Rise In Bone Mineral Density Research Articles

Associations between life's essential 8 and femoral neck bone mineral density among adults: A national population-based study.

Osteoporosis represents a significant public health issue, impacting both health outcomes and economic costs. This research investigates how cardiovascular health, as indicated by the LE8 score, correlates with bone mineral density (BMD). Data from the National Health and Nutrition Examination Survey (NHANES) spanning 2011 to 2018 were analyzed in this cross-sectional analysis, including 9018 subjects following the exclusion of individuals lacking BMD or LE8 data. The LE8 score, comprising factors such as diet, physical activity, smoking status, sleep quality, body mass index, lipid profiles, blood glucose, and blood pressure, was used to evaluate cardiovascular health. BMD was determined through dual-energy X-ray absorptiometry (DXA). Relationships between the LE8 scores and BMD at the femoral neck were assessed using linear regression and smooth curve fitting techniques. Enhanced LE8 scores were linked to improved BMD at the femoral neck. Notably, a 10-point increment in the LE8 score was associated with a rise in BMD by 0.04 g/cm² [β = 0.04, 95% CI: 0.03-0.05]. The data indicate a strong positive association between cardiovascular health, as measured by LE8, and BMD. These results support the development of holistic health strategies that promote cardiovascular health to potentially improve bone density.

Vertebral fractures, trabecular bone score and their determinants in chronic hypoparathyroidism.

Patients with hypoparathyroidism are at risk of vertebral fractures (VFs) despite high bone mineral density (BMD). We investigated this paradox by assessing trabecular bone score (TBS) and hip structural analysis (HSA) in non-surgical chronic hypoparathyroidism (cHypoPT) with and without VFs. 152 cHypoPT patients (age 40.2 ± 13.4years, M: F = 81:71) with a median follow-up of 8 (2-13) years were assessed for BMD, VFs, TBS, and HSA and compared with 152 healthy controls. VFs at T7-L4 were assessed by Genant's method. Average serum total calcium and phosphorus during follow-up were assessed. The lumbar spine and hip BMD were higher by 25.4 and 13.4% in cHypoPT than controls (P < 0.001). Paradoxically, VFs (30.9 vs.7.9%), including multiple (12.5 vs. 2.6%) were higher in cHypoPT (P < 0.001). Though overall average TBS (1.411 ± 0.091) was normal in cHypoPT, 25.4% of the females had subnormal TBS, more in post than pre-menopausal women (52.3 vs. 14%, P = 0.002) and as compared to males (6.1%, P = 0.001). TBS correlated with menopausal status and follow-up serum calcium-phosphorus product. For every gm/cm2 rise in BMD, TBS increase was only 0.227 in cHypoPT compared to 0.513 in controls. Frequency of VFs increased with declining TBS (P = 0.004). HSA was comparable between cHypoPT with and without VFs. 23.4% of cHypoPT with VFs had subnormal TBS. 31% of cHypoPT patients had VFs. TBS indicated degraded bone microarchitecture in 50% of the post-menopausal cHypoPT women. However, TBS has limitations to detect abnormal bone microarchitecture in cHypoPT as only one-fourth of patients with VFs showed low TBS.

