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PubMed1983

Studies on osteoporosis X. Effect of estrogen-progestin combination on heparin-induced osteoporosis.

Neutron activation analysis was employed to determine total body calcium in C3H/St(Ha) female mice. As 99% of body calcium is in bone, loss of calcium was used as an index of bone loss (osteoporosis). Heparin (500 U/kg b.i.d. caused bone loss in 3 months. Premarin (2 mg/kg q.d.) or norethindrone (40 mg/kg q.d.) alone prevented this osteoporosis. A Premarin-norethindrone combination (2 mg - 10 mg q.d. respectively) appeared to be somewhat more effective than either agent alone, but this difference was not significant at the 5% level. Combinations of estrogen and progestins may prevent metabolic bone disease at the same time reducing the danger of estrogen induced neoplasia.

Animals↗
PubMed1999

Diagnosis and management of osteoporosis in postmenopausal women: clinical guidelines. International Committee for Osteoporosis Clinical Guidelines.

The authors, all physicians involved in clinical research on bone and practicing clinicians, propose practical guidelines for identifying persons with osteoporosis or those at high risk of developing the disease and for managing patients who may benefit from therapy. These guidelines are based on an analysis of peer-reviewed articles published before November 1998. A flowchart of women who might benefit from treatment is provided, including clinical presentation (recent fracture of the spine, hip, or other bone or no fracture; risk factors for osteoporosis); relevant investigations (bone mineral density measurement and laboratory tests required for the differential diagnosis); and therapeutic management (general measures such as calcium and vitamin D supplementation and specific pharmacologic interventions such as estrogen, bisphosphonates, intranasal calcitonin, raloxifene, fluoride salts, and other compounds that have been assessed in randomized clinical trials). The strongest evidence for antifracture efficacy (reduction of vertebral and nonvertebral fracture risk) was observed with alendronate.

Adult↗
PubMed1989

Prevention and rehabilitation of osteoporosis program: exercise and osteoporosis.

Osteoporosis is a common crippling bone disease affecting post-menopausal and elderly women. It results in fractures, spinal deformity and chronic pain leading to decreased mobility and functional disability. A preventive program in Toronto, described in this article, aims to prevent bone loss and maximise the functional capacity of osteoporotic patients through a program with educational, social and exercise components. Evaluation of the program, also reported here, showed that 80 per cent of patients complied with the requirements of the exercise program and that those who exercised reported improvement in general well being, stamina, mobility and pain tolerance. The exercise group also showed a significant improvement in VO 2 max (p less than 0.001) and bone mass (p less than 0.02) after one year of exercise. None of the patients developed fracture as a direct result of the exercise. The exercise prescribed for osteoporosis is safe and beneficial. The program is a social success.

Aged↗
PubMed1995

Histomorphometric classification of postmenopausal osteoporosis: implications for the management of osteoporosis.

AIMS: To define and group static and dynamic iliac crest histomorphometric parameters in women with established osteoporosis. METHODS: Iliac crest biopsy specimens from 146 white women were sectioned undecalcified and examined using image analysis. RESULTS: Five distinct groups were defined on the basis of histomorphometric changes in cell function: group 1, decreased osteoblastic and osteoclastic activity; group 2, decreased osteoblastic and increased osteoclastic activity; group 3, increased osteoblastic and osteoclastic activity; group 4, no bone surface cell activity; and group 5, apparently normal osteoblastic and osteoclastic activity. CONCLUSIONS: Five distinct subgroups of patients with postmenopausal osteoporosis can be defined based on changes in bone cell function. Defining cellular dysfunction in this way may be important for tailoring treatment regimens to the needs of individual patients.

Age Factors↗
PubMed2000

Efficacy and safety of daily risedronate in the treatment of corticosteroid-induced osteoporosis in men and women: a randomized trial. European Corticosteroid-Induced Osteoporosis Treatment Study.

