect of bracing on bone mass in adolescents with idiopathic scoliosis are nonexistent. We were concerned that bone mass loss resulting from long-term brace use may be permanent and may predispose to problems with osteoporosis. METHODS: Healthy adolescent females (n = 85) with scoliosis measuring 20-45 degrees and treated either by brace or observation were studied. Dietary calcium, activity level, body mass index, and pubertal status were evaluated. Scoliosis was measured by Cobb angle. Bone mineral density at the hip and spine were measured by dual energy x-ray absorptiometry to differentiate local versus systemic effects of bracing. Lateral scans of the L3 vertebral body were used to minimize the influence of the pedicles, the effect of the scoliosis, and the interference of the ilium. RESULTS: Mean age, height, and weight were similar between braced and observed groups. After adjusting for curve, Cobb angle, body mass index, activity, and diet, two-way analysis of covariance showed L3 and femoral bone mineral density was the same for braced and observed patients, and pubertal status affected spinal bone mineral density but had no effect on femoral bone mineral density. Pubertal status and body mass index accounted for 53% of the variation in spine bone mineral density and was not affected by brace use. Cobb angle, curve pattern, activity, and diet were not associated with bone mineral density. CONCLUSION: Brace treatment does not adversely affect bone mass at the spine and hip in children with idiopathic scoliosis.

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Relative influence of physical activity, muscle mass and strength on bone density.

In a population-based sample of 348 men (age 22-90 years) and 351 women (age 21-93 years), we evaluated the relationship of bone density assessed at a variety of skeletal sites by dual-energy X-ray absorptiometry (DXA) with various muscle mass estimates obtained also from the DXA scan and with physical activity by interview and strength assessed both subjectively and objectively. All these parameters declined with age as judged from these cross-sectional data. All estimates of total skeletal muscle mass were strongly correlated with bone density at different skeletal sites. Muscle mass, in turn, was correlated with physical activity and hand strength. In multivariate models including these variables, muscle mass was the strongest determinant of bone density, accounting for 6-53% (mean 27%) of the variance at the different skeletal sites. Physical activity (and/or a physical activity x age interaction) was an independent predictor of bone mass in 48% of the site-specific models and accounted for 0.03-39% (mean 10%) of the variance, while hand strength (and/or a hand strength x age interaction) accounted for up to 4% (mean 1%) of the variance as an independent predictor of bone density in a third of the models. Although these variables together accounted for a large proportion of the variance in bone density, other potential predictors were not assessed in these analyses. The dramatic decline in physical activity over life seemed unable to completely explain the age-related loss of bone mass, and additional research is needed to determine whether the relationship of muscle mass with bone density is a direct one or due instead to other factors such as circulating hormone levels.

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Differences in intestinal calcium and phosphate transport between low and high bone density mice.

The purpose of this study was to determine whether there are differences in intestinal Ca and phosphate transport in mice having different peak bone densities. Intestinal transport was measured in C57BL/6 (C57, low bone density) and C3H/He (C3H, high bone density) female mice. Unidirectional (mucosal to serosal) transport of Ca was 58% higher in C3H compared with C57 mice, as measured by everted duodenal sacs. The capacity of the duodenal mucosa to take up Ca was also higher in the C3H mice. This uptake highly correlated with Ca transport across the intestine. 1,25-Dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], which stimulates intestinal Ca absorption, markedly stimulated unidirectional Ca transport and uptake to similar levels in both strains of mice. On the other hand, unidirectional phosphate transport in C3H mice was only 36% that of C57 mice. mRNA levels of the plasma membrane Ca pump were 90% higher in the duodenum of C3H mice. There was no difference between strains in duodenal calbindin or 24-hydroxylase mRNA levels. Regarding vitamin D metabolism, there was no difference in serum 1,25(OH)(2)D(3) levels or in renal 1alpha-hydroxylase mRNA levels. The combination of high intestinal Ca transport and low phosphate transport may contribute to the high peak bone density seen in the C3H relative to the C57 mouse.

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Targeted expression of calcitonin gene-related peptide to osteoblasts increases bone density in mice.

