Individuals with type 2 diabetes mellitus (T2DM) have an increased risk of bone fragility fractures compared to nondiabetic subjects. This increased fracture risk may occur despite normal or even increased values of bone mineral density (BMD), and poor bone quality is suggested to contribute to skeletal fragility in this population. These concepts explain why the only evaluation of BMD could not be considered an adequate tool for evaluating the risk of fracture in the individual T2DM patient. Unfortunately, nowadays, the bone quality could not be reliably evaluated in the routine clinical practice. On the other hand, getting further insight on the pathogenesis of T2DM-related bone fragility could consent to ameliorate both the detection of the patients at risk for fracture and their appropriate treatment. The pathophysiological mechanisms underlying the increased risk of fragility fractures in a T2DM population are complex. Indeed, in T2DM, bone health is negatively affected by several factors, such as inflammatory cytokines, muscle-derived hormones, incretins, hydrogen sulfide (H2S) production and cortisol secretion, peripheral activation, and sensitivity. All these factors may alter bone formation and resorption, collagen formation, and bone marrow adiposity, ultimately leading to reduced bone strength. Additional factors such as hypoglycemia and the consequent increased propensity for falls and the direct effects on bone and mineral metabolism of certain antidiabetic medications may contribute to the increased fracture risk in this population. The purpose of this review is to summarize the literature evidence that faces the pathophysiological mechanisms underlying bone fragility in T2DM patients.

The two-dimensional strain allows the assessment of carotid arterial mechanics. Probably the assessment of arterial stiffness allows a better risk stratification of patients.

Introduction Aromatase inhibitors (AIs) dramatically increased breast cancer (BC) survival, leading to enhanced attention to their long-term consequences on psychological functioning. Conflicting data has been examined regarding the association between AIs administration and the clinical psychological features in BC survivors (BCSs). Purpose As psychological symptoms often occur in such chronic diseases, our study aimed at exploring anxious and depressive symptoms and the perceived quality of life (QoL) in BCSs assessed for osteoporosis. Methods The total sample consisted of a clinical sample of 51 outpatient postmenopausal women, diagnosed with BC, and a control group composed of 51 healthy postmenopausal women. All recruited participants were evaluated through the clinical gold standard interview and completed the following self-rating scales: the Hamilton Anxiety Rating Scale, Beck Depression Inventory II edition, and 36-Item Short Form Health Survey, which were administered at baseline and after 6 months in BCSs in AIs treatment, compared with controls. Moreover, all participants were assessed for vitamin D status, bone mineral density (BMD) and subclinical vertebral fractures. Data regarding age, age at menopause, body mass index (BMI), smoking habits and alcohol consumption was collected.

Background: This systematic review analyzed the relationship between alexithymia, considered as the inability to recognize and express thoughts and emotions, and type 2 diabetes mellitus (T2DM), one of the most common chronic illness, characterized by a metabolic disorder burdened by high morbidity and mortality worldwide due to its outcomes. Methods: PRISMA guidelines were followed throughout this systematic review of the recent literature indexed in the databases PubMed, PsycInfo, Scopus, and Web of Science. Search terms for eligible studies were: “Type 2 diabetes” OR “T2DM” AND “Toronto Alexithymia Scale” OR “TAS-20”[All Fields]. Results: The initial search identified 61 indexed scientific publications. After screening we found that seven publications met the established scientific inclusion and exclusion criteria. It emerged that alexithymic patients ranged from 25 to 50% across the examined publications and it appeared that patients with T2DM generally reflected greater values of alexithymia, revealing particular differences among TAS domains. Moreover, emlpoyed participants were alexithymic to a greater extent compared to non-working participants (77.8 vs. 35.4%) and alexithymia was 2.63 times more severe among working participants when examining predictors of alexithymia. When evaluating the correlations between alexithymia and HbA1c or fasting blood glucose levels we found strong associations equal to 0.75 and 0.77 for TAS-20 total scores, respectively. While alexithymic participants showed significantly higher levels of HbA1c and blood glucose when compared to the non-alexithymic participants. Conclusions: The results of this systematic review of the current literature highlight the need of alexithymia evaluation in patients with T2DM. The high prevalence in T2DM and strong associations with poorly regulated diabetes and psychological distress, indicate a significant relationship between poor glycemic control and psychological distress, such as anxiety and depression, and quality of life. Further studies are needed focusing on age and gender differences in order to be able to improve clinical psychological care and prevention.

There is cumulating evidence for a contribution of Wnt signaling pathways in multiple processes involved in atherosclerosis and vascular aging. Wnt signaling plays a role in endothelial dysfunction, in the proliferation and migration of vascular smooth muscle cells (VSMCs) and intimal thickening. Moreover, it interferes with inflammation processes, monocyte adhesion and migration, as well as with foam cell formation and vascular calcification progression. Sclerostin is a negative regulator of the canonical Wnt signaling pathway and, accordingly, the consequence of increased sclerostin availability can be disruption of the Wnt signalling cascade. Sclerostin is becoming a marker for clinical and subclinical vascular diseases and several lines of evidence illustrate its role in the pathophysiology of the vascular system. Sclerostin levels increase with aging and persist higher in some diseases (e.g., diabetes, chronic kidney disease) that are known to precipitate atherosclerosis and enhance cardiovascular risk. Current knowledge on the association between sclerostin and vascular diseases is summarized in this review.