Long-term use of high-dose corticosteroids often results in bone loss, which may lead to osteoporosis-related fractures. This was a multicenter, double-blind study in which 290 ambulatory men and women receiving high-dose oral corticosteroid therapy (prednisone > or = 7.5 mg/day or equivalent) for 6 or more months were randomized to receive placebo, risedronate 2.5 mg/day, or risedronate 5 mg/day for 12 months. All patients received calcium 1 g and vitamin D 400 IU daily. The primary endpoint was lumbar spine bone mineral density (BMD) at month 12. Additional measurements included BMD at the femoral neck and trochanter and the incidence of vertebral fractures. Overall, there were statistically significant treatment effects on BMD at 12 months at the lumbar spine (p < 0.001), femoral neck (p = 0.004), and trochanter (p = 0.010). Risedronate 5 mg increased BMD at 12 months by a mean (SEM) of 2.9% (0.49%) at the lumbar spine, 1.8% (0.46%) at the femoral neck, and 2.4% (0.54%) at the trochanter, whereas BMD was maintained only in the control group. Although not powered to show fracture efficacy, we observed a reduction in the incidence of vertebral fractures of 70% in the combined risedronate treatment groups, relative to placebo (p = 0.042). Risedronate was well tolerated, had a good safety profile, and was not associated with gastrointestinal adverse events. We conclude that risedronate increases BMD and potentially reduces the incidence of vertebral fractures in patients with corticosteroid-induced osteoporosis.

Adolescent↗
PubMed1991

[The effect of estrogen and, sex-steroids and thyroid hormone preparation on bone mineral density in senile osteoporosis--a comparative study of the effect of 1 alpha-hydroxycholecalciferol (1 alpha-OHD3) on senile osteoporosis].

In order to assess the effect of sex steroids on bone mineral density in Japanese with senile osteoporosis, the bone mineral density in 1/3 distal site of radius was measured serially before and after treatment for 2 years using single photon absorptiometry. Sixty seven old females with senile osteoporosis were divided into 4 groups, Group 1 (n = 28, mean age; 74.4 +/- 1.3 y.o., mean +/- SEM) was the control group, Group 2 (n = 14, mean age; 73.7 +/- 1.7 y.o.) was treated with 0.5-1.0 micrograms/day of 1 alpha -OHD3, Group 3 (n = 12, mean age; 75.4 +/- 2.9 y.o.) was treated with conjugated estrogen (Premarin) in a dose of 0.3125 mg/day (3 approximately 4 weeks administration followed by 1 week rest) and Group 4 (n = 13, mean age; 76.4 +/- 1.8 y.o.) was treated with sex-steroids (pregnenolone : androstenedione : androstenediol : testosterone : estrone = 1.0 mg : 1.0 mg : 0.5 mg : 0.1 mg : 5 micrograms/tablet) and thyroid hormone (thyroid-sicca 7.5 mg/tablet) preparation in a dose of 2 tablets/day. When the radial bone mineral density (RMD) before the treatment was taken as 100%, RMDs of each group at 6, 12, 18 and 24 months were 96.4 +/- 3.1%, 97.3 +/- 2.0%, 93.7 +/- 2.1% and 96.1 +/- 1.8% in Group 1, 100.8 +/- 2.8%, 106.4 +/- 2.1%, 101.3 +/- 3.4% and 108.8 +/- 2.9% in Group 2, 103.0 +/- 2.8%, 106.2 +/- 3.5%, 105.9 +/- 4.3% and 100.2 +/- 4.7% in Group 3, 105.3 +/- 2.2%, 104.7 +/- 2.3%, 112.6 +/- 6.4% and 112.1 +/- 6.7% in Group 4, respectively. Therefore, significant increases in RMD were observed in Groups 2, 3 (transient) and 4 when compared with Group 1. In Group 3, serum level of parathyroid hormone (PTH) was significantly (p less than 0.05) increased from 0.28 +/- 0.03 ng/ml before the treatment to 0.55 +/- 0.15 ng/ml at 24 months after the treatment. In Group 2, transient (6 months after the treatment) but significant (p less than 0.01) increase in urinary Ca/Creatinine ratio from 0.15 +/- 0.04 to 0.20 +/- 0.03 was found. Serum A1-P activities in Group 4 was shown to increase transiently from 131 +/- 10 IU to 151 +/- 12 IU (p less than 0.05) at 6 months and to 158 +/- 13 IU (p less than 0.01) at 12 months followed by subsequent decrease to 135 +/- 6 IU at 18 months and 133 +/- 10 IU at 24 months after the treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed2004

[Biochemical bone marrow markers and their significance in postmenopausal osteoporosis--a new method in the diagnosis of osteoporosis?].