Male Hypogonadism And Osteoporosis: A Systematic Review

Background: Male hypogonadism can be defined as a disorder caused by decreased testosterone levels leading to low sperm count, multiorgan dysfunction and inadequate quality of life. Osteoporosis is defined as a debilitating condition which causes loss of bone mass and structure leading to considerable risk of fragility fracture and increased mortality. About 6% of men and 21% women between ages 50 to 84 years suffer from osteoporosis, changing the lives of 27.6 million males and females in the European Union (EU) in 2010. Osteoporosis is responsible for&gt;8.9 million fractures yearly around the world, about 1000 cases an hour. The prevalence of osteoporosis increases as the population advances in age. Fracture risk increases in those with reduced bone mineral density(BMD) than those with osteoporosis.Although the risk of osteoporotic fracture is less in men than women however men are twice at risk of dying from the consequences of such fractures than women. World Health Organization (WHO) defined osteoporosis as a BMD of 2.5 standard deviation (SD) or more below the mean in young healthy female, with a T score of-2.5 or lower. The American college of physicians recommend early evaluation of men&lt;65 years old who are at high risk of osteoporosis using Dual energy x-ray absorptiometry (DXA) scan. Objective: The aim of this review is to conduct a systematic review of available literature to evaluate epidemiology and risk factors for osteoporosis in men. The focus of this work was to critically review evidence related to impact of hypogonadism on bone health in men. Methods: A thorough search of different electronic databases was done including PubMed, google scholar, Cochrane database and FINDIT in the university of South Wales library and data collected. Results: Some studies reported that only 4.5% men were treated for osteoporosis compared to 27% women. The annual death rate was 32% in men and 17% in women. In 1-5 years follow up, only 27% men were on any form of therapy while 71% women were on treatment. A study of 241 men who received 10mg of alendronate daily for 2 years compared to placebo showed a notable rise in BMD, and a notable decrease in fracture of the vertebra was documented with OR of 0.10, CI; 95%; 0.00-0.88. A study of 284 men treated with risedronate showed successful increase in BMD in contrast to placebo. Obesity is one of the most common causes of male hypogonadism, usually associated with normal or reduced follicle stimulating hormone (FSH), luteinizing hormone (LH) and low testosterone levels. Conclusion: The burden of osteoporosis is severe and is shown in the increased level of disability and death in the affected patients and yet only a small number of men are given adequate treatment. Recognition and treatment of male hypogonadism and osteoporosis has received some attention lately, however, it remains under detected and under treated, much needs to be done in investigating for hypogonadism in men with fragility fractures.

Effect of immobilization, off-loading and zoledronic acid on bone mineral density in patients with acute Charcot neuroarthropathy: A prospective randomized trial

Bisphosphonates are commonly used as an adjuvant in the management of acute Charcot neuroarthropathy (CNA), although the clinical efficacy of the treatment is controversial. The aim of the present study is to investigate the effect of immobilization and zoledronic acid on bone mineral density (BMD) changes during the treatment of acute CNA. Thirty-five patients with acute midfoot CNA were randomly assigned to treatment with either zolendronic acid or placebo. BMD of the lumbar spine and both hips was measured at baseline and after six months of treatment. Comparison between BMD at presentation and at 6 months demonstrated a significant fall in BMD in the placebo group at the CNA-affected femoral neck (-3.2%, p=0.016) and in the CNA-free hip (-1.2%, p=0.026). Conversely, a significant rise in BMD was observed in the zolendronic acid group at all measured areas of the CNA-free hip. Immobilization and off-loading does not lead to marked disuse osteoporosis in patients with acute CNA after 6 months of treatment. Treatment with zoledronic acid led to a statistically significant increase in hip BMD compared to placebo.

Study of bone mineral density in patients with ankylosing spondylitis.

Ankylosing spondylitis (AS) is an inflammatory rheumatic disease characterized by spine and sacroiliac joint involvement that mainly affects young male subjects. Bone Mineral Density (BMD) loss occurs in AS disease course. Bone loss in AS appears to be multifactorial and perhaps involves different mechanisms at different stages of disease. The disease typically affects young males and is associated with progressive functional impairment, increased work disability and decreased quality of life. Osteoporosis is frequent in AS and there is a close association of bone mineral density, bone metabolism and inflammatory activity. Osteoporosis is frequently associated with AS and BMD decreased predominantly in patients with active disease. The aim of the present study was to study bone mineral density in cases of Ankylosing Spondylitis (AS) in comparison to age and sex matched controls. The present study was conducted on 100 established cases of AS based on modified New York criteria and 150 controls healthy, age, race, socio-economic matched controls patients. The results were statistically analyzed. Hundred cases of AS were subjected to undergo BMD by Dual Energy X-ray Absorption (DEXA) scan of different age groups in cases 35.19± 8.23(min age 23- max age 67years) and controls 33.27±5.22(min age 22years - max age 44years) with height observed in cases is 169.67±6-87 and controls 170.99±7.16 with weight varied in cases 65.63±10.27 and controls 70.14±10.67. Osteoporosis is a significant complication in ankylosing spondylitis and needs to be monitored and managed at the earliest. Significant osteoporosis can occur even in early disease. Osteoporosis of spine is much more prevalent than femur.BMD spine is still the most important site to define osteoporosis in ankylosing spondylitis. Rise in BMD in LS spine with duration, is not exclusive for subjects with radiologically evident syndesmophytes. Statistically, presence of syndesmophytes did not affect estimation of osteoporosis of spine.

