Epidemiology of fractures in type 2 diabetes

Schwartz, Ann V.

doi:10.1016/j.bone.2015.05.032

Cited by 72 publications

(64 citation statements)

References 86 publications

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“…The mechanisms by which such impairments occur remain unclear, but long-term exposure to high glucose levels in patients with T2DM may lead to decreased bone remodelling which, in turn, may lead to structural deterioration. This could explain the well-documented higher risk for fracture despite preservation or an increase in BMD in patients with type 2 diabetes [1–3, 13, 14]. We have studied whether high glucose alone or, with the addition of AGEs in the primary culture of osteoblast-like cells (hOB) from diabetic patients, is able to promote changes in the proliferation, differentiation and/or function of these cells as a possible explanation for bone fragility in T2DM patients.…”

Section: Discussionmentioning

confidence: 99%

“…Diabetes-related complications (retinopathy, neuropathy, kidney diseases, or vascular damages) may alter skeletal bone remodelling, since they impose a direct effect on bone strength and/or the probability of falls, thus increase the risk of fractures. Other aspects of diabetes, such as high levels of AGEs in bone collagen and/or hyperglycaemia in bone microenvironments, have also been considered as triggers to increased bone fragility [3]. Although many factors have been proposed, very few studies have analyzed the importance of each factor and the intimate mechanism of action on the deterioration of bone metabolism.…”

Section: Introductionmentioning

confidence: 99%

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Influence of high glucose and advanced glycation end-products (ages) levels in human osteoblast-like cells gene expression

Miranda

Giner

Montoya

et al. 2016

BMC Musculoskelet Disord

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BackgroundType 2 diabetes mellitus (T2DM) is associated with an increased risk of osteoporotic fracture. Several factors have been identified as being potentially responsible for this risk, such as alterations in bone remodelling that may have been induced by changes in circulating glucose or/and by the presence of non-oxidative end products of glycosylation (AGEs). The aim of this study is to assess whether such variations generate a change in the gene expression related to the differentiation and osteoblast activity (OPG, RANKL, RUNX2, OSTERIX, and AGE receptor) in primary cultures of human osteoblast-like cells (hOB).MethodsWe recruited 32 patients; 10 patients had osteoporotic hip fractures (OP group), 12 patients had osteoporotic hip fractures with T2DM (T2DM group), and 10 patients had hip osteoarthritis (OA group) with no osteoporotic fractures and no T2DM. The gene expression was analyzed in hOB cultures treated with physiological glucose concentration (4.5 mM) as control, high glucose (25 mM), and high glucose plus AGEs (2 μg/ml) for 24 h.ResultsThe hOB cultures from patients with hip fractures presented slower proliferation. Additionally, the hOB cultures from the T2DM group were the most negatively affected with respect to RUNX2 and OSX gene expression when treated solely with high glucose or with high glucose plus AGEs. Moreover, high levels of glucose induced a major decrease in the RANKL/OPG ratio when comparing the OP and the T2DM groups to the OA group.ConclusionsOur data indicates an altered bone remodelling rate in the T2DM group, which may, at least partially, explain the reduced bone strength and increased incidence of non-traumatic fractures in diabetic patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Influence of high glucose and advanced glycation end-products (ages) levels in human osteoblast-like cells gene expression

Miranda

Giner

Montoya

et al. 2016

BMC Musculoskelet Disord

View full text Add to dashboard Cite

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“…The markedly increased fracture rate in patients with Type 1 (T1D) and Type 2 (T2D) diabetes mellitus, despite in most cases, normal bone mineral density, has led to substantial efforts to explain the pathophysiologic basis for the development of this unique but important diabetic complication [1]. On the other hand, this manifestation also has provided investigators with evidence of a close link between bone and energy metabolism.…”

Section: Introductionmentioning

confidence: 99%

Skeletal integration of energy homeostasis: Translational implications

Lecka‐Czernik

Rosen

2016

Bone

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New evidence has recently emerged defining a close relationship between fat and bone metabolism. Adipose tissue is one of the largest organs in the body but its functions vary by location and origin. Adipocytes can act in an autocrine manner to regulate energy balance by sequestering triglycerides and then, depending on demand, releasing fatty acids through lipolysis for energy utilization, and in some cases through uncoupling protein 1 for generating heat. Adipose tissue can also act in an endocrine or paracrine manner by releasing adipokines that modulate the function of other organs. Bone is one of those target tissues, although recent evidence has emerged that the skeleton reciprocates by releasing its own factors that modulate adipose tissue and beta cells in the pancreas. Therefore, it is not surprising that these energy-modulating tissues are controlled by a central regulatory mechanism, primarily the sympathetic nervous system. Disruption in this complex regulatory circuit and its downstream tissues is manifested in a wide range of metabolic disorders, for which the most prevalent is type 2 diabetes mellitus. The aim of this review is to summarize our knowledge of common determinants in the bone and adipose function and the translational implications of recent work in this emerging field.

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“…Two logical candidates include diabetes mellitus, and osteoarthritis. Diabetes is recognized to have adverse consequences upon bone and muscle [40,41] and to increase fracture risk above that predicted by FRAX [42]. Similarly, some studies find osteoarthritis to be associated with increased risk for falls and fractures [43,44].…”

Section: оригінальні дослідження / Original Researchesmentioning

confidence: 99%

Синдром Дисмобільності: Зміна Парадигми В Царині Профілактики Переломів

Binkley

Krueger

2021

PJS

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Abstract. Fragility fractures engender major healthcare cost, reduce independence/quality and life and increase mortality risk. Despite availability of multiple therapies to reduce risk for future fracture, few patients are treated even following hip fracture. Clearly, approaches of the past aimed at reducing fragility fracture risk, primarily by diagnosing osteoporosis and initiating bone-active medications, have failed. A di erent approach is required; such a change in focus is proposed here. Brie y, the dysmobility syndrome concept recognizes fragility fracture as the clinical outcome of consequence and appreciates that osteoporosis is only part of the syndrome leading to "osteoporosis-related" fracture. Other components of this syndrome include sarcopenia, obesity, diabetes, osteoarthritis, and potentially multiple other factors that increase risk for falls with attendant increased fracture risk. In summary, the dysmobility syndrome concept moves the eld, and also, importantly, older adults at risk for fragility fracture, beyond a singular focus on bone to more appropriately focus on a holistic approach to fracture risk reduction.

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Epidemiology of fractures in type 2 diabetes

Cited by 72 publications

References 86 publications

Influence of high glucose and advanced glycation end-products (ages) levels in human osteoblast-like cells gene expression

Influence of high glucose and advanced glycation end-products (ages) levels in human osteoblast-like cells gene expression

Skeletal integration of energy homeostasis: Translational implications

Синдром Дисмобільності: Зміна Парадигми В Царині Профілактики Переломів

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