This study analyzes the qualification of biochemical markers in the diagnosis of osteoporosis and evaluates the potential of a multiparametric classification of premenopausal and non-osteoporotic as well as osteoporotic postmenopausal women, which is based on biochemical marker profiles. For this evaluation data of 29 women in the age between 28-74 years were used. The classification of osteoporosis was done by the trabecular density of the lumbar spine using qCT-measurements. The biochemical markers of formation and resorption AP, bAP, OC, ucOC, PICP, PYD, DPD, NTX, BSP and vitamin K were analyzed on day 1 and 42 in all patients. For vitamin K we found significant distribution differences between non-osteoporotic and osteoporotic women (p<0.005). The crosslinks PYD and DPD showed weakly significant differences. All other parameters exhibited non-significant results. Vitamin K acted with a sensitivity of 64% and a specificity of 82%. The used multiparameter classification process improved sensitivity and specificity considerably. The parameter profiles of OC/PYD, vitamin K/PYD and vitamin K/bAP revealed the highest sensitivities with specificities of more than 82%.

Adult↗
PubMed1998

Alendronate prevents postmenopausal bone loss in women without osteoporosis. A double-blind, randomized, controlled trial. Alendronate Osteoporosis Prevention Study Group.

BACKGROUND: Preventing bone loss associated with menopause and aging and maintaining the normal micro-architecture of bone provide important opportunities for the prevention of osteoporosis and fractures. OBJECTIVE: To determine the safety and efficacy of alendronate, an aminobisphosphonate, for preventing postmenopausal bone loss. DESIGN: 3-year double-blind, randomized, placebo-controlled trial. SETTING: 15 osteoporosis centers throughout the world. PARTICIPANTS: 447 women who had recently experienced menopause (6 to 36 months before study entry). INTERVENTION: Participants were randomly assigned to one of five regimens: oral placebo; oral alendronate, 1, 5, or 10 mg/d; or oral alendronate, 20 mg/d for 2 years followed by placebo during the third year (20/0 mg/d). MEASUREMENTS: Bone mineral density was measured by dual-energy x-ray absorptiometry. Bone turnover and bone quality were assessed with biochemical markers and bone histomorphometry. RESULTS: Alendronate at 5, 10, and 20/0 mg/d increased bone mineral density from baseline at the lumbar spine, femoral neck, and trochanter by 1% to 4% and in the total body by 0.3% to 1.0%; placebo led to losses of 2% to 4% at these sites. Alendronate, 1 mg/d, attenuated losses relative to those seen with placebo. Alendronate decreased markers of bone resorption to a new steady state by 3 months and decreased markers of bone formation by 6 to 12 months. Bone quality remained normal. At all dosages studied, alendronate had a safety and tolerability profile similar to that of placebo. CONCLUSIONS: In early postmenopausal women, alendronate given for 3 years at dosages of 5 mg/d or greater prevented the loss of bone mineral density at the spine and hip and in the total body. Alendronate seems to be a safe and effective nonhormonal option for prevention of postmenopausal bone loss.

Adult↗
PubMed1999

Evidence-based medicine and osteoporosis: a comparison of fracture risk reduction data from osteoporosis randomised clinical trials.

The goal of osteoporosis therapy is to prevent fractures, and many therapies are available for this disease. Regarding proven fracture benefit, however, the quality of the randomised clinical trial evidence varies substantially among therapies. The purpose of this paper is, therefore, to review the published osteoporosis randomised clinical trial literature and to assess the quality of the evidence. Although more than 35 randomised trials for different therapies were reviewed, only alendronate and vitamin D plus calcium have clearly demonstrated a fracture benefit, with alendronate providing the greatest relative risk reduction. Quality clinical trial fracture data for calcitonin, etidronate, fluoride, hormone replacement therapy, parathyroid hormone, calcitriol (and other vitamin D preparations), vitamin D and calcium monotherapy, and selective oestrogen receptor modulators are either lacking or inconclusive or published only as abstracts.

Alendronate↗
PubMed2001

[Osteoporosis in all young daughters of a mother with multiple osteoporotic fractures. A case of familial osteoporosis].

We herein describe a family whose female members are all osteoporotic: a postmenopausal mother and her three premenopausal daughters. The mother aged 60 presented axial and peripheral fractures, and very low bone mineral density (BMD). She reported that her grandmother had suffered a hip fracture. The eldest daughter aged 30 suffered multiple vertebral fractures during pregnancy and lactation associated with very low BMD. In view of these observations, the other two daughters aged 29 and 27 years respectively were evaluated. BMD was found to be severely diminished according to densitometric values for osteoporosis established by WHO, but they had no history of bone fractures. Probably the strong genetic component in bone mass is responsible for the severely diminished BMD observed in all the women in this family, as well as the occurrence of bone fractures in two of them. To our knowledge, there are no similar reports in the literature. Our results evidence the importance of evaluating bone mass in the offspring of an individual presenting severe osteoporosis, in order to detect family members with low bone mass and at high risk of developing bone fractures.