Changes in bone mineral density (BMD) around the cemented Exeter stem: A prospective study in 18 women with 5 years follow‐up

Background and purpose THA changes the pattern of strain distribution in the proximal femur. We quantified the changes in BMD for 5 years after insertion of the cemented Exeter stem in women.Methods 18 women aged 55–79 years, undergoing unilateral THA with the cemented Exeter stem, were included in the study. The BMD was measured in 7 femoral regions of interest according to Gruen, and the contralateral hip and spine using dual‐energy X‐ray absorptiometry postoperatively, at 18 and at 60 months of follow‐up. Results were tested using Wilcoxon matched‐pairs signed‐rank test.Results During the first 18 months, a significant decrease in BMD was seen in zones 2, 3, 6, and 7. No significant changes were seen in zones 4 and 5, in the contralateral hip, or at the spine. In zone 1, there was a small but significant rise in BMD. From 18 to 60 months, we observed a statistically significant rise in BMD in all zones except 4 and 7. Despite this, the total periprosthetic BMD decreased during the follow‐up relative to the immediate postoperative situation. There was no significant reduction in BMD in the contralateral hip. In the spine, we observed a significant rise in BMD.Interpretation 18 months after THA, BMD had decreased in Gruen zones 2, 3, 6, and 7. The bone loss was similar to that seen after other implants and appears to be related to the changes in stress pattern within the proximal femur. At 5 years, BMD had increased again in these zones. It remained lower than baseline, however.

Effect of Bisphosphonates on Bone Mineral Density After Renal Transplantation as Assessed by Bone Mineral Densitometry

Introduction Steroid-induced osteoporosis is a major problem after organ transplantation. There is considerable evidence that bisphosphonates are effective in decreasing osteoporosis. Aim This prospective study was carried out to see the effects of bisphosphonates on bone mineral density (BMD) after successful renal transplantation. Material and methods Fifty consecutive patients of successful renal transplantation were randomized into two groups. Group A ( n = 27) received 35 mg/wk of Alendronate for 6 months after transplantation. Group B ( n = 23) did not receive Alendronate and served as a control. Both groups underwent a pretransplant baseline dual-energy X-ray absorptiometry (DEXA) scan of their hips and lumber spines. Both groups received oral calcium and vitamin D supplement. Both groups were matched for the regimen and dose of immunosuppressive drugs. BMD was measured at 3 months and 6 months after transplantation. Results Both groups showed a decline in BMD in early months posttransplantation. However, the 6-month DEXA scans showed a significant rise in BMD in group A as compared to group B. Conclusion Bisphosphonates appear to have a beneficial effect on steroid-induced bone loss.

