Osteoporosis: Sambrook PN

Sambrook PN. · Kolling Institute, Royal North Shore Hospital, University of Sydney, Sydney, Australia. · Nat Clin Pract Rheumatol. · Pubmed #19030005 No free full text.

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Sambrook PN, Diamond T, Ferris L, Fiatarone-Singh M, Flicker L, MacLennan A, Nowson C, O'Neill S, Greville H, Anonymous00086, Anonymous00087. · University of Sydney. · Aust Fam Physician. · Pubmed #11681155 No free full text.

Abstract: BACKGROUND: Last year, Australian Family Physician published 'Guidelines for Management of Postmenopausal Osteoporosis', which were developed by Osteoporosis Australia. Recently, significant advances in our understanding of the treatment of corticosteroid osteoporosis have occurred. OBJECTIVE: The following guidelines, also developed by Osteoporosis Australia, and supported by the National Asthma Campaign, are to help general practitioners identify those patients at risk of this problem and to provide information about current treatment strategies. DISCUSSION: Corticosteroids are widely used and effective agents for the control of many inflammatory diseases. Corticosteroid osteoporosis is a common problem associated with the long term high dose use of these medications.

Sambrook PN. · No affiliation provided · N Engl J Med. · Pubmed #18003966 No free full text.

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Sambrook PN. · No affiliation provided · J Rheumatol. · Pubmed #11093430 No free full text.

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Sambrook PN, Ebeling P. · Kolling Institute of Medical Research, University of Sydney (E25), Royal North Shore Hospital, Saint Leonards NSW 2065, Sydney, Australia. · Curr Rheumatol Rep. · Pubmed #18460263 No free full text.

Abstract: Bisphosphonates are effective therapy for osteoporosis, Paget's disease, and metastatic bone disease. Generally, the side effects of bisphosphonates are minimal. Recently, an uncommon adverse reaction affecting the maxilla or mandible, called osteonecrosis of the jaw, has been reported, especially in those patients receiving high doses of bisphosphonates in the oncology setting. Regarding doses used to treat osteoporosis, clinicians must keep the very small potential absolute risk of jaw osteonecrosis in perspective and consider it in relation to the demonstrated benefit of bisphosphonates. Still, in a very small number of patients taking bisphosphonates, intractable, painful, nonhealing exposed bone may occur following dental extractions or denture irritation.

Geusens PP, Roux CH, Reid DM, Lems WF, Adami S, Adachi JD, Sambrook PN, Saag KG, Lane NE, Hochberg MC. · Department of Internal Medicine, Division of Rheumatology, University Hospital, P Debyelaan 25, Box 5800, 6202 AZ Maastricht, The Netherlands. · Nat Clin Pract Rheumatol. · Pubmed #18398411 No free full text.

Abstract: Many randomized controlled trials (RCTs) have investigated drug treatment for women at high risk of fracture, with a reduction in fracture risk as their end point. There has also been progress in identifying women at the highest risk of fractures. The most important clinical determinant contributing to the clinical decision of initiating and choosing drug therapy for fracture prevention is a woman's fracture risk, which, in RCTs, was determined by menopausal state, age, bone mineral density, fracture history, fall risks and glucocorticoid use. Women with secondary osteoporosis were excluded, except in studies of glucocorticoid use. A second determinant of drug therapy is the evidence for fracture prevention in terms of spectrum (vertebral, nonvertebral and/or hip fractures), size and speed of effect. In the absence of head-to-head RCTs with fracture risk as the end point, however, the efficacy of antifracture drugs cannot be directly compared. Other determinants include the potential extraskeletal benefits and safety concerns of the drug, patient preferences and reimbursement issues.

Sambrook PN. · Institute of Bone and Joint Research, University of Sydney, Sydney, Australia. · J Rheumatol Suppl. · Pubmed #16142850 No free full text.

