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An Italian multidisciplinary working group discussed the current Italian scenario of osteoporosis management during a meeting and highlighted the essential role of calcium and vitamin D supplementation in the prevention of fragility fractures., Purpose: This paper aims to review and discuss data on calcium and vitamin D requirements and the role of combined calcium and vitamin D supplementation in the treatment of patients with osteoporosis., Methods: The discussion of the experts covered literature data on calcium and vitamin D supplementation, gaps in the diagnosis and treatment of osteoporosis, and the role of the primary care physician in identifying and treating patients with osteoporosis. Articles for consideration were identified through PubMed searches using different combinations of pertinent keywords., Results: The discussion highlighted that insufficient calcium or vitamin D intake increases the risk of fragility fractures. The experts also drew attention to the essential role of calcium and vitamin D supplementation in achieving an anti-fracture effect and supporting the efficacy of anti-osteoporotic agents without increasing nephrolithiasis and cardiovascular risks. In addition, the discussion underlined the role of the primary care physician in the initial clinical approach to patients with osteoporosis., Conclusions: The experts believe that efficient treatment for patients with osteoporosis should include calcium and vitamin D supplementation to achieve adequate levels that are able to inhibit the parathyroid hormone and bone resorption., (© 2024. The Author(s).)

Male osteoporosis is a still largely underdiagnosed pathological condition. As a consequence, bone fragility in men remains undertreated mainly due to the low screening frequency and to controversies in the bone mineral density (BMD) testing standards. Up to the 40% of overall osteoporotic fractures affect men, in spite of the fact that women have a significant higher prevalence of osteoporosis. In addition, in males, hip fractures are associated with increased morbidity and mortality as compared to women. Importantly, male fractures occur about 10 years later in life than women, and, therefore, due to the advanced age, men may have more comorbidities and, consequently, their mortality is about twice the rate in women. Gender differences, which begin during puberty, lead to wider bones in males as compared with females. In men, follicle-stimulating hormones, testosterone, estrogens, and sex hormone-binding levels, together with genetic factors, interact in determining the peak of bone mass, BMD maintenance, and lifetime decrease. As compared with women, men are more frequently affected by secondary osteoporosis. Therefore, in all osteoporotic men, a complete clinical history should be collected and a careful physical examination should be done, in order to find clues of a possible underlying diseases and, ultimately, to guide laboratory testing. Currently, the pharmacological therapy of male osteoporosis includes aminobisphosphonates, denosumab, and teriparatide. Hypogonadal patients may be treated with testosterone replacement therapy. Given that the fractures related to mortality are higher in men than in women, treating male subjects with osteoporosis is of the utmost importance in clinical practice, as it may impact on mortality even more than in women.

Aim: Bone fragility is increasingly recognized as a relevant complication of type 2 diabetes (T2D) and diabetic patients with fragility fractures have higher mortality rates than non diabetic individuals or diabetic patients without fractures. However, current diagnostic approaches for fracture risk stratification, such as bone mineral density measurement or the use of risk assessment algorithms, largely underestimate fracture risk in T2D patients. A multidisciplinary expert panel was established in order to in order to formulate clinical consensus recommendations on bone health assessment and management of fracture risk in patients with T2D., Data Synthesis: The following key questions were addressed: a) which are the risk factors for bone fragility in T2D?, b) which diagnostic procedures can be currently used to stratify fracture risk in T2D patients?, c) which are the effects of antidiabetic treatments on bone?, and d) how to prevent and treat bone fragility in T2D patients? Based on the available data members of this panel suggest that the stratification of fracture risk in patients with diabetes should firstly rely on the presence of a previous fragility fracture and on the individual risk profile, with the inclusion of T2D-specific risk factors (namely T2D duration above 10 yrs, presence of chronic T2D complications, use of insulin or thiazolidinediones and persistent HbA1c levels above 8% for at least 1 year). Two independent diagnostic approaches were then suggested in the presence or the absence of a prevalent fragility fracture, respectively., Conclusions: Clinical trials in T2D patients at risk for fragility fractures are needed to determine the efficacy and safety of available antiresorptive and anabolic agents in this specific setting., (Copyright © 2021 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