Oral bisphosphonate treatment for osteogenesis imperfecta—an Indian perspective

Various treatments for the management of osteogenesis imperfecta (OI) have been tried, of which bisphosphonates seem to have the maximum benefit in reducing fracture rate and improving bone density. This study investigated the value of oral alendronate for treating OI in Indian children. Between 2002 and 2005, 11 patients with OI were referred for bisphosphonate therapy. The various types of OI were classified using the Sillence criteria. All patients underwent baseline biochemistry, radiographic studies and bone mineral density (BMD) measurements before commencing therapy. Patients were commenced on oral alendronate (0.5 mg/kg/day) and followed up for a period ranging from 1 month to 2 years. A retrospective analysis of pre- and post-treatment changes in fracture rate and bone density was undertaken using the paired sample t-test. One patient lost to follow-up was excluded from the study and three completed only 2 months of therapy. Pre-treatment fracture rate per year before treatment ranged from 0.5 to 6 with a mean (SD) of 2.95 (1.57) and median of 2.5. The post-treatment fracture rate was 1.1 (0.59)/year (p=0.02). Seven children underwent BMD analysis while on treatment and all had a rise in BMD, of which the change in lumbar spine BMD was statistically significant (p=0.001), and lumbar (p=0.005) and femoral neck t-score (p=0.04) showed a significant change. No significant change was seen in serum biochemistry except for disappearance ofhypercalciuria (p=0.04). No child had an adverse reaction to alendronate. After a median of 9.5 months of treatment, oral alendronate is associated with a lower fracture rate, improvement in BMD and a decrease in hypercalciuria.

Bisphosphonates Are Effective Prophylactic of Early Bone Loss After Renal Transplantation

Introduction Rapid bone loss and fractures occur early after solid organ transplantation. We examined the preliminary results of a prospective study evaluating the efficacy of prophylactic use of bisphosphonates in renal allograft recipients. Methods Bone mineral density (BMD) was measured at the lumbar spine and the hip by dual energy X-ray absorptiometry at 1, 6, 12 months. Alendronian or risedronian were initiated for patients with osteopenia or osteoporosis at 1 month who had no contraindications to bisphosphonates. The treatment lasted at least 6 months. Sixty-six patients were included in the study; 39 were treated with bisphosphonates (A), and 27 were drug-free (B). Presently, 24 group A and 13 group B patients have completed the 12-month observation period. Results In group A 53.8% (21) subjects had osteoporosis and 46.2% (18), osteopenia. Mean T-score L 2–L 4 in group A at 1, 6, and 12 months were: (−)2.22 ± 1.06; (−)2.07 ± 1.25; (−)1.89 ± 1.07, respectively. The T-score increase between 6 and 12 months was significant ( P = 0.0014). The relative rise in BMD L 2–L 4 between 1 and 12 months was 2.26%. In group B mean T-score L 2–L 4 at 1, 6, and 12 months were: (−)0.26 ± 1.34; (−)0.80 ± 1.19; (−)1.2 ± 1.59, respectively. The T-score decrease between 1 and 12 months in group B was significant ( P = .0082). The 12-month relative decrease in femoral neck and trochanter BMD in group B was (−)2.1% and (−)2.75%, respectively. Conclusion Bisphosphonates are effective for prophylaxis of rapid bone loss early after renal transplantation.

Restoration of the coupling process and normalization of bone mass following successful treatment of endogenous Cushing’s syndrome: A prospective, long-term study

Endogenous Cushing's syndrome (CS) is associated with bone loss and an increased risk of fractures. However, the long-term outcome of treatment on bone health has not been adequately clarified. We followed 33 patients with active CS prospectively before and twice after treatment (mean follow-up 33 (n = 25) and 71 months (n = 18), respectively). The patients were compared to age-, sex- and body mass index (BMI)-matched controls, also followed longitudinally. Bone mineral indices (bone mineral density (BMD), bone mineral content (BMC) and bone area) were evaluated in the lumbar spine (LS), femoral neck (FN), and total body (TB) by dual-energy X-ray absorptiometry (DXA). Biochemical markers of bone turnover were assessed by serum levels of osteocalcin and C-terminal telopeptides of Type-1 collagen (CTX-1). Mann-Whitney rank sum tests showed that BMD of the LS, FN and TB was reduced by 14.8% (P < 0.001), 15.7% (P < 0.001), and 9.2% (P < 0.001) in CS vs. controls at baseline, with markedly reduced serum osteocalcin (P = 0.014) and increased CTX-1 (P = 0.012) levels, but no correlation between markers. At first follow-up, BMD was increased in LS (7.9%, P < 0.001) and FN (3.5%, P = 0.003) compared to baseline. The time-dependent rise in BMD (LS (r = 0.59; P = 0.002) and FN (r = 0.52; P = 0.007); Spearman's rank correlation), in CS was paralleled by increased osteocalcin (275%, P < 0.001) and correlation between biochemical markers (r = 0.92, P < 0.001; Pearson's correlation). TB BMD did not increase significantly before the second follow-up, when BMD Z-scores were normalized in all three compartments. Our observations demonstrate restoration of coupled bone remodeling and normalization of bone mineral density in all measured skeletal compartments of treated CS patients after prolonged recovery, first significant in predominantly trabecular bone (i.e. lumbar spine).