Adult↗
PubMed1980

Studies on osteoporosis IV. Effect of benzo[b]thiophene-2- and dibenzothiophene-4-carboxylic acid on heparin accelerated osteoporosis.

Total skeletal calcium was determined in female mice with the aid of whole body neutron activation analysis. Three months treatment with heaprin produced significant osteoporosis in C3-H/St(Ha) mice but not in C57/BL6(J) mice. This was more pronounced in the younger (5-8 months) than in the older (15-18 months) animals. Two 2-thiophene carboxylic acid derivatives showed significant osteoporosis preventive activity.

Animals↗
PubMed1998

Quality of life in osteoporosis: reliability, consistency, and validity of the Osteoporosis Assessment Questionnaire.

OBJECTIVE: To determine the reliability, consistency, and clinical utility of the Osteoporosis Assessment Questionnaire (OPAQ), an AIMS2 based self-assessment questionnaire. METHODS: Reliability of individual questions, scales, and domains were evaluated in 40 subjects by test-retest and intraclass correlation coefficients and internal consistency by Cronbach's alpha. Construct validity was evaluated by disease state. The relationships between domains and scales were modeled by confirmatory factor analysis. RESULTS: Mean kappa (79 questions) and intraclass correlation (18 health scales) coefficients were 0.58+/-0.16 (mean+/-SD) and 0.82+/-0.07, respectively. Internal consistency was greater than 0.8 in all but 3 scales. Construct validity was confirmed. Patients with hip fracture recorded lower OPAQ scores than patients with vertebral fracture. Correlation and confirmatory factor analyses grouped the 18 health scales into 7 domains. CONCLUSION: These findings suggest that OPAQ is a reliable, consistent, and valid instrument capable of distinguishing hierarchy of functional loss in disease states in osteoporosis.

Aged↗
PubMed2002

Meta-analyses of therapies for postmenopausal osteoporosis. IV. Meta-analysis of raloxifene for the prevention and treatment of postmenopausal osteoporosis.

OBJECTIVE: To review the effect of raloxifene on bone density and fractures in postmenopausal women. DATA SOURCE: We searched MEDLINE from 1966 to 2000 and examined citations of relevant articles and the proceedings of international osteoporosis meetings. STUDY SELECTION: We included seven trials that randomized women to raloxifene or placebo, with both groups receiving similar calcium and vitamin D supplementation, and measured bone density for at least one year. DATA EXTRACTION: For each trial, three independent reviewers abstracted the data and assessed the methodological quality using a validated tool. DATA SYNTHESIS: Data from one large dominating trial suggest a reduction in vertebral fractures with a relative risk (RR) of 0.60 [95% confidence interval (CI) 0.50-0.70, P < 0.01]. The RR of nonvertebral fractures in patients given 60 mg or more of raloxifene in the larger study was 0.92 (95% CI 0.79-1.07, P = 0.27). Raloxifene resulted in positive effects on the percentage change in bone density, which increased over time and was independent of dose. At the final year, point estimates and 95% CIs for the differences in percent change in bone density (95% CI) between raloxifene and placebo groups were 1.33 (95% CI 0.37-2.30) for total body, 2.51 (95% CI 2.21-2.82) for lumbar spine, 2.05 (95% CI 0.71-3.39) for combined forearm, and 2.11 (95% CI 1.68-2.53) for combined hip (P < 0.01 at all four sites). Results were similar across studies, and formal tests of heterogeneity did not approach conventional statistical significance. Raloxifene slightly increased rates of withdrawal from therapy as a result of adverse effects (RR 1.15, 95% CI 1.00-1.33, P = 0.05). The pooled RR was significant for hot flashes 1.46 (95% CI 1.23-1.74, P < 0.01) and nonsignificant for leg cramps 1.64 (95% CI 0.84-3.20, P = 0.15). CONCLUSION: Raloxifene increases bone density, and the effect increases over 2 yr. The data suggest a positive impact of raloxifene on vertebral fractures. There was little effect of raloxifene on nonvertebral fractures.

Female↗
PubMed2002

Meta-analyses of therapies for postmenopausal osteoporosis. V. Meta-analysis of the efficacy of hormone replacement therapy in treating and preventing osteoporosis in postmenopausal women.

