MECHANISMS IN ENDOCRINOLOGY: Mechanisms and evaluation of bone fragility in type 1 diabetes mellitus

Hough, F. S.; Pierroz, Dominique D.; Cooper, Cyrus; Ferrari, Serge; _, _

doi:10.1530/eje-15-0820

Cited by 127 publications

(109 citation statements)

References 122 publications

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“…