Abstract: In addition to bisphosphonates, D-hormones appear to be effective agents in the prevention of post-transplant osteoporosis. In this article studies on D-hormone agents for prevention of post-transplant bone loss are reviewed. Potential reduction in immunosuppressive requirements with D-hormone is an additional consideration. Based upon available evidence, prophylaxis should involve a bisphosphonate, with D-hormone considered as adjunctive or alternative therapy.

Sambrook PN. · Royal North Shore Hospital, St Leonards, Sydney, Australia 2065. · Ann Rheum Dis. · Pubmed #15647424 links to  free full text

Abstract: The first choice for prevention of corticosteroid osteoporosis is a potent oral bisphosphonate-for example, alendronate or risedronate. Intravenous bisphosphonates should be considered for patients intolerant of the oral route. For patients receiving chronic low dose corticosteroids treatment with calcium and vitamin D may prevent further bone loss. Use of parathyroid hormone is promising.

Sambrook PN. · Institute of Bone & Joint Research, University of Sydney, Sydney, Australia. · Curr Pharm Des. · Pubmed #12171526 No free full text.

Abstract: Postmenopausal women are at greatest risk of rapid bone loss and fracture with glucocorticoids and should be actively considered for prophylactic measures. In men and premenopausal women receiving glucocorticoids, the decision to use anti-osteoporosis prophylaxis is less clear and depends upon baseline bone mineral density [BMD], anticipated dose and duration of glucocorticoids. Based upon evidence the order of choice for prophylaxis would be a bisphosphonate followed by a vitamin D metabolite or hormone replacement therapy [HRT]. Calcium alone appears unable to prevent rapid bone loss in patients starting glucocorticoids. HRT should clearly be considered if hypogonadism is present. In patients receiving chronic low dose glucocorticoids, treatment with calcium and vitamin D may be sufficient to prevent further bone loss. However since fracture risk is a function of multiple factors including the degree of reduction in BMD as well as the duration of exposure, treatment with therapy to increase BMD will reduce fracture risk even in patients receiving chronic low dose glucocorticoids.

Sambrook PN, Seeman E, Phillips SR, Ebeling PR, Anonymous00166, Anonymous00167. · No affiliation provided · Med J Aust. · Pubmed #12049064 links to  free full text

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Sambrook PN. · Institute of Bone & Joint Research, University of Sydney, Sydney, Australia. · Ann Acad Med Singapore. · Pubmed #11885496 No free full text.

Abstract: INTRODUCTION: Corticosteroids have major effects on calcium metabolism, leading to accelerated osteoporosis and fracture. METHODS: This review will attempt to summarise current knowledge about their effects in light of new information and important remaining questions, especially with respect to management of this common condition. RESULTS: Corticosteroids affect bone through multiple pathways, influencing both bone formation and bone resorption. Evidence from randomised trials suggests that postmenopausal women receiving corticosteroids are at greatest risk of rapid bone loss and consequent fracture and should be actively considered for prophylaxis. Based upon available evidence, the rank order of choice for prophylaxis would be a bisphosphonate followed by a vitamin D metabolite or hormone replacement. CONCLUSIONS: With early therapy, corticosteroid bone loss can be effectively prevented or reversed.

Hunter DJ, Sambrook PN. · Rheumatology Department, Royal North Shore Hospital, Sydney, Australia. · Arthritis Res. · Pubmed #11094456 links to  free full text

Abstract: Bone loss occurs when the cellular events of bone formation are quantitatively larger than bone formation. This manuscript discusses the measurement of bone loss, occurrence in the population, risk factors and consequences of bone loss. Recent developments in bone mass measurement and biomarkers have improved our ability to assess bone loss. This process is a normal concomitant of ageing. There are a number of other risk factors, including sex hormone deficiency, physical inactivity, calcium/vitamin D deficiency, inflammatory arthritis, corticosteroids, smoking and alcohol. The major consequence of bone loss in our ageing society is fracture.