OBJECTIVE: To review the effect of hormone replacement therapy (HRT) on bone density and fractures in postmenopausal women. DATA SOURCE: We searched MEDLINE and EMBASE from 1966 to 1999, the Cochrane Controlled Register, citations of relevant articles, and proceedings of international meetings for eligible randomized controlled trials. We contacted osteoporosis investigators to identify additional studies, and primary authors for unpublished data. STUDY SELECTION: We included 57 studies that randomized postmenopausal women to HRT or a control (placebo or calcium/vitamin D) and were of at least 1 yr in duration. Seven of these studies reported fractures. DATA ABSTRACTION: For each study, three independent reviewers assessed the methodological quality and abstracted the data. DATA SYNTHESIS: HRT showed a trend toward reduced incidence of vertebral fractures [relative risk (RR) 0.66, 95% confidence interval (CI) 0.41-1.07; 5 trials] and nonvertebral fractures (RR 0.87, 95% CI 0.71-1.08; 6 trials). HRT had a consistent effect on bone mineral density (BMD) at all sites. The difference between HRT and control in the percent change in bone density at 2 yr was 6.76 (5.83, 7.89; 21 trials) at the lumbar spine and 4.53 (3.68, 5.36; 14 trials) and 4.12 (3.45, 4.80; 9 trials) at the forearm and femoral neck, respectively. CONCLUSIONS: HRT has a consistent, favorable and large effect on bone density at all sites. The data show a nonsignificant trend toward a reduced incidence in vertebral and nonvertebral fractures.

Estrogen Replacement Therapy↗
PubMed2002

Meta-analyses of therapies for postmenopausal osteoporosis. VII. Meta-analysis of calcium supplementation for the prevention of postmenopausal osteoporosis.

OBJECTIVE: To summarize controlled trials examining the effect of calcium on bone density and fractures in postmenopausal women. DATA SOURCE: We searched MEDLINE and EMBASE up to 1998 and the Cochrane Controlled Register up to 2000, and we examined citations of relevant articles and proceedings of international meetings. We contacted osteoporosis investigators to identify additional studies, and primary authors for unpublished data. STUDY SELECTION: We included 15 trials (1806 patients) that randomized postmenopausal women to calcium supplementation or usual calcium intake in the diet and reported bone mineral density of the total body, vertebral spine, hip, or forearm, or recorded the number of fractures, and followed patients for at least 1 yr. DATA EXTRACTION: For each trial, three independent reviewers assessed the methodological quality and extracted data. DATA SYNTHESIS: We found calcium to be more effective than placebo in reducing rates of bone loss after two or more years of treatment. The pooled difference in percentage change from baseline was 2.05% [95% confidence interval (CI) 0.24-3.86] for total body bone density, 1.66% (95% CI 0.92-2.39) for the lumbar spine, 1.64% (95% CI 0.70-2.57) for the hip, and 1.91% (95% CI 0.33-3.50) for the distal radius. The relative risk (RR) of fractures of the vertebrae was 0.77, with a wide CI (95% CI 0.54-1.09); the RR for nonvertebral fractures was 0.86 (95% CI 0.43-1.72). CONCLUSIONS: Calcium supplementation alone has a small positive effect on bone density. The data show a trend toward reduction in vertebral fractures, but do not meaningfully address the possible effect of calcium on reducing the incidence of nonvertebral fractures.

Calcium↗
PubMed2002

Meta-analyses of therapies for postmenopausal osteoporosis. VIII: Meta-analysis of the efficacy of vitamin D treatment in preventing osteoporosis in postmenopausal women.

