Parkinson's disease and osteoporosis

Parkinson's disease is associated with an increased risk of falls. The risk is greatest in patients with advanced disease. Because Parkinson's disease usually occurs late in life, the risk factors related to the neurological impairments add to those associated with aging. The incidence of fractures is high in patients with Parkinson's disease, with femoral neck fractures in older women being particularly common. Risk factors for fractures include a low body mass index, limited exposure to sunlight, an inadequate vitamin D intake with low 25-OH vitamin D levels, and bone loss. Several studies found decreased bone mineral density values at the femoral neck and lumbar spine in patients with Parkinson's disease. Although this decrease is ascribable in part to factors unrelated with Parkinson's disease, such as older age and female gender, Parkinson's disease itself also plays a role, most notably in patients with severe neurological impairments (Hoehn and Yahr stages III and IV).     

Impaired bone mineralization accompanied by low vitamin D and secondary hyperparathyroidism in patients with femoral neck fracture

Summary

Although it is well established that a decrease in bone mass increases the risk of osteoporotic fractures, the proportion of fractures attributable to areal bone mineral density (BMD) is rather low. Here, we have identified bone mineralization defects together with low serum 25-hydroxyvitamin D (25-(OH) D) levels as additional factors associated with femoral neck fractures.

Introduction

Osteoporotic fractures of the femoral neck are associated with increased morbidity and mortality. Although it is well established that a decrease in bone mass increases the risk of osteoporotic fractures, the proportion of fractures attributable to areal BMD is rather low. To identify possible additional factors influencing femur neck fragility, we analyzed patients with femoral neck fracture.

Methods

We performed a detailed clinical and histomorphometrical evaluation on 103 patients with femoral neck fracture including dual-energy X-ray absorptiometry, laboratory parameters, and histomorphometric and bone mineral density distribution (BMDD) analyses of undecalcified processed biopsies of the femoral head and set them in direct comparison to skeletal healthy control individuals.

Results

Patients with femoral neck fracture displayed significantly lower serum 25-(OH) D levels and increased serum parathyroid hormone (PTH) compared to controls. Histomorphometric analysis revealed not only a decreased bone volume and trabecular thickness in the biopsies of the patients, but also a significant increase of osteoid indices. BMDD analysis showed increased heterogeneity of mineralization in patients with femoral neck fracture. Moreover, patients with femoral neck fracture and serum 25-(OH) D levels below 12 μg/l displayed significantly thinner trabecular bone.

Conclusion

Taken together, our data suggest that impaired bone mineralization accompanied by low serum 25-(OH) D levels is of major importance in the etiology of femoral neck fractures. Therefore, balancing serum 25-(OH) D levels and thereby normalizing PTH serum levels may counteract pronounced mineralization defects and might decrease the incidence of femoral neck fractures.     

Bone status and fractures in 85 adults with Wilson’s disease

Summary

Wilson’s disease is characterized by copper deposition, especially in the liver and central nervous system. We assessed the prevalent fractures and bone mineral density (BMD) and related risk factors in 85 patients. BMD was normal, but patients with severe neurological involvement, low BMI, and/or amenorrhea are at risk for fractures.

Introduction

Wilson’s disease (WD) is characterized by copper deposition, especially in the liver and central nervous system. Two studies showed a high prevalence of osteoporosis in WD patients. We wanted to assess the prevalent fractures and bone mineral density (BMD) and to identify risk factors for bone loss and fractures in a large group of WD patients.

Methods

In this prospective cross-sectional survey at National center of reference for WD, we included 85 patients, 47 women, and 38 men, with a mean age of 35?±?10 years, and mean time from diagnosis to study of 21?±?9 years; 57 (67 %) patients had neurological signs. Peripheral fractures, prevalent radiological vertebral fractures (VFx), and dual-energy X-ray absorptiometry BMD measurements at the femoral neck (FN) and lumbar spine (LS) were studied.