Sambrook PN, Eisman JA. · Institute of Bone and Joint Research, University of Sydney, Royal North Shore Hospital, NSW. · Med J Aust. · Pubmed #10776395 links to  free full text

Abstract: Patients with low bone density or any prior low trauma fracture should be considered for therapeutic intervention. Oestrogen replacement therapy remains the first choice for prevention of bone loss in early postmenopausal women with low bone density. In postmenopausal women with existing fractures, the rank order of treatments is firstly alendronate, secondly raloxifene and thirdly less potent bisphosphonates, such as etidronate, or active vitamin D metabolites, such as calcitriol. For men with osteoporosis, if hypogonadism is present, it should be treated with testosterone replacement therapy. Despite limited data, a bisphosphonate should then be considered in conjunction with calcium. Supplementation with simple vitamin D should be considered in elderly patients who are housebound or live in institutions, as they are at risk of vitamin D deficiency and osteomalacia.

Sambrook PN. · Sydney University Dept. of Rheumatology, Royal North Shore Hospital, Australia. · Z Rheumatol. · Pubmed #10769436 No free full text.

Abstract: Corticosteroids are widely used in the treatment of patients with chronic inflammatory diseases. Since the most rapid bone loss occurs in the first 12-24 months after commencing high dose corticosteroids, it is important to consider two different therapeutic situations, (a) prevention in patients starting corticosteroids and (b) treatment of patients on chronic corticosteroids who will already have some significant degree of corticosteroid related bone loss. An adequate calcium intake is recommended and any contributing factors to osteoporosis should be treated. A bone density will give information about the future risk of osteoporotic fracture and the need for active pharmacological treatment. Patients commencing high dose long-term corticosteroid therapy should be treated prophylactically with a bisphosphonate and/or active vitamin D metabolites (alphacalcidol or calcitriol) and the treatment may need to be continued for 1-2 years. Patients on chronic corticosteroids may improve their bone density by treatment with bisphosphonates and vitamin D metabolites (including the calciferols). In postmenopausal women, concomitant use of estrogen replacement therapy is also appropriate. It is important in a patient on long-term therapy to review the need for continuing treatment or the possibility of dosage reduction.

Sambrook PN, Rodriguez JP, Wasnich RD, Luckey MM, Kaur A, Meng L, Lombardi A. · Institute of Bone and Joint Research, University of Sydney, Royal North Shore Hospital, St. Leonards, Level 4, Block 4, 2065 Sydney, Australia. · Osteoporos Int. · Pubmed #15205720 No free full text.

Abstract: In a 3-year study followed by a 2-year open-label extension, alendronate sodium (ALN) maintained or increased bone mineral density (BMD) in 445 recently postmenopausal women with a spine BMD T-score >-2. In a second 2-year extension, 84 women previously treated with either 5 or 10 mg ALN daily during the first 3 years and 5 mg ALN during the first extension (group A) were randomized to either 5 mg ALN or placebo (PBO). Another group of 59 women (group B) received 20 mg ALN during the first 2 years, PBO during year 3, and were then followed up without treatment during years 4-7. In group A, continuous ALN treatment for 7 years increased spine and trochanter BMD by 2.7-4.1 and 3.3-4.2%, respectively, while femoral neck BMD was maintained. Patients initially receiving 10 mg ALN maintained total body BMD, whereas those treated with 5 mg ALN experienced a small but significant loss after 7 years. Among women who received ALN 5 mg during years 4-7, those who had been treated with ALN 10 mg in the first 3 years had slightly greater increases in BMD at most sites at the end of the study, compared with women who received ALN 5 mg during the first 3 years. During years 6-7, patients who switched to PBO during the previous 2 years showed a significant loss in femoral neck BMD, whereas changes at the other sites were not significant. Women in group B showed significant loss in BMD at all skeletal sites during years 4-7, when they received no treatment. In conclusion, ALN 5 or 10 mg daily for up to 7 years prevents bone loss in recently postmenopausal women. Patients started on ALN 10 mg appear to gain more BMD than those initially treated with 5 mg ALN. Early postmenopausal women who discontinue ALN after 2 years of treatment experience significant bone loss at all skeletal sites despite the higher (20 mg) initial dosing. The ALN was generally well tolerated during 7 years of treatment.

