Search

Osteoporosis and atherosclerosis are significant public health problems that often coexist, especially in the elderly. Although some studies have reported an age-dependent relationship, others have suggested a causal relationship between osteoporosis and atherosclerosis. The aim of our study was to evaluate the cardiovascular risk in a population of patients with osteoporosis by measuring carotid intima-media thickness (cIMT) and carotid-femoral pulse wave velocity (cf-PWV). A total of 58 patients with osteoporosis and an equal number of healthy control subjects were enrolled. All subjects underwent (1) a bone densitometry examination using dual X-ray absorptiometry, (2) a vascular evaluation for the measurements of cIMT and cf-PWV and (3) a blood sample for the evaluation of lipids and phosphocalcic metabolism. Patients with osteoporosis had a significant increase in cIMT and cf-PWV. There was also a significant inverse correlation between the femoral neck BMD and cf-PWV values. In conclusion, osteoporotic outpatients have earlier vascular ageing, with an increase of arterial stiffness. These data support a possible association between osteoporosis and atherosclerosis independent of age.

Background: Breast cancer is the most commonly occurring cancer in women worldwide. Early breast cancer is a kind of invasive neoplasm that has not proliferated beyond the breast or the axillary lymph nodes. Current therapeutic strategies for breast cancer mainly include local therapies such as surgery or radiotherapy and systemic therapies like chemotherapy, endocrine, and targeted therapy. Nowadays, the adjuvant treatment for hormone receptor-positive early breast cancer in postmenopausal women remains the main effective systemic therapy which can improve disease- free survival and overall survival; it involves several endocrine treatment regimens, including Selective Estrogen Receptor Modulators (SERMs), Aromatase Inhibitors (AIs), or a combination of them. AIs have been shown to be more effective in preventing recurrence in postmenopausal women with early breast cancer when compared with tamoxifen, thus representing the standard of care for adjuvant endocrine therapy. Although AIs are usually well-tolerated, they can have some side effects. Apart from the appearance of arthralgias or myalgias and cardiovascular events, AI therapies, reducing already low endogenous postmenopausal estradiol levels, cause increased bone loss and increase fracture risk in postmenopausal women. Objectives: The objective of this review is to evaluate the therapeutic options in the management of Aromatase Inhibitor-Associated Bone Loss (AIBL). Methods: We reviewed the current literature dealing with different therapeutic options in the treatment of AIBL. Results: Clinical practice guidelines recommend a careful evaluation of skeletal health in all women with breast cancer before AI therapy initiation. Adequate calcium and vitamin D intake have also been suggested. Pharmacological attempts to minimize AI-related bone loss have focused on the use of antiresorptive agents, such as bisphosphonates and denosumab to protect bone integrity and reduce the risk of fractures. Furthermore, clinical trials have shown that by making the bone microenvironment less susceptible to breast cancer metastasis, these drugs are able to increase disease- free survival. Conclusions: AI, that are the pillar of the systemic treatment for patients with hormone receptor-- positive breast cancer, are associated with different side effects, and in particular, osteoporosis and fractures. Both bisphosphonates and denosumab are able to prevent this negative effect.

Due to increasing life expectancy in thalassemia major (TM), osteoporosis is emerging as a significant problem. Its aetiology is multifactorial, culminating in increased bone resorption and impaired remodelling. Hypogonadism and marrow expansion seem to play an important role, but iron overload, deferoxamine toxicity, a defective growth hormone-insulin-like growth factor-1 axis and multiple endocrinopathies may represent additional causes of bone damage. Many of these patients, though under appropriate treatment programs, do not achieve normal peak bone mass. The receptor activator of nuclear factor kappa-ß (RANK)/RANK ligand/osteoprotegerin and the Wnt/β-catenin systems work as major mediators of imbalanced bone turnover and bone loss. Additional genetic factors, such as collagen type 1 alpha 1 and vitamin D receptor gene polymorphisms, may exert some influence on the enhanced fracture risk observed in TM. To date, in spite of adequate hormone replacement, chelating therapy and acceptable haemoglobin levels, subjects with TM display impaired bone density and imbalanced bone turnover, thus the puzzle of the pathogenesis of TM-induced osteoporosis remains far from being solved.