Results

Mean LS and FN Z-score was normal (?0.37?±?1.20 at LS and ?0.06?±?1.20 at FN). BMI <19 kg/m² and amenorrhea were associated with low BMD. Prevalent peripheral fractures were noted in 43 (51 %) and VF in 7 (8 %) patients. Severity of neurological involvement and male sex was associated with peripheral fractures, whereas older age, severe neurological involvement, and low BMD and Z-score values were associated with VF.

Conclusion

Our data showing normal BMD overall do not support routine bone status evaluation in adults with WD. However, patients with severe neurological involvement, low BMI, and/or amenorrhea are at risk factors for fractures and may require specific monitoring.     

Bone Disease in Patients Awaiting Liver Transplantation. Has the Situation Improved in the Last Two Decades?

In recent years, there has been speculation about the possibility of a reduction in the incidence of fractures after liver transplantation (LT) because of changes in the characteristics of candidates and the use of different immunosuppressive therapies. We analyzed the characteristics of LT candidates (CTC) and compared them with historical data from a group of LT candidate patients (HTC). Data from 60 CTC patients consecutively included in a screening program of metabolic bone disease were compared with data from 60 HTC patients prospectively evaluated between 1992 and 1993. In all patients, we analyzed the clinical and laboratory characteristics, bone mineral density (BMD) dual-energy X-ray absorptiometry, and skeletal fractures. Patients in the CTC group were older than patients in the HTC group. The CTC group had lower femoral neck T scores. No differences were observed between groups in the proportion of patients with osteoporosis (22 vs. 30 %, p = ns) or fractures (36 vs. 33 %, p = ns). The percentage of patients with normal BMD decreased from 38 to 20 %. 25(OH)D values were low in both groups. Only 7.5 % of the CTC patients received calcium and/or vitamin D supplementation. The prevalence of fractures among CTC patients was similar to that seen two decades ago. At present, candidates for LT are older and have lower femoral bone mass. Vitamin D deficiency remains frequent; however, calcium and/or vitamin D supplementation is uncommon.     

Is vitamin D necessary for skeletal integrity in the elderly?

Serum 1.25 dihydroxyvitamin D concentrations were reduced in elderly patients with femoral neck fractures, irrespective of the presence of osteomalacia. This reduction was not attributable to a decrease in vitamin D binding protein. The low rate of bone turnover in these elderly patients might reduce the requirement for vitamin D and protect against the development of osteomalacia. Serum vitamin D metabolite concentration cannot be used as a screening test for osteomalacia in these patients.     

Relative contributions of bone density, bone turnover, and clinical risk factors to long-term fracture prediction.

Long-term fracture prediction using bone mineral density remains controversial, as does the additional contribution from assessing bone turnover or clinical risk factors. We measured bone mineral density at various sites, along with biochemical markers of bone turnover, sex steroid levels, and over 100 clinical variables, at baseline on an age-stratified sample of 304 Rochester, MN women in 1980. The 225 postmenopausal women were subsequently followed for 3146 person-years (median, 16.2 years per subject), wherein they experienced 302 new fractures: 81% resulted from minimal or moderate trauma and 60% of these involved the proximal femur, thoracic or lumbar vertebrae, or distal forearm. Accounting for multiple fractures per subject, these osteoporotic fractures together were best predicted by baseline femoral neck bone mineral density (age-adjusted hazard ratio [HR] per SD decrease, 1.37; 95% CI, 1.10-1.70); 19 moderate trauma forearm fractures were best predicted by distal radius bone mineral content, whereas 28 hip fractures and 100 vertebral fractures were best predicted by femoral neck bone mineral density. Femoral neck bone mineral density performed comparably in predicting osteoporotic fracture risk within the first decade of follow-up (HR, 1.38; 95% CI, 1.10-1.74) as well as more than 10 years after baseline (HR, 1.39; 95% CI, 1.05-1.84). The older biochemical markers were not associated with fractures, but serum "free" estradiol index was independently predictive of short- and long-term fracture risk. Consistent clinical risk factors were not identified, but statistical power was limited. Identifying patients at increased long-term risk of fracture is challenging, but it is reassuring that femoral neck bone mineral density can predict osteoporotic fractures up to 20 years later.     