Bisphosphonate mechanism of action.

Nitrogen-containing bisphosphonates (N-BPs) are potent inhibitors of bone resorption widely used in the treatment of osteoporosis and other bone degrading disorders. At the tissue level, N-BPs reduce bone turnover, increase bone mass and mineralization, measured clinically as a rise in bone mineral density, increase bone strength and reduce fracture risk. At the cellular level, N-BPs, localize preferentially at sites of bone resorption, where mineral is exposed, are taken up by ostoclasts and inhibit osteoclast activity. The bone formation that follows incroporates the N-BP in the matrix, where it becomes pharmacologically inactive until released at a future time during bone remodeling. At the molecular level, N-BPs inhibit an enzyme in the cholesterol synthesis pathway, farnesyl diphosphate synthase. As a result, there is a reduction in the lipid geranylgeranyl diphosphate, which prenylates GTPases required for cytoskeletal organization and vesicular traffic in the osteoclast, leading to osteoclast inactivation.

Prevention of Bone Loss With Tibolone in Postmenopausal Women: Results of Two Randomized, Double-Blind, Placebo-Controlled, Dose-Finding Studies

Tibolone is a synthetic agent with tissue-specific effects, including an antiresorptive effect on bone. Clinical trials have documented prevention of bone loss in postmenopausal women; a daily oral dose of 2.5 mg has generally been used. The present study evaluated tibolone therapy over 2 years with daily doses of 0.3, 0.625, 1.25, or 2.5 mg of tibolone as compared with placebo in 770 generally healthy women who were 1 to 4 years past menopause and who had normal bone density for their age. All of them took supplemental calcium carbonate as well in a daily dose of 500 mg. Bone mineral density (BMD) was measured in the lumbar spine and right proximal femur by dual-energy x-ray absorptiometry for up to 2 years. The patient population was drawn from two identically designed randomized, placebo-controlled, dose-finding studies. A total of 519 women completed the 2-year studies. Tibolone led to a progressive increase in spinal and total hip BMD over 2 years of treatment in all doses except 0.3 mg. Hip BMD was maintained by the 0.3-mg dose. Only doses of 1.25 or 2.5 mg daily progressively increased BMD at the femoral neck. Differences in mean percentage of change from baseline in spinal and total hip BMD were significant for all dose groups compared with placebo. The rise in BMD at the lumbar spine over baseline, with 1.25 or 2.5 mg daily, was 2.0 to 2.6% at 2 years, a statistically significant and clinically meaningful effect. Increasing BMD was not limited to the first year of tibolone therapy. All tibolone doses except the lowest were associated with decreased serum osteocalcin levels, whereas in placebo recipients osteocalcin increased over baseline. Comparable reductions in bone-specific alkaline phosphatase were noted in patients given 1.25 and 2.5 mg of tibolone. Total cholesterol levels decreased in all tibolone dose groups, but declines in high-density lipoprotein cholesterol, triglycerides, and apolipoprotein A-1 seemed to be dose-related. All doses of tibolone were generally well tolerated during the 2 years of administration. No deep venous thrombosis or pulmonary embolism was observed. Hot flashes were less frequent with tibolone therapy than with placebo and were at their lowest with the 2.5-mg dose. Average body weight changes were similar in the actively treated and placebo groups. Endometrial hyperplasia was comparably frequent in the two groups. Vaginal bleeding became less prevalent with continued tibolone treatment. A 1.25-mg daily dose of tibolone is recommended for preventing osteoporosis. The ability of this drug to dose-dependently increase BMD in the lumbar spine and total hip should allow individualized antiresorptive treatment for postmenopausal women according to their clinical response.