OBJECTIVE: To review the effect of vitamin D on bone density and fractures in postmenopausal women. DATA SOURCE: We searched MEDLINE and EMBASE from 1966 to 1999 and examined citations of relevant articles and proceedings of international meetings. We contacted osteoporosis investigators and primary authors to identify additional studies and to obtain unpublished data. STUDY SELECTION: We included 25 trials that randomized women to standard or hydroxylated vitamin D with or without calcium supplementation or a control and measured bone density or fracture incidence for at least 1 yr. DATA EXTRACTION: For each trial, three independent reviewers assessed the methodological quality and abstracted data. DATA SYNTHESIS: Vitamin D reduced the incidence of vertebral fractures [relative risk (RR) 0.63, 95% confidence interval (CI) 0.45-0.88, P < 0.01) and showed a trend toward reduced incidence of nonvertebral fractures (RR 0.77, 95% CI 0.57-1.04, P = 0.09). Most patients in the trials that evaluated vertebral fractures received hydroxylated vitamin D, and most patients in the trials that evaluated nonvertebral fractures received standard vitamin D. Hydroxylated vitamin D had a consistently larger impact on bone density than did standard vitamin D. For instance, total body differences in percentage change between hydroxylated vitamin D and control were 2.06 (0.72, 3.40) and 0.40 (-0.25, 1.06) for standard vitamin D. At the lumbar spine and forearm sites, hydroxylated vitamin D doses above 50 microg yield larger effects than lower doses. Vitamin D resulted in an increased risk of discontinuing medication in comparison to control as a result of either symptomatic adverse effects or abnormal laboratory results (RR 1.37, 95% CI 1.01-1.88), an effect that was similar in trials of standard and hydroxylated vitamin D. CONCLUSIONS: Vitamin D decreases vertebral fractures and may decrease nonvertebral fractures. The available data are uninformative regarding the relative effects of standard and hydroxylated vitamin D.

Female↗
PubMed1999

The contribution of vitamin D receptor gene polymorphisms in osteoporosis and familial osteoporosis.

It is well established that genetic factors play a major role in the pathogenesis of osteoporosis. Previous reports have suggested that vitamin D receptor (VDR) gene polymorphisms, particularly the BB, tt and AA genotypes, are associated with low bone mineral density (BMD). If these VDR genotypes are indeed an important determinant of BMD, then a population of related osteoporotic individuals (mother-daughter or sister-sister relationship) should have a high prevalence of the BB, tt or AA VDR genotypes. To test this hypothesis we determined the VDR genotypes in 26 osteoporotic persons (age 44.3 +/- 12.7 years, mean +/- SD) belonging to 12 families. Furthermore, for comparison with existing studies, we applied the VDR genotype analysis in a population of 53 unrelated healthy subjects (age 45.2 +/- 9.8 years, mean +/- SD) and 59 unrelated osteoporotic subjects (age 52.1 +/- 9.0 years, mean +/- SD). The menopausal status of the healthy and osteoporotic populations was pre-, peri- and mostly early postmenopausal. The proportions of the three genotypes, BB, tt and AA, within the 12 osteoporotic families were 15%, 12% and 27%, respectively, whereas the proportions of the other three homozygous genotypes (bb, TT, aa) were 50%, 50% and 23%. The distribution of the BB, tt and AA genotypes in the normal population was 21%, 21% and 36%, respectively (vs bb, TT, aa: 36%, 38%, 21%), whereas in the osteoporotic population it was 24%, 20% and 34% (vs bb, TT, aa: 27%, 34%, 14%). Our data indicate that there is not a statistically significant (p>0.05) difference in the VDR genotype frequencies within osteoporotic families as compared with the same genotypes in the population of unrelated normal or osteoporotic subjects. VDR genotype analysis showed no significant relation between VDR polymorphisms and BMD or Z-score values at the lumbar spine. This study demonstrates the lack of a heritability pattern between the BB, tt and AA genotypes and low BMD.

Adult↗
PubMed1998

A unitary model for involutional osteoporosis: estrogen deficiency causes both type I and type II osteoporosis in postmenopausal women and contributes to bone loss in aging men.

We propose here a new unitary model for the pathophysiology of involutional osteoporosis that identifies estrogen (E) deficiency as the cause of both the early, accelerated and the late, slow phases of bone loss in postmenopausal women and as a contributing cause of the continuous phase of bone loss in aging men. The accelerated phase in women is most apparent during the first decade after menopause, involves disproportionate loss of cancellous bone, and is mediated mainly by loss of the direct restraining effects of E on bone cell function. The ensuing slow phase continues throughout life in women, involves proportionate losses of cancellous and cortical bone, and is associated with progressive secondary hyperparathyroidism. This phase is mediated mainly by loss of E action on extraskeletal calcium homeostasis which results in net calcium wasting and increases in the level of dietary calcium intake required to maintain bone balance. Because elderly men have low circulating levels of both bioavailable E and bioavailable testosterone (T) and because recent data suggest that E is at least as important as T in determining bone mass in aging men, E deficiency may also contribute substantially to the continuous bone loss of aging men. In both genders, E deficiency increases bone resorption and may also impair a compensatory increase in bone formation. For the most part, this unitary model is well supported by observational and experimental data and provides plausible explanations to traditional objections to a unitary hypothesis.

Aged↗