老年患者25( OH) D、PTH与骨折的相关分析

目的了解骨科老年患者25-羟基维生素D(25(OH)D)、甲状旁腺激素(PTH)水平及与骨折的相关性。方法2011.8~2014.12我院骨科老年患者428名,72.47±6.19岁,其中骨折192名。测定血清25(OH)D和PTH,腰椎(L1-4)、全髋、股骨颈骨密度。比较骨折与非骨折组25(OH)D,PTH及骨密度的差异;分析25(OH)D、PTH各组骨折和骨密度的差异;分析25(OH)D和PTH、骨密度的相关性;用相对工作特征曲线(relative operating characteristic,ROC curve)分析25(OH)D对骨折的预测价值。结果骨折组与非骨折组相比,25(OH)D水平及全髋和股骨颈骨密度偏低。不同25(OH)D水平组骨折发生的差异具有统计学意义,维生素D严重缺乏组、缺乏组骨折发生率较高。维生素D严重缺乏组、缺乏组、不足组的骨密度偏低,PTH增高组骨密度也偏低。25(OH)D与PTH、腰椎(L1-4)、全髋、股骨颈BMD存在相关性。ROC曲线下面积为0.529,不能以25(OH)D的水平预测骨折。结论骨科老年患者存在严重的维生素D缺乏,维生素D缺乏者骨折发生率明显增高,对其应从补充维生素D、预防跌倒、提高骨质量等多方面进行综合干预。     

Epidemiology of osteoporosis

Osteoporosis represents a major and increasing public health problem with the aging of population. Major clinical consequences and economic burden of the disease are fractures. Many risk factors are associated with the fractures including low bone mass, hormonal disorders, personal and family history of fractures, low body weight, use of certain drugs (e.g. glucocorticoids), cigarette smoking, elevated intake of alchohol, low physical activity, insufficient level of vitamin D and low intake of calcium. This epidemiological review describes frequency, importance of risk factors and impact of osteoporosis and osteoporotic fractures. Objective measures of bone mineral density along with clinical assessment of risk factors can help identify patients who will benefit from prevention and intervention efforts and eventually reduce the morbidity and mortality associated with osteoporosis-related fractures.     

Anti-epileptic medication and bone health

Background Epilepsy is a common chronic neurological disorder, usually requiring long-term treatment with anti-epileptic drugs (AED). Many studies have reported that AED therapy is associated with metabolic bone disease and is a major iatrogenic risk factor for fractures. There remains uncertainty about the type(s) of bone disease due to AED treatment, and the pathogenesis of AED-associated fractures. Rationale Deficits in bone mineral density (BMD) are widely reported in AED-treated patient populations. However, much of the research conducted to date has been limited by factors such as small sample size, potentially biased subject selection, a lack of selection of appropriate control data, and failure to take account of important confounding influences. The pathogenesis of AED-associated fractures is likely to be multifactorial, due to factors including reduced BMD, impaired bone quality (due to osteoporosis and/or osteomalacia), increased propensity to fall, and fractures associated with seizures or loss of consciousness. Recommendations Patients receiving long-term AED should be monitored for indices of bone health, including BMD and vitamin D status. Lifestyle factors should be optimized, vitamin D status maintained, and fall prevention strategies introduced as appropriate. Good seizure control is important. The use of additional, specific osteoporosis therapy is not evidence-based in this setting, but would appear reasonable in patients with clinically significant decreases in BMD, applying current treatment guidelines for osteoporosis. Conclusion There is a pressing need for improved understanding of the pathogenesis of AED-associated bone disease, for better definition of the risk associated with specific AED regimens, and for the development of evidence-based preventive and treatment approaches in this common but neglected disorder.     