Changes in bone density during childhood and adolescence: an approach based on bone's biological organization.

Bone densitometry has great potential to improve our understanding of bone development. However, densitometric data in children rarely are interpreted in light of the biological processes they reflect. To strengthen the link between bone densitometry and the physiology of bone development, we review the literature on physiological mechanisms and structural changes determining bone mineral density (BMD). BMD (defined as mass of mineral per unit volume) is analyzed in three levels: in bone material (BMD(material)), in a bone's trabecular and cortical tissue compartments (BMD(compartment)), and in the entire bone (BMD(total)). BMD(material) of the femoral midshaft cortex decreases after birth to a nadir in the first year of life and thereafter increases. In iliac trabecular bone, BMD(material) also increases from infancy to adulthood, reflecting the decrease in bone turnover. BMD(material) cannot be determined with current noninvasive techniques because of insufficient spatial resolution. BM(compartment) of the femoral midshaft cortex decreases in the first months after birth followed by a rapid increase during the next 2 years and slower changes thereafter, reflecting changes in both relative bone volume and BMD(material). Trabecular BMD(compartment) increases in vertebral bodies but not at the distal radius. Quantitative computed tomography (QCT) allows for the determination of both trabecular and cortical BMD(compartment), whereas projectional techniques such as dual-energy X-ray absorptiometry (DXA) can be used only to assess cortical BMD(compartment) of long bone diaphyses. BMD(total) of long bones decreases by about 30% in the first months after birth, reflecting a redistribution of bone tissue from the endocortical to the periosteal surface. In children of school age and in adolescents, changes in BMD(total) are site-specific. There is a marked rise in BMD(total) at locations where relative cortical area increases (metacarpal bones, phalanges, and forearm), but little change at the femoral neck and midshaft. BMD(total) can be measured by QCT at any site of the skeleton, regardless of bone shape. DXA allows the estimation of BMD(total) at skeletal sites, which have an approximately circular cross-section. The system presented here may help to interpret densitometric results in growing subjects on a physiological basis.

Statement on the diagnosis and management of osteoporosis from the Consensus Development Conference at the Second International Conference on Osteoporosis, Osaka 1997

Osteoporosis is an established and well-defined "disease" that affects more than 75 million people in the United States, Europe, and Japan. It is a major health problem resulting in progressive health deterioration, morbidity, and escalating annual health care costs. A panel of specialists met in Nara, Japan, to review current knowledge in certain areas of osteoporosis and to document it in a form that may be helpful to practitioners. The focus was on providing general information, rather than specific advice. This statement is based on the combined experience of the members of the panel, on the papers and posters presented at the Second International Conference on Osteoporosis in Osaka November 13–16, 1997, and, in particular, on the presentations by invited experts at the Consensus Development Conference that followed in Nara. A draft of the statement was prepared before the meeting, based on contributions by the panel. After the meeting, the statement was rewritten by Drs. Morii and Genant to incorporate the conclusions of the panel, and it was then reviewed by the panel. The pathophysiology of osteoporosis is multifactorial; there is no single cause but there are many risk factors. Bone mineral density is one component of fracture risk that can be measured with reasonable accuracy and precision. It generally forms the basis for the diagnosis of osteoporosis. The accuracy of bone mineral density (BMD) measurements in predicting fracture is as good as blood pressure in predicting stroke. The main risk factors are calcium and protein deficiency, low levels of estrogen or androgen, low body mass, lack of weight-bearing exercise, immobilization, and the use of corticosteroid hormones, thyroid hormones, parathyroid hormones, alcohol, tobacco, diuretics, or anticoagulants. The risk of fracture in patients with osteoporosis can be greatly reduced with a variety of approved treatments of established safety and efficacy that prevent bone loss and that may produce some rise in BMD, although the long-term bone gain remains uncertain. The major disability produced by hip or vertebral fracture makes prevention the first priority.

