“…In general, excessive bone marrow adipogenesis and the presence of advanced glycation products that are toxic to the bone cells in DM are bad for bone health [ 116 ]. However, the BMD phenotypes diverge between Type 1 and 2 DM [ 117 , 118 , 119 ]. Type 1 DM is associated with low BMD, probably due to the lack of bone anabolic signals from insulin; Type 2 DM is often associated with increased BMD due to increased circulating insulin and leptin, which provide anabolic signals to osteoblasts.…”
Osteoporosis refers to excessive bone loss as reflected by the deterioration of bone mass and microarchitecture, which compromises bone strength. It is a complex multifactorial endocrine disease. Its pathogenesis relies on the presence of several endogenous and exogenous risk factors, which skew the physiological bone remodelling to a more catabolic process that results in net bone loss. This review aims to provide an overview of osteoporosis from its biology, epidemiology and clinical aspects (detection and pharmacological management). The review will serve as an updated reference for readers to understand the basics of osteoporosis and take action to prevent and manage this disease.
“…In general, excessive bone marrow adipogenesis and the presence of advanced glycation products that are toxic to the bone cells in DM are bad for bone health [ 116 ]. However, the BMD phenotypes diverge between Type 1 and 2 DM [ 117 , 118 , 119 ]. Type 1 DM is associated with low BMD, probably due to the lack of bone anabolic signals from insulin; Type 2 DM is often associated with increased BMD due to increased circulating insulin and leptin, which provide anabolic signals to osteoblasts.…”
Osteoporosis refers to excessive bone loss as reflected by the deterioration of bone mass and microarchitecture, which compromises bone strength. It is a complex multifactorial endocrine disease. Its pathogenesis relies on the presence of several endogenous and exogenous risk factors, which skew the physiological bone remodelling to a more catabolic process that results in net bone loss. This review aims to provide an overview of osteoporosis from its biology, epidemiology and clinical aspects (detection and pharmacological management). The review will serve as an updated reference for readers to understand the basics of osteoporosis and take action to prevent and manage this disease.
“…Data regarding the age of onset of osteopenia in patients with T1DM are conflicting, as studies show low Z-scores in children and young adults, but no differences in adults with T1DM in comparison to nondiabetics. A recent meta-analysis showed a significant reduction of BMD in children with T1DM[ 22 ]. Normalization of BMD or bone size over time in patients with T1DM is seen in longitudinal studies.…”
The risk of fracture is increased in both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). However, in contrast to the former, patients with T2DM usually possess higher bone mineral density. Thus, there is a considerable difference in the pathophysiological basis of poor bone health between the two types of diabetes. Impaired bone strength due to poor bone microarchitecture and low bone turnover along with increased risk of fall are among the major factors behind elevated fracture risk. Moreover, some antidiabetic medications further enhance the fragility of the bone. On the other hand, antiosteoporosis medications can affect the glucose homeostasis in these patients. It is also difficult to predict the fracture risk in these patients because conventional tools such as bone mineral density and Fracture Risk Assessment Tool score assessment can underestimate the risk. Evidence-based recommendations for risk evaluation and management of poor bone health in diabetes are sparse in the literature. With the advancement in imaging technology, newer modalities are available to evaluate the bone quality and risk assessment in patients with diabetes. The purpose of this review is to explore the pathophysiology behind poor bone health in diabetic patients. Approach to the fracture risk evaluation in both T1DM and T2DM as well as the pragmatic use and efficacy of the available treatment options have been discussed in depth.
“…In adults, the evidence for an adverse impact of T1DM on bone mass, bone architecture, and bone strength is compelling. In contrast, results in children are conflicting: a meta-analysis [11] including 9 studies in children with T1DM showed a lower BMD Z -score in 5 [12-16], whereas 4 studies did not show any difference in BMD [17-20]. Another systematic review including 25 studies showed that the influence of T1DM was related to gender and younger age of disease onset (i.e., below 20 years) and that the impact of T1DM was beyond that expected for known age- and gender disparities in healthy controls [6].…”
This paper gives an overview of the impact of type 1 diabetes on bone health in children and adolescents. First, we analyse studies using DXA (dual x-ray absorptiometry) to assess BMC (bone mineral content) and BMD (bone mineral density). Then, we discuss modern, non-invasive techniques including pQCT (peripheral quantitative computer tomography) and HRpQCT (high-resolution peripheral quantitative computer tomography) for the detailed assessment of bone health aspects including bone mass, bone geometry, bone microarchitecture and bone strength. Thereafter, we explore some of the mechanisms that are responsible for diabetic bone disease in children, like low bone turnover and high sclerostin levels. Finally, we summarise some of the evidence for the importance of microvascular disease in the pathophysiology of diabetic bone disease.
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