Prevalence and risk factors of low bone mineral density and 25-hydroxyvitamin D status in young healthy epileptic adult patients in a tropical Asian country taking antiepileptic drug

PurposeAntiepileptic drugs have been reported to reduce bone mineral density (BMD) in several countries with varying prevalence but in studies with small sample size and inadequate assessment of confounders, and rarely including young adults. We sought to determine the prevalence, vitamin D status and risk factors for low BMD in young adult epileptic patients in a tropical setting.MethodsWe prospectively examined left femoral neck and spine with dual-energy X-ray absorption. Demographic data, basic laboratory studies, history of clinical epilepsy, parathyroid hormone and vitamin D level were obtained.ResultsOne hundred and twenty three patients were included. The mean (± SD) T-score was ? 0.31 ± 1.24 at the spine and ? 0.19 ± 1.11 at the left femoral neck. 36% had osteopenia and 4.1% had osteoporosis at either site. Four patients had vitamin D deficiency. Vitamin D levels were not correlated with BMD. Twenty-five patients had vitamin D insufficiency. Multivariate logistic regression analysis identified low body mass index (BMI) and male sex as risk factors for low BMD at the spine and low BMI and duration of treatment as risk factors for low BMD at the left femoral neck.ConclusionChronic use of antiepileptic drug (AED) in young adult patients is associated with low BMD.     

Glucocorticoid-induced osteoporosis: is the bone density decrease the only explanation?

BACKGROUND: Glucocorticoids may increase bone fragility via mechanisms independent from their bone mass reducing effect. OBJECTIVE: To study relationships between osteoporotic fractures and bone mineral density in patients on long-term glucocorticoid therapy. PATIENTS AND METHODS: We studied 121 women with a mean age of 60.4 +/- 14.3 years on long-term glucocorticoid therapy (cumulative dose > or = 1 g of prednisone equivalent, duration > or = 6 months) for rheumatoid arthritis (n = 38), polymyalgia rheumatica or giant cell arteritis (n = 26), connective tissue disease (n = 15), asthma (n = 14), another inflammatory joint disease (n = 14), or another condition (n = 14). The control group was composed of 125 subjects who had the same mean age and met the same exclusion criteria as the case group. Bone mineral density was measured at the lumbar spine and femoral neck using a Hologic QDR 4500 unit. In subjects with back pain, radiographs of the thoracic and lumbar spine were obtained to look for fractures. RESULTS: The odds ratio for a bone mineral density decrease of one standard deviation at the femoral neck was 1.68 (1.20-2.35) in patients with a cumulative glucocorticoid dose of 10 g of prednisone equivalent and 1.67 (1.22-2.29) in those with a glucocorticoid therapy duration of 2 years. Sixty-eight fractures were recorded in 56 patients (46% of the overall patient group). Even after adjustment on age, glucocorticoid therapy duration, and dose, mean bone mineral density values at the lumbar spine and femoral neck were significantly lower in the subgroup of patients with fractures than in the subgroup without fractures. Sensitivity and specificity of bone mineral density at the femoral neck and/or lumbar spine for the diagnosis of vertebral fracture and/or peripheral fracture were 73% and 51%, respectively. In the stepwise logistic regression model, factors explaining the presence of fractures were as follows, in hierarchical order: age; absence of calcium/vitamin D supplementation, femoral neck T-score, and glucocorticoid dose. CONCLUSION: Our data are compelling evidence that bone mineral density is a major determinant of the fracture risk in patients with glucocorticoid-induced osteoporosis.     

Atraumatic diplaced bilateral femoral neck fracture in a patient with hypophosphatemic rickets in postpartum period: A missed diagnosis