Treatment of osteoporosis is aimed to prevent fragility fractures and to stabilize or increase bone mineral density. Several drugs with different efficacy and safety profiles are available. The long-term therapeutic strategy should be planned, and the initial treatment should be selected according to the individual site-specific fracture risk and the need to give the maximal protection when the fracture risk is highest (i.e. in the late life). The present consensus focused on the strategies for the treatment of postmenopausal osteoporosis taking into consideration all the drugs available for this purpose. A short revision of the literature about treatment of secondary osteoporosis due both to androgen deprivation therapy for prostate cancer and to aromatase inhibitors for breast cancer was also performed. Also premenopausal females and males with osteoporosis are frequently seen in endocrine settings. Finally particular attention was paid to the tailoring of treatment as well as to its duration.

Summary: By investigating the relationship between serum testosterone, estradiol, and bone mineral density (BMD) in a large cohort of HIV-infected men, estradiol was associated with BMD, relative estrogen deficiency being involved in bone loss in men with hypogonadism, in addition to all HIV-related factors. Increased aromatization in adipose tissue does not counteract HIV-related bone loss., Introduction: The purpose of this study is to evaluate the relationship between serum testosterone, estradiol, and BMD in a large cohort of HIV-infected men., Methods: We investigated biochemical, hormonal parameters, and BMD in 1204 HIV-infected men (age 45.64 ± 7.33 years) participating in a cross-sectional, observational study. Among other parameters, the main outcome measures were serum total testosterone and estradiol, gonadotropins, 25-hydroxyvitamin D [25(OH)D], parathormone (PTH), calcium, phosphorous, femoral, and lumbar BMD., Results: In men with HIV, the prevalence of osteoporosis and osteopenia is 15.1 and 63.2% with 25(OH)D insufficiency being very common (60.1%). After age adjustment, BMD is positively associated with estradiol, but not testosterone, at linear (p < 0.001) and stepwise (p < 0.05) multiple regression. Lumbar BMD significantly increases across the estradiol quartiles but not among testosterone quartiles. Femoral and lumbar BMD are significantly higher in men with estradiol ≥ 27 pg/mL than in those with estradiol <27 pg/mL. Apart from estradiol, only age, calcium, and BMI predict BMD at stepwise linear multiple regression, but the strength of this association is weak., Conclusions: Estradiol, but not testosterone, is associated with BMD in HIV-infected men and exerts a protective role on bone especially when it is above 27 pg/mL. Relative estrogen deficiency is a potential mechanism involved in bone loss in hypogonadal HIV-infected men, in addition to all HIV-related factors. Increased aromatization in adipose tissue does not counteract HIV-related bone loss. Finally, reduced BMD in young-to-middle-aged HIV-infected men might be considered a peculiar hallmark of HIV infection due to its relevant prevalence, representing one of the several pieces composing the complicated puzzle of premature aging related to HIV infection.

Human immunodeficiency virus (HIV)-infected patients have an increased risk of developing osteopenia or osteoporosis compared with healthy individuals. Our aim was to compare dual X-ray absorptiometry (DXA), the gold standard for measuring bone mineral density (BMD), with bone quantitative ultrasound (QUS), an alternative technique for predicting fractures and screening low BMD, at least in postmenopausal populations. We analyzed DXA and QUS parameters to investigate their accuracy in the diagnosis and prediction of bone alterations in a cohort of 224 HIV-1-positive patients. The speed of sound (SOS), broadband ultrasound attenuation (BUA) and stiffness index (SI) parameters showed a moderate correlation with DXA, especially with total-body BMD (r coefficient of 0.38, 0.4 and 0.42 respectively), particularly in the female subgroup. In addition, multivariate analysis of HIV-positive patients assessed for vertebral fractures indicated that QUS was more effective than DXA at predicting the risk of fracture. QUS can be used as an additional tool for analyzing bone density in HIV-positive patients and its case of use and low cost make it especially suitable for resource-limited settings where DXA is not employed.