Assessment of Bone Mineral Density before and after Exercise Training in Postmenopausal Women.

Bone mineral density (BMD) of lumbar spine (vertebrae 3, 4, and 5) as well as parathormone and estradiol (E2) levels were studied in two groups of postmenopausal women. The first group A, included 25 subjects who participated in exercise training. The second group B, comprised 15 subjects who did not participate in training. In group A, a significant rise in BMD, a significant decrease in parathormone level and no significant changes in E2 level were observed 6 months after the exercise training. In group B, no significant changes in parathormone level or BMD but a significant decrease in E2, were observed 6 months after starting the study.

Adult growth hormone deficiency and bone mass.

Bone mineral density (BMD) is reduced in adults with growth hormone (GH) deficiency and the decrease in BMD appears more marked if the GH deficiency is childhood onset rather than adult onset. Recent epidemiological studies suggest an increased fracture rate in GH-deficient adults. The skeletal response to GH therapy depends on the variety of GH deficiency, the type of bone studied and the duration of therapy. In the childhood-onset, GH-deficient adult there is either no change or a reduction in cortical and integral bone mass over the first 6 months, whereas at 6 months there is an increase in vertebral trabecular BMD. Subsequently there is a steady rise in BMD at all sites over the next 12-18 months. In the adult-onset, GH-deficient adult, the long-term results are more contentious. It is too early to determine whether GH therapy modifies fracture risk.

The use of bisphosphonates in the treatment of osteoporosis

Three therapeutic protocols using 3 different bisphosphonate molecules have been evaluated in three groups of women in physiological menopause, whose bone mineral density (BMD) at the ultradistal (UD) or mediodistal (MD) radius showed risk of fracture. Treatment with alendronate (5 mg/day, for 12 months) increases BMD (38 patients, mean age 63 +/- 6 years) by about 5%; treatment with ethidronate (400 mg/day form days, then 1.250 mg/day calcium carbonate for 76 days), repeated 4-times (31 patients, mean age 66 +/- 6 years) did not cause any significant rise in BMD of either UD or MD radius; treatment with clodronate (10 mg/day i.m. for 20 days, a 10-day-interval, followed by 400 mg/day for 60 days) resulted in an insignificant increase (about 4%) in the BMDUD value (8 patients, mean age 62 +/- 5 years). No vertebral fractures nor deformations were observed in any of the 3 groups during treatments. All groups showed an optimal tolerance to the drugs.

The effect of vertebral collapse on spinal bone mineral density measurements in osteoporosis

Bone mineral density (BMD) of the lumbar spine (L1-L4) was measured using dual-energy x-ray absorptiometry (DXA) in 57 postmenopausal women with spinal osteoporosis aged 50-82 years (average age 64). For each vertebra between L1 and L4, the BMD was compared to age-matched normal population values and a Z score obtained. Twenty three patients had between one and three collapsed vertebrae from L1 to L4. The average Z score for fractured vertebrae was -1.62 but for uncollapsed vertebrae was -2.26 (P less than 0.001). The difference in Z scores obtained for collapsed and uncollapsed vertebrae was greater where only one fracture was present (0.803) compared to two (0.577) or three fractures (0.245). The average increase in density for a fractures vertebra was 0.070 g/cm2. For L1 vertebral fractures alone the average increase in BMD was 0.096 g/cm2, L2 vertebral fractures 0.041 g/cm2, L3 fractures 0.029 g/cm2 and L4 fractures 0.062 g/cm2. It is concluded that as vertebral collapse is not alway detected using DXA and usually causes a rise in BMD, spinal x-rays are necessary to avoid misinterpretation of a falsely elevated BMD in osteoporotic patients, particularly in longitudinal studies or when monitoring therapy, where small changes in BMD are important.