IntroductionSimultaneous bilateral femoral neck fracture is an uncommon condition. There are very few cases reported in the literature and most of these cases have underlying bone pathologies such as renal osteodystrophy and osteomalacia. In some cases bilateral femoral neck fractures occur due to generalized seizures or high-energy trauma.Presentation of caseIn this case report “atraumatic bilateral femoral neck fracture in a 26 year old woman in postpartum period with hypophosphatemic rickets disease” is presented.DiscussionFemoral neck fractures are more frequently seen in elderly because of the reduction of bone quality and developing osteoporosis. In the literature generalized epilepsy, osteomalacia, hypovitaminosis D and chronic renal failure are shown as facilitating causes of bilateral femoral neck fractures. In patients without any additional pathology electric shock, electroconvulsive therapy, and high-energy trauma can lead to femoral neck fractures. In our patient there was also an underlying pathology, she has been followed due to autosomal recessive hypophosphatemic rickets disease since she was one year old. In the treatment of bilateral femoral neck fractures open/closed reduction internal fixation or hip arthroplasty are applied.ConclusionFor patients with bone metabolic diseases and/or the patients in pregnancy and postpartum period, preventive measures should be increased to reduce the risk of pathologic fracture. Admitting to the hospital physicians must be more careful about detecting fractures in these patients.     

Femoral Neck and Intertrochanteric Fractures Have Different Risk Factors: A Prospective Study

The aim of this study was to determine whether both types of hip fracture, femoral neck and intertrochanteric, have similar risk factors. A prospective cohort study was carried out on community-dwelling elderly women in four areas of the United States: Baltimore, MD; Pittsburgh, PA; Minneapolis, MN and Portland, OR. The participants were 9704 Caucasian women, 65 years and older, of whom 279 had fractured their femoral neck and 222 had fractured their trochanteric region of the proximal femur. The predictors used were the bone mass of the calcaneus and proximal femur, anthropometry, history of fracture (family and personal), medication use, functional status, physical activity and visual function. The main outcome measures were femoral neck and intertrochanteric fractures occurring during an average of 8 years of follow-up. In multivariate proportional hazards models, several risk factors increased the risk of both types of hip fracture; including femoral neck bone density and increased functional difficulty. In hazard regression models that directly compared risk factors for the two types of hip fracture, calcaneal bone mineral density (BMD) predicted femoral neck fractures more strongly than intertrochanteric fractures (OR = 1.16; 95% CI = 1.02–1.31). Steroid use and impaired functional status also predicted femoral neck fractures instead of intertrochanteric fractures. Poor health status (OR = 0.74; 95% CI = 0.55–1.00) predicted intertrochanteric fractures more strongly than femoral neck fractures. We conclude that femoral neck fractures are largely predicted by BMD and poor functional ability while aging and poor health status predispose to intertrochanteric fractures. Received: 8 February 2000 / Accepted: 10 June 2000     

L’hypercalciurieHypercalciuria.

Hypercalciuria is a biological syndrome defined as excretion in the urine of more than 0.1 mmol/kg/24 hours of calcium in the absence of dietary restrictions. A number of endocrine, renal, and bone diseases can cause hypercalciuria. Urinary calcium excretion is substantially influenced by the intakes of calcium, sodium, protein, carbohydrates, alcohol, and potassium, so that a poorly balanced diet can result in hypercalciuria. Recently, there has been a burst of interest in molecular studies of rare lithiasis syndromes, all of which are due to mutations in the ClCN5 chlorine channel gene. Mutations affecting the calcium-sensitive receptor (CaSR) have been identified in other forms of hypercalciuria. Idiopathic hypercalciuria is defined as hypercalciuria that persists after correction of dietary imbalances and has no detectable cause. The classification suggested by Pak (class I, class II, class III, and “renal” hypercalciuria) is controversial and of little assistance in clinical practice. Three mechanisms can be incriminated in idiopathic hypercalciuria: increased intestinal absorption of calcium, defective reabsorption of calcium by the renal tubule, and increased bone resorption. Overexpression of the vitamin D receptor and a deficiency in renal tubule enzymes may be involved also. Bone mineral density is moderately decreased in idiopathic hypercalciuria, particularly of the renal type. The risk of vertebral fracture seems increased, however. Overproduction of calcitriol and of cytokines that stimulate bone resorption have been incriminated in the bone loss. Treatment of the cause is essential in secondary hypercalciuria (dietary advice, treatment of an underlying disease…). A diet low in sodium and meat and containing no more than 800 mg of calcium per day has been advocated in idiopathic hypercalciuria. Hydrochlorothiaide therapy is warranted in patients with osteopenia and an inadequate response to dietary therapy.     