The neuropeptide calcitonin gene-related peptide (CGRP) is concentrated in fine sensory nerve endings innervating all tissues, including bone. CGRP inhibits osteoclasts, stimulates insulin-like growth factor I and inhibits tumor necrosis factor alpha production by osteoblasts in vitro. To investigate the role of CGRP in bone in vivo, mice were engineered to express CGRP in osteoblasts by placing the human CGRP gene under the control of the rat osteocalcin promoter (Ost-CGRP tg+ mice). Calvaria cultures from transgene positive (tg+), but not tg- mice, produced bioactive CGRP. Trabecular bone density and bone volume, determined by peripheral quantitative computed tomography and bone histomorphometry, respectively, were higher in tg+ than tg- littermates. This increase in bone volume was associated with an increased bone formation rate. Trabecular bone density decreased in tg+ mice as a result of ovariectomy, but remained higher than in sham tg- mice. Targeting CGRP to osteoblasts appears to favor the establishment of a higher trabecular bone mass in mice.

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Impact of parathyroid hormone on bone density in long-term renal transplant patients with good graft function.

BACKGROUND: It remains unknown whether low-grade hyperparathyroidism persisting beyond the first year postrenal transplantation has any impact on bone density. METHODS: Parathyroid hormone (PTH), glomerular filtration rate (GFR), and bone density (by dual-energy x-ray absorptiometry [DXA]) were monitored in the follow-up of our transplant patients. Of 260 long-term renal transplant patients, 41 fulfilled the following criteria: Two DXA measurements performed at least five years apart (median 6.8 years, range 5-9); GFR>or=35 ml/min per 1.73 m body surface area (median 50, range 35-76); no bisphosphonate treatment or parathyroidectomy in the study period. RESULTS: In all, 40% had mean PTH values above the normal limit 6.9 pmol/L (65 pg/ml), and the range was 0.9-17 pmol/L. In the first DXA, 8 of 41 patients had osteoporosis and 17 more had osteopenia. Hip bone density Z-score was -0.60 SD, range (-2.6 to +2.3). The absolute median value (g/cm) remained unchanged until the second DXA, but among patients there was a variation which ranged from -2.3% to +1.7% per year. In a simple linear regression analysis, these changes were significantly correlated to mean PTH (r=0.16, P=0.010). Median lumbar spine bone density was also reduced in the first DXA and was not different at follow-up, but with this variable individual changes did not correlate to mean PTH. CONCLUSION: Bone density is often reduced and PTH remains elevated in long-term renal transplant patients with good transplant function. Slight to moderate elevation of PTH is associated with reduction in hip bone mineral density.

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Increase in bone mass of older postmenopausal women with low mineral bone density after one year of percutaneous oestradiol implants.

OBJECTIVE: To evaluate the effect of 75 mg oestradiol implants on the bone mass of older postmenopausal women with osteoporosis. DESIGN: One year prospective-controlled study. SUBJECTS: Thirty-two postmenopausal women over 60 years of age and more than five years postmenopausal with low bone density were recruited. Thirty women completed treatment for one year with 75 mg oestradiol implants. The changes in bone density were compared with a control group of 14 women. The side effects with treatment were documented. MAIN OUTCOME MEASURES: Dual energy X-ray absorptiometry of the lumbar spine and proximal femur using Hologic 1000 QDR before treatment and at one year. Plasma oestradiol assays were performed before and after one year. RESULTS: The median percentage changes in the treated group after one year was 12.6% at the lumbar spine and 5.22% at the total hip. The increase in vertebral bone density was greatest in women with low initial bone density (r = -0.35, P < 0.05) and those with highest treatment plasma oestradiol levels (r = 0.47, P < 0.01). Side effects were common but most were transient and mild in nature. CONCLUSION: 75 mg oestradiol implants significantly increase the bone mineral density at the spine and hip of older postmenopausal women with established osteoporosis.

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Bone density, biochemistry and life-style.

We have assessed the relationship between bone density, biochemistry and life-style factors in a cross-sectional study of 434 pre- and 357 postmenopausal women. Bone-mineral content (BMC) was measured in the non-dominant forearm using single-photon densitometry. Bone mass was corrected for bone size (BMC2) in a sub-set of 263 subjects. Correlation statistics and multiple regression analyses were used to identify physical and biochemical measurements that could be used to best predict BMC or BMC2. These were combined with lifestyle factors, using multiple logistic regression analysis, to identify women at risk of low bone density. Cut-off values were taken as the 5th percentile of the bone density distributions in pre-menopausal women. In postmenopausal women, using BMC2 values to define "risk", and using age, creatinine, alkaline phosphatase, thyroxine treatment, and calcium supplementation as predictors, a sensitivity of 73% and a specificity of 95% were achieved. Such a model may be of use as a "first pass" screening test for osteoporosis.