A high salt intake has been correlated with several pathological conditions such as hypertension, cardiovascular disease, renal calcium stones, and osteoporosis. Some of these diseases present a high prevalence in the elderly and common pathogenetic mechanisms are proposed for some of them. A high salt intake has been associated with hypertension as well as osteoporosis and one of the proposed pathogenetic mechanisms is an increased calcium excretion in urine. Urinary calcium loss induces a negative calcium balance that may predispose hypertensive subjects to developing greater bone loss. The gene which encodes for the thiazide- sensitive sodium-chloride cotransporter (NCCT) represents a possible link between hypertension and osteoporosis. Subjects heterozygous for an inactivating mutation of NCCT present a positive effect on bone density as shown by the significantly higher Z-scores at the lumbar spine and total femur. Recent clinical studies also support the benefit of ACE inhibitors in reducing fracture risk or improving bone metabolism. These data suggest that the renin-angiotensin system may be one of the several factors involved in bone metabolism. Hypertension, together with stroke, has been demonstrated to be a risk factor for osteoporosis. Although the risk associated with hypertension was limited in terms of relative risk, it may have a significant impact on the general population owing to the high prevalence of hypertension. The treatment of hypertension may thus be very useful in also giving protection against fractures.

Aim: We evaluated whether the number of teeth lost is associated with risk factors for osteoporosis and whether bone mass measurements can add further information., Methods: A total of 455 healthy women were enrolled. All the subjects filled in a questionnaire on risk factors for osteoporosis. The bone mineral density (BMD) was measured both by dual X-ray absorptiometry (DXA) and quantitative ultrasound measurements (QUS)., Results: On the basis of the questionnaire score 65.1% of the subjects were in the low risk category, 11% in the moderate risk category, 19.3% in the fairly high risk category and 4.6% in the high risk category. Close relationships (P<0.001) were observed between bone mass loss and the questionnaire risk categories. The number of teeth lost significantly increased from normal to osteoporosis groups. High correlations were also found between osteosonographic parameters and the number of teeth lost. Among questionnaire items a significant positive correlation was found only between the number of teeth lost and both age class (P<0.001) and years since menopause (P<0.001). A multiple regression showed that only age class (P<0.001) and ultrasound bone profile index (UBPI) (P=0.041) were independently linked to tooth loss., Conclusions: The results obtained showed that age is the main determinant of tooth loss and that QUS adds further information in identifying patients at a higher risk of tooth loss.

Osteoporosis (OP) is a very common disease associated with increased morbidity, mortality and costs. For a 50-yr-old woman the lifetime risk of an osteoporotic fracture is 40%, while for a man of the same age the risk is 13%. Good evidence exists as to the correlation between bone mineral density (BMD) and fracture risk in post-menopausal women. The diagnosis of OP can be made when BMD is more >2.5 SD below the mean of normal young women (T-score < or = -2.5). In men it has not been possible, until now, to identify a definite T-score under which the diagnosis of OP can be made. Several studies produced conflicting results when they tried to answer the question as to whether males and females fracture at the same absolute BMD value. Men have a greater bone size than women even when this parameter is corrected for weight and body mass. As densitometric devices measure areal density, men appear to have a higher BMD than women. Some studies have shown that, for a given BMD, males and females have the same fracture risk, while other papers have demonstrated that fractured men have a higher BMD than fractured women. Another problem concerns the diagnosis of osteoporosis. In fact, when the T-score is calculated in men on the basis of a young female reference range the prevalence of osteoporosis can be underestimated. The official position of International Society for Clinical Densitometry (ISCD) may represent an "interim" answer in order to identify men at risk of fracture.