Bone Disease After Liver Transplantation: A Long-Term Prospective Study of Bone Mass Changes, Hormonal Status and Histomorphometric Characteristics

After liver transplantation there is a high incidence of fractures, with important rates of bone loss during the first months. However, the long-term evolution of bone mass and metabolism parameters have been scarcely studied. In order to determine the incidence and risk factors involved in the development of skeletal fractures and to analyze the long-term evolution of bone mass, bone turnover and hormonal status after liver transplantation, a 3-year prospective study was performed in 45 patients following liver transplantation. Serum osteocalcin, parathyroid hormone (PTH), 25-hydroxyvitamin D (25-OH D) and testosterone levels (men), and bone mass at the lumbar spine and femur were measured before and sequentially at different time points during 3 years. Spinal X-rays were obtained during the first year. Histomorphometric analysis of bone biopsies obtained in 24 patients within the first 12 hours after surgery and 6 months after transplantation was performed. Fifteen patients (33%) developed fractures after liver transplantation, and pre- transplant risk factors for fractures were age and low bone mass (odd”s ratio for osteoporosis, 95% confidence interval: 5.69, 1.32–24.53). Serum PTH, osteocalcin, 25-OH D, testosterone and creatinine levels increased after transplantation. Moreover, PTH correlated with creatinine and osteocalcin values. Bone mass decreased during the first 6 months and reached baseline values at the lumbar spine the second year, with posterior significant recovery at the femoral neck. Long term evolution of femoral neck BMD correlated with PTH levels. Six months after transplantation bone histomorphometric data showed an increase in bone formation parameters. After liver transplantation there is a high incidence of fractures, specially in elderly patients and those with osteoporosis. Bone mass decreased in the short-term period and improved, initially at the lumbar spine and later at the femur, according to histomorphometric evidences of an increase in bone formation. The increase in creatinine values induces a secondary hyperparathyroidism that influences the changes in femoral bone mass. Treatment of osteoporosis shortly after liver transplantation may be important in the prevention of bone fractures, particularly in patients with low bone mass. Received: June 2000 / Accepted: November 2000     

Bone loss and fracture after lung transplantation.

BACKGROUND: Osteoporosis is very common in patients with end-stage pulmonary disease. However, there are few prospective data on fracture incidence after lung transplantation. METHODS: We prospectively evaluated changes in bone mass, fracture incidence, and biochemical indices of bone and mineral metabolism in 30 patients who completed 1 year of observation after lung transplantation. All received calcium, vitamin D, and therapy with one or more agents that inhibit bone resorption, initiated shortly after transplantation. RESULTS: Before transplantation, only 20% of the patients had normal lumbar spine (LS) and femoral neck bone mineral density (BMD). After transplantation, 15 patients (50%) sustained significant bone loss at either the LS (-8.6+/-1.0%) or the femoral neck (-11.3+/-2.2%). Eleven (37%) patients (10 women) sustained a total of 54 atraumatic fractures. Pretransplantation LS BMD and T scores were significantly lower in those who sustained fractures (-2.809+/-0.32 versus -1.569+/-0.29; P<0.01). Fracture patients were more likely to have had pretransplantation glucocorticoid therapy (chi-square 5.687; P<0.02). The duration of pretransplantation glucocorticoid therapy was also longer in fracture patients (4.9+/-0.8 versus 1.3+/-0.4 years; P<0.001). Biochemical markers of bone resorption were significantly higher in patients who sustained bone loss and/or fractures. CONCLUSIONS: We conclude that fractures are a significant problem in the first year after lung transplantation, even in patients who receive therapy to prevent bone loss. Women with low pretransplantation BMD and a history of pretransplantation glucocorticoid therapy are at greatest risk.     

Skeletal health after intestinal bladder augmentation: findings in 54 patients

OBJECTIVE: To evaluate the risk of osteopenia in patients after intestinal bladder augmentation. PATIENTS AND METHODS: In all, 54 patients with bladder augmentation were evaluated during the regular follow-up programme. Augmentation was performed because of paediatric neurogenic or non-neurogenic reasons. Areal bone mineral densities (aBMD) for the lumbar spine (L1-L4), femoral neck and whole body were measured with dual-energy X-ray absorptiometry. In addition, acid-base balance and plasma 25-hydroxyvitamin D (vitamin D), kidney and gonadal functions as well as body mass index (BMI) were measured. Findings were correlated with clinical characteristics. RESULTS: BMD was reduced in 34 (63%) of the 54 patients. There was a significant difference in the prevalence of decreased aBMDs between neurogenic and non-neurogenic groups 31 of 42 patients (74%) and three of 12 patients, respectively (P < 0.01). There were spinal compression fractures in 23% of patients. Risk factors for osteoporosis were inability to walk, renal insufficiency, hypogonadism, vitamin D deficiency, acidosis, and a low BMI. There was moderate or severe vitamin D deficiency in 42% of patients but the vitamin D status did not correlate with BMD. The glomerular filtration rate correlated to the whole-body aBMD (P = 0.04). In 26% of patients (predominantly males with myelomeningocele) plasma follicle-stimulating hormone levels were elevated, indicating variable degrees of hypogonadism. Hypogonadism was associated with reduced lumbar spine aBMD (P = 0.03). CONCLUSION: Patients with paediatric reasons for bladder augmentation are at risk of osteopenia and compression fractures. The risk factors are mostly related to the patient's underlying illness and not to the augmentation per se.     

Bone mineral density in patients on maintenance dialysis

Disorders of bone and mineral metabolism affect almost all patients with advanced chronic kidney disease (CKD). High prevalence of decreased bone mineral density has been reported in this population; however, the role and diagnostic utility of bone density measurements are not well established. The incidence of bone fractures is high in patients with ESRD, but the association between fractures and bone density is not obvious. A recent meta-analysis suggested that decreased density at the radius might be associated with higher overall fracture risk. Changes in bone mineral density reflect several underlying pathological processes, such as vitamin D deficiency, estrogen deficiency and changes in bone turnover. The response of bone to these factors and processes is not uniform: it can vary in different compartments of the same bone or in different bones of the skeleton. Therefore, it is important to differentiate between the various types of bone. This may be possible by proper selection of the measurement site or using methods such as quantitative bone computed tomography. Previous studies used different methods and measured bone mineral density at diverse sites of the skeleton, which makes the comparison of their results very difficult. The association between changes in bone mineral metabolism and cardiovascular mortality is well known in ESRD patients. Studies also suggest that low bone density itself might be an indicator for high risk of cardiovascular events and poor overall outcome in this population. Some of the risk factors of low bone mineral density, such as vitamin D or estrogen deficiency, are potentially modifiable. Further studies are needed to elucidate if interventions modifying these risk factors will have an impact on clinical outcomes. In this review, we discuss the options for and problems of assessment of bone density and summarize the literature about factors associated with low bone density and its link to clinical outcomes in patients on maintenance dialysis.     

Acetabular fractures in the elderly. Results of a sophisticated treatment concept

Acetabular fractures in elderly patients are rare injuries, but their incidence is increasing. Poor bone quality due to osteoporosis and an increased operative risk due to concomitant disease are factors complicating surgical therapy. Literature does not provide generally accepted treatment protocols.In a 4-year period, 27 patients who were 65 years or older and who had an acute displaced fracture of the acetabulum were admitted to our department. Four minimally displaced and stable fractures were managed conservatively. Internal fixation was performed in 16 cases. According to the Merle d'Aubigné score, in 15 out of 18 surviving patients excellent or good results were found.Treatment strategy should be planned individually for each fracture, taking into account the patients biological age and general condition, fracture type, bone quality and associated injuries. Primary endoprosthetic replacement should only be considered when the acetabular bone stock allows stable cup fixation. Osteosynthesis in combination with early endoprosthetic replacement should be considered in acetabular fractures with associated femoral head or neck fractures or when significant articular steps and/or bone defects remain after open reduction and internal fixation.