Adult↗

The relation between bone density, free androgen index, and estradiol in men 60 to 70 years old.

The cause of age-related bone loss in men is poorly understood. Previous studies of the relationship between bone density and serum androgens have yielded inconsistent results, perhaps partly because age is a determinant of both. Recent studies suggest that serum estrogen levels influence bone density in adult men. In order to determine whether bone mineral density (BMD) and bone turnover are associated with serum sex steroids, we investigated 37 normal men within a narrow age range (60-70 years). Bone mineral density at the forearm, hip, and spine, testosterone, sex hormone binding globulin (SHBG), free androgen index (FAI:T/SHBG), estradiol (E), free estradiol index (FEI:E/SHBG), and markers of bone formation (alkaline phosphatase, osteocalcin, procollagen type I C-terminal extension peptide) and bone resorption (hydroxyproline/creatinine [OHPr/Cr], deoxypyridinoline/creatinine [Dpd/Cr], pyridinoline/creatinine, collagen type I cross-linked telopeptide) were measured. Bone mineral density was positively related (r > 0.35, p < 0.05 at all sites) to log FAI, whereas there was no significant relationship between BMD and either serum total testosterone, serum E, or FEI. Bone density at the spine and hip were inversely related to both OHPr/Cr (r > -0.41, p < 0.05 for all sites) and Dpd/Cr (r > -0.36, p < 0.05 for all sites). OHPr/Cr (r = -0.41, p < 0.05) and Dpd/Cr (r = -0.41, p < 0.05) were both inversely related to log FAI. We conclude that BMD and bone turnover in adult men are related to plasma free androgens.

Aged↗

Measurement of mandibular bone density after iliac crest grafting.

Nonvascularized and microsurgically revascularized iliac bone grafts used for mandibular reconstruction behave differently during healing. Quantitative computer tomography (QCT) was used to investigate these differences with respect to mineralization and macrostructure of the grafts after a period of adequate functional loading. It was shown that in nonvascularized grafts, reactive sclerosis occurs, as a sign of an irregularly reparative metaplastic process and mineralization. In comparison with the intact iliac crest, the bone density of the graft was markedly increased. The microsurgically revascularized grafts, however, showed retention of structural differentiation into homogeneous cancellous bone, and a smoothly demarcated cortex with essentially unchanged bone density. Possible explanations of these differences are discussed.

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Serum insulin and bone density in normal subjects.

A relationship between circulating insulin and bone mass has been postulated. To test this hypothesis we measured fasting serum insulin and quantitated bone density in the forearm, spine and femoral neck by single and dual photon absorptiometry of 70 normal women. There was no statistically significant relationship between insulin and bone density at any site by correlation or regression analysis. Although the relationship between a single measurement of a hormone (at one point in time) and bone density (the result of lifelong factors) should be interpreted with caution, our findings do not support the hypothesis that there is an association between serum insulin and bone mass.

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The relationship between plasma estradiol and the increase in bone density in postmenopausal women after treatment with subcutaneous hormone implants.

Twenty-three postmenopausal women with a median of 2 years past menopause (range, 1 to 12 years) and a median age of 52 years (range, 39 to 62 years) were recruited to participate in a longitudinal study designed to investigate the factors that influence the increase in bone density with subcutaneous estradiol and testosterone implants. All women received 75 mg of estradiol with 100 mg testosterone subcutaneously. Bone density was measured at the spine and hip by dual-photon absorptiometry before therapy and after 1 year of subcutaneous hormonal therapy. The mean pretreatment bone density at the lumber vertebrae and neck of the femur was 0.84 grams of hydroxyapatite per square centimeter (SD, 0.11) and 0.73 grams of hydroxyapatite per square centimeter (SD, 0.10), respectively. The bone density at both sites increased with values of 0.91 grams of hydroxyapatite per square centimeter (SD, 0.11) and 0.75 grams of hydroxyapatite per square centimeter (SD, 0.11), respectively. These values represent an increase of 8.3% (p less than 0.0001) at the spine and 2.8% (p less than 0.01) at the neck of the femur. The plasma estradiol level increased from a median of 80.5 pmol/L to 453 pmol/L (p less than 0.001). The percentage increase of vertebral bone density was not related to age, number of years past the menopause, pretreatment bone density, or serum testosterone levels, but a significant correlation was found between the percentage increase in bone density at the spine and the serum estradiol level (p less than 0.02, r = 0.45).

Adult↗