Sambrook PN, Geusens P, Ribot C, Solimano JA, Ferrer-Barriendos J, Gaines K, Verbruggen N, Melton ME. · Institue of Bone and Joint Research, Royal North Shore Hospital, University of Sydney, St Leonards NSW, Australia. · J Intern Med. · Pubmed #15049885 No free full text.

Abstract: OBJECTIVES: Alendronate and raloxifene are antiresorptive agents with different mechanisms of action, each used to treat osteoporosis in postmenopausal women. This study was undertaken to compare the efficacy and tolerability of alendronate to raloxifene in postmenopausal women with low-bone density. DESIGN: Randomized, double-masked, double-dummy multicentre international study. SETTING: Clinical trial centres in Europe, South America and Asia-Pacific. SUBJECTS: A total of 487 postmenopausal women with low bone density, based on bone mineral density (BMD) of the lumbar spine or hip (T-score < or =-2.0). Interventions. Patients received either alendronate 70 mg once weekly and daily placebo identical to raloxifene or raloxifene 60 mg daily and weekly placebo identical to alendronate for 12 months. MAIN OUTCOME MEASURES: Evaluations included BMD of the lumbar spine and hip and markers of bone turnover at 6 and 12 months and adverse event reporting. RESULTS: Alendronate demonstrated substantially greater increases in BMD than raloxifene at both lumbar spine and hip sites at 12 months. Lumbar spine BMD increased 4.8% with alendronate vs. 2.2% with raloxifene (P < 0.001). The increase in total hip BMD was 2.3% with alendronate vs. 0.8% with raloxifene (P < 0.001). Reductions in bone turnover were significantly larger with alendronate than raloxifene. Overall tolerability was similar, however, the proportion of patients reporting vasomotor events was significantly higher with raloxifene (9.5%) than with alendronate (3.7%, P = 0.010). The proportion of patients reporting gastrointestinal events was similar between groups. CONCLUSION: In postmenopausal women with low bone density, improvements in BMD and markers of bone turnover were substantially greater during treatment with alendronate compared to raloxifene.

Sambrook PN, Hughes DR, Nelson AE, Robinson BG, Mason RS. · Institute of Bone and Joint Research, Royal North Shore Hospital, University of Sydney, Australia. · Ann Rheum Dis. · Pubmed #14644862 links to  free full text

Abstract: BACKGROUND: Glucocorticoid induced osteoporosis is a common clinical problem. OBJECTIVE: To determine the pathophysiology of glucocorticoid induced osteoarthritis at the organ level. METHODS: Iliac crest biopsy specimens were obtained from nine patients receiving prednisone treatment for rheumatoid arthritis. Osteocyte viability and histomorphometric indices were assessed. RESULTS: Compared with controls, glucocorticoid treated subjects had reduced trabecular thickness and increased erosion. The number of viable osteocytes was significantly decreased in glucocorticoid treated patients compared with controls. CONCLUSION: The impaired bone formation, increased erosion and, importantly, loss of viable osteocytes are all likely to contribute to the increased risk of fracture in these patients.

Sambrook PN, Kotowicz M, Nash P, Styles CB, Naganathan V, Henderson-Briffa KN, Eisman JA, Nicholson GC. · Institute of Bone & Joint Research, University of Sydney, Sydney, Australia. · J Bone Miner Res. · Pubmed #12733733 No free full text.