Secondary osteoporosis is a common clinical problem faced by bone specialists, with a higher frequency in men than in women. One of several causes of secondary osteoporosis is hematological disease. There are numerous hematological diseases that can have a deleterious impact on bone health. In the literature, there is an abundance of evidence of bone involvement in patients affected by multiple myeloma, systemic mastocytosis, thalassemia, and hemophilia; some skeletal disorders are also reported in sickle cell disease. Recently, monoclonal gammopathy of undetermined significance appears to increase fracture risk, predominantly in male subjects. The pathogenetic mechanisms responsible for these bone loss effects have not yet been completely clarified. Many soluble factors, in particular cytokines that regulate bone metabolism, appear to play an important role. An integrated approach to these hematological diseases, with the help of a bone specialist, could reduce the bone fracture rate and improve the quality of life of these patients.

Anticoagulant agents are widely used in the treatment of thromboembolic events and in stroke prevention. Data about their effects on bone tissue are in some cases limited or inconsistent (oral anti-vitamin K agents), and in others are sufficiently strong (heparins) to suggest caution in their use in subjects at risk of osteoporosis. This review analyses the effects of this group of drugs on bone metabolism, on bone mineral density, and on fragility fractures. A literature search strategy was developed by an experienced team of specialists by consulting the MEDLINE platform, including published papers and reviews updated to March 2019. Literature supports a detrimental effect of heparin on bone, with an increase in fracture rate. Low molecular weight heparins (LMWHs) seem to be safer than heparin. Although anti-vitamin K agents (VKAs) have a significant impact on bone metabolism, and in particular, on osteocalcin, data on bone mineral density (BMD) and fractures are contrasting. To date, the new direct oral anticoagulants (DOACs) are found to safe for bone health.

Osteoporosis and cardiovascular disease are worldwide public health issues. Recent evidence indicates a possible role of the canonical Wnt/β-catenin signalling pathway as a common mediator between these two diseases. The aim of the present study was to investigate the relationship between serum concentrations of sclerostin and Dkk1, two extracellular inhibitors of Wnt/β-catenin signalling, with carotid intima-media thickness (CIMT) and with arterial stiffness, evaluated by measuring the pulse wave velocity (PWV) in an ambulatory population of adults. To this aim, 67 subjects were recruited in the 'Atherosclerosis and osteoporosis: identification of common pathogenetic factors' investigation. Serum sclerostin levels correlated positively with CIMT (r=0.314, p=0.03) and inversely with the augmentation index, a marker of arterial stiffness (r=-0.286, p

Osteoporosis and atherosclerosis are two chronic degenerative diseases that share several biochemical pathways and risk factors. Previous studies have associated osteoporosis with carotid atherosclerosis, cardiovascular mortality and stroke, but data on the relationship with peripheral artery disease are few and conflicting. The OPG/RANK/RANKL system and Wnt/beta catenin signaling seem to be deeply involved in the pathogenesis of bone alterations and atherosclerotic processes also affect arteries of the lower extremities. Hypovitaminosis D could also play a role in the relationship of these two diseases. New and larger studies are necessary to shed light on this association and to design new drugs able to act in both these chronic degenerative diseases.

Thalassemia major is a common cause of skeletal morbidity, as shown by the increased fracture risk in thalassemic patients. The etiology of this bone disease is multifactorial and culminates in a state of increased bone turnover with excessive bone resorption and remodeling. Despite hormonal replacement therapy, calcium and vitamin D administration, effective iron chelation, and normalization of hemoglobin levels, patients with thalassemia major continue to lose bone mass. The increased bone turnover rate observed in thalassemic patients justifies the use of powerful anti-resorption drugs, such as bisphosphonates. To date, alendronate, pamidronate, and zoledronate seem to be effective in increasing bone mineral density and normalizing bone turnover, but more trials are necessary to evaluate their efficacy in reducing fracture risks in larger thalassemic populations.