Purpose: To evaluate the effects of alendronate, vitamin D, and calcium supplementation on bone metabolism and bone mineral density (BMD) in both HIV-infected men and women treated with highly active antiretroviral therapy (HAART)., Method: We performed a 52-week prospective, multicenter, randomized, open-label clinical trial. Eligible participants were on stable HAART and had BMD values at the femoral neck or lumbar spine that corresponded to a t score less than -1. Patients were randomized to receive alendronate 70 mg weekly or no alendronate; calcium 1000 mg daily and vitamin D 500 IU daily were provided to all study recipients. Primary endpoint of the study was the change in bone metabolism evaluated by N-telopeptide of type 1 collagen and bone-specific alkaline phosphatase; the secondary endpoint was BMD variation., Results: 18 patients were randomized to the alendronate and 23 to the no-alendronate group (controls). The alendronate-treatment group compared to controls had a significant decrease in serum N-telopeptides, 1914 +/- 1433.4 vs. 3967 +/- 1650.5 pM/L (p = .005) after 1 year. Lumbar spine BMD increased by 4% in the alendronate group (p = .004) vs. 3.7% (p = .062) in controls, compared to baseline values. Femoral neck BMD decreased by 0.5% in the alendronate group (p = .05) and by 3.5% in the control group (p = .04). No between-groups differences for BMD were found (Delta lumbar-BMD 0.0351 +/- 0.0406 in cases and 0.0356 +/- 0.073 in controls [p = .977], Delta femoral-BMD -0.085 +/- 0.160 in cases and -0.100 +/- 0.165 in controls [p = .795])., Conclusion: Alendronate plus vitamin D and calcium was effective in reducing bone resorption. Alendronate improved lumbar BMD and minimized femoral BMD decrease after 52 weeks compared to treatment with vitamin D and calcium alone in patients on HAART with osteopenia/osteoporosis.

Several studies have indicated that up to 60% of idiopathic calcium stone formers present hypercalciuria. Many authors have described reduced bone mineral density (BMD) in stoneformers with hypercalciuria, but osteopenia has also been found in normocalciuric patients. Moreover, Jaeger's group found that bone mass was reduced in all patients with calcium stone disease, independently of hypercalciuria. Many factors may contribute to the pathogenesis of osteopenia in stone formers. A predominant role has been given to the low-calcium diet that is still prescribed in nephrolithiasis. Also slight metabolic acidosis, which is frequently present in stone formers eating a diet rich in animal protein, can contribute to bone loss. Finally, some authors described a pathogenetic role for cytokines, prostaglandins and vitamin D receptor gene polymorphisms., (Copyright 2004 S. Karger AG, Basel)

Background: Several authors have observed that idiopathic calcium stone formers show a bone mass reduction, which is more evident in those with idiopathic hypercalciuria. The aim of this work was the evaluation of osteopenia and osteoporosis rate in a group of idiopathic calcium stone formers. The influence of hypercalciuria, nutritional factors and anthropometric parameters on bone mass was evaluated in these patients as well., Methods: We enrolled 196 idiopathic calcium stone formers; 102 males, and 94 females. All subjects underwent a metabolic study. BMC and BMD were evaluated as well as QUS., Results: Males showed greater weight, height, BMI, densitometric values and plasma creatinine, uric acid, urea, sodium, magnesium, GFR and urinary osmolarity than females. Moreover males excreted more uric acid, urea, creatinine, sulphate, phosphate, oxalate and citrate than females. The prevalence of osteopenia and osteoporosis, according to T-score, was 54% and 14% respectively. Hypercalciuria was demonstrated in 21.7% of the patients. Hypercalciuric men showed a higher excretion of urea, phosphate, sulphate and magnesium., Conclusions: Our results confirm the importance of QUS in the evaluation of stone formers' bone mass. Anthropometric characteristics and dietary habits seem to play a role in bone loss. We did not demonstrate any influence of hypercalciuria on bone mass. Although the pathogenesis of bone loss in stone formers still remains unclear, it can be hypothesized that a slight degree of metabolic acidosis, probably of alimentary origin, may be involved in the reduction of bone mass.