Abstract: High-dose corticosteroids, used for many medical conditions, are associated with rapid bone loss from sites such as the vertebrae, and compression fractures can be observed within months. Recent trials suggest treatment with bisphosphonates or active vitamin D analogs can reduce bone loss and the risk of fracture associated with glucocorticoids, but few studies have directly compared such agents. We conducted a randomized, multicenter, open-label trial to compare the efficacy of alendronate, calcitriol, and simple vitamin D in prevention and treatment of glucocorticoid-induced bone loss. A total of 195 subjects (134 females and 61 males) commencing or already taking glucocorticoids were randomized to one of three groups: calcitriol, 0.5 to 0.75 microg/day; simple vitamin D (ergocalciferol, 30,000 IU weekly) plus calcium carbonate (600 mg daily); or alendronate, 10 mg/day plus calcium carbonate (600 mg daily). Over 2 years, mean lumbar bone mineral density change was +5.9% with alendronate, -0.5% with ergocalciferol, and -0.7% with calcitriol (p < 0.001). At the femoral neck, there was no significant difference in bone mineral density change between the treatments over 2 years: alendronate (+0.9%), ergocalciferol (-3.2%), and calcitriol (-2.2%). Lumbar bone loss varied according to whether patients were starting or receiving chronic glucocorticoids, and there was a significant treatment x prior glucocorticoid use interaction effect. Six of 66 calcitriol subjects, 1 of 61 ergocalciferol subjects, and 0 of 64 alendronate subjects sustained new vertebral fractures. These data do not suggest any difference between simple vitamin D and calcitriol but do show that alendronate was superior to either treatment for glucocorticoid induced bone loss.

Reid DM, Devogelaer JP, Saag K, Roux C, Lau CS, Reginster JY, Papanastasiou P, Ferreira A, Hartl F, Fashola T, Mesenbrink P, Sambrook PN, Anonymous00081. · University of Aberdeen, Aberdeen, UK. · Lancet. · Pubmed #19362675 No free full text.

Abstract: BACKGROUND: Persistent use of glucocorticoid drugs is associated with bone loss and increased fracture risk. Concurrent oral bisphosphonates increase bone mineral density and reduce frequency of vertebral fractures, but are associated with poor compliance and adherence. We aimed to assess whether one intravenous infusion of zoledronic acid was non-inferior to daily oral risedronate for prevention and treatment of glucocorticoid-induced osteoporosis. METHODS: This 1-year randomised, double-blind, double-dummy, non-inferiority study of 54 centres in 12 European countries, Australia, Hong Kong, Israel, and the USA, tested the effectiveness of 5 mg intravenous infusion of zoledronic acid versus 5 mg oral risedronate for prevention and treatment of glucocorticoid-induced osteoporosis. 833 patients were randomised 1:1 to receive zoledronic acid (n=416) or risedronate (n=417). Patients were stratified by sex, and allocated to prevention or treatment subgroups dependent on duration of glucocorticoid use immediately preceding the study. The treatment subgroup consisted of those treated for more than 3 months (272 patients on zoledronic acid and 273 on risedronate), and the prevention subgroup of those treated for less than 3 months (144 patients on each drug). 62 patients did not complete the study because of adverse events, withdrawal of consent, loss to follow-up, death, misrandomisation, or protocol deviation. The primary endpoint was percentage change from baseline in lumbar spine bone mineral density. Drug efficacy was assessed on a modified intention-to-treat basis and safety was assessed on an intention-to-treat basis. This trial is registered with ClinicalTrials.gov, number NCT00100620. FINDINGS: Zoledronic acid was non-inferior and superior to risedronate for increase of lumbar spine bone mineral density in both the treatment (least-squares mean 4.06% [SE 0.28] vs 2.71% [SE 0.28], mean difference 1.36% [95% CI 0.67-2.05], p=0.0001) and prevention (2.60% [0.45] vs 0.64% [0.46], 1.96% [1.04-2.88], p<0.0001) subgroups at 12 months. Adverse events were more frequent in patients given zoledronic acid than in those on risedronate, largely as a result of transient symptoms during the first 3 days after infusion. Serious adverse events were worsening rheumatoid arthritis for the treatment subgroup and pyrexia for the prevention subgroup. INTERPRETATION: A single 5 mg intravenous infusion of zoledronic acid is non-inferior, possibly more effective, and more acceptable to patients than is 5 mg of oral risedronate daily for prevention and treatment of bone loss that is associated with glucocorticoid use.

Sebba AI, Emkey RD, Kohles JD, Sambrook PN. · University of South Florida, Tampa, FL, USA. · Bone. · Pubmed #19049913 No free full text.

Abstract: This meta-analysis pooled data from the four phase III clinical trials of ibandronate to assess the relationship between ibandronate dose, changes in bone mineral density, and rates of both clinical and non-vertebral fractures. Individual patient data from the intent-to-treat population of the BONE, IV fracture prevention, MOBILE, and DIVA studies were included for analysis. The relationship between ibandronate dose and bone mineral density at both the lumbar spine and at the total hip was assessed qualitatively. The relationship between lumbar spine bone mineral density and clinical fracture rate, and the relationship between total hip bone mineral density and non-vertebral fracture rate, were assessed both qualitatively and using mathematical models. A total of 8710 patients were included in this analysis. Both lumbar spine and total hip bone mineral density were observed to increase with increasing ibandronate dose. The incidence of all clinical fractures was observed to decrease as lumbar spine bone mineral density increased. A statistically significant inverse linear relationship was observed between percent change in lumbar spine bone mineral density and the rate of clinical fractures (P=0.005). A non-significant curvilinear relationship was observed between percent change in total hip bone mineral density and non-vertebral fracture rate. Increased ibandronate exposure is associated with increasing gains in the lumbar spine bone mineral density and decreasing clinical fracture rates. A non-linear relationship may exist between increases in the total hip bone mineral density and non-vertebral fracture rate.

Chen JS, Hogan C, Lyubomirsky G, Sambrook PN. · Institute of Bone & Joint Research, Royal North Shore Hospital, Sydney, Australia. · Osteoporos Int. · Pubmed #18633666 No free full text.

Abstract: This study reviewed factors influencing osteoporosis management in primary care settings in Australia and examined risk profiles of patients (n = 37,957) for osteoporosis. Only 29.7% of patients with a prior fracture were currently on specific medication for osteoporosis. The results highlight the need for further exploration of barriers to osteoporosis management. INTRODUCTION: Osteoporosis management in primary care is suboptimal even for high-risk people with a history of prior fracture. METHODS: This study reviewed factors influencing the management of individuals at risk for osteoporosis in primary care settings in Australia and examined risk profiles of patients for osteoporosis. Patients (n = 37,957, mean age 71) were recruited over a 12-month period (February 2006-Jan 2007) and interviewed. RESULTS: With regard to risk factors for osteoporosis, 12.6% of patients reported a history of prior minimal trauma fracture, 7.5% reported a family history of osteoporosis, 7.4% reported they were current smokers, 11.4% reported low dietary calcium intake, 31.8% reported no regular weekly physical exercise and 10.3% reported current use of glucocorticoids. Of those with a prior fracture, only 29.7% were currently on specific medication for osteoporosis. Radiography (n = 17,754) demonstrated a prior vertebral fracture in 30.1%, but only 3.8% of the 17,754 patients reported current use of specific osteoporosis medication. CONCLUSIONS: This study has confirmed low rates of treatment in primary care even in individuals who have already suffered a prior fracture or have other risk factors. This study highlights the need for further exploration of barriers to osteoporosis management in the primary care setting.

Makovey J, Nguyen TV, Naganathan V, Wark JD, Sambrook PN. · Institute of Bone and Joint Research, Royal North Shore Hospital, University of Sydney, Sydney, Australia. · J Bone Miner Res. · Pubmed #17620052 No free full text.

Abstract: This longitudinal twin study was designed to assess the heritability of bone loss in peri- and postmenopausal women. A sample of 724 female twins was studied. Baseline and repeat BMD measurements were performed. Results of genetic model-fitting analysis indicated genetic effects on bone loss account for approximately 40% of the between-individual variation in bone loss at the lumbar spine, forearm, and whole body. INTRODUCTION: BMD and bone loss are important predictors of fracture risk. Although the heritability of peak BMD is well documented, it is not clear whether bone loss is also under genetic regulation. This study was designed to assess the heritability of bone loss in peri- and postmenopausal women. MATERIALS AND METHODS: A sample of 724 female twins (177 monozygotic [MZ] and 185 dizygotic [DZ] pairs), 45-82 yr of age, was studied. Each individual had baseline BMD measurements at the lumbar spine, hip, forearm, and total body by DXA and at least one repeat measure, on average 4.9 yr later. Change in BMD (DeltaBMD) was expressed as percent of gain or loss per year. Intraclass correlation coefficients for DeltaBMD were calculated for MZ and DZ pairs. Genetic model-fitting analysis was conducted to partition the total variance of DeltaBMD into three components: genetic (G), common environment (C), and specific environment, including measurement error (E). The index of heritability was estimated as the ratio of genetic variance over total variance. RESULTS: The mean annual DeltaBMD was -0.37 +/- 1.43% (SD) per year at the lumbar spine, -0.27 +/- 1.32% at the total hip, -0.77 +/- 1.66% at the total forearm, -0.36 +/- 1.56% at the femoral neck, and -0.16 +/- 0.81% at the whole body. Intraclass correlation coefficients were significantly higher in MZ than in DZ twins for all studied parameters, except at the hip sites. Results of genetic model-fitting analysis indicated that the indices of heritability for DeltaBMD were 0.38, 0.49, and 0.44 for the lumbar spine, total forearm, and whole body, respectively. However, the genetic effect on DeltaBMD at all hip sites was not significant. CONCLUSIONS: These data suggest that, although genetic effects on bone loss with aging are less pronounced than on peak bone mass, they still account for approximately 40% of the between-individual variation in bone loss for the lumbar spine, total forearm, and whole body in peri- and postmenopausal women. These findings are relevant for studies aimed at identification of genes that are involved in the regulation of bone loss.

Sambrook PN. · Rheumatology at Kolling Institute, University of Sydney, Sydney, Australia. · Nat Clin Pract Endocrinol Metab. · Pubmed #17245334 No free full text.

This publication has no abstract.

Sambrook PN, Cameron ID, Chen JS, Cumming RG, Lord SR, March LM, Schwarz J, Seibel MJ, Simpson JM. · Institute of Bone & Joint Research, University of Sydney, Sydney, Australia. · Osteoporos Int. · Pubmed #17216131 No free full text.

Abstract: INTRODUCTION: When subjects are selected on the basis of fall risk alone, therapies for osteoporosis have not been effective. In a prospective study of elderly subjects at high risk of falls, we investigated the influence of bone strength and fall risk on fracture. METHODS: At baseline we assessed calcaneal bone ultrasound attenuation (BUA) as well as quantitative measures of fall risk in 2005 subjects in residential care. Incident falls and fractures were recorded (median follow-up 705 days). RESULTS: A total of 6646 fall events and 375 low trauma fracture events occurred. The fall rate was 214 per 100 person years and the fracture rate 12.1 per 100 person years. 82% of the fractures could be attributed to falls. Although fracture rates increased with decreasing BUA (incidence rate ratio 1.94 for lowest vs. highest BUA tertile, p<0.002), incident falls also affected fracture incidence. Subjects who fell frequently (>3.15 falls/per person year) were 3.35 times more likely to suffer a fracture than those who did not fall. Some fall risk factors such as balance were associated with the lowest fracture risk lowest in the worst performing group. Multivariate analysis revealed higher fall rate, history of previous fracture, lower BUA, lower body weight, cognitive impairment and better balance as significant independent risk factors for fracture. CONCLUSIONS: In the frail elderly, both skeletal fragility and fall risk including the frequency of exposure to falls are important determinants of fracture risk.

Sambrook PN, Schacht E. · Institute of Bone and Joint Research, University of Sydney, Sydney, Australia. · J Rheumatol Suppl. · Pubmed #16142844 No free full text.

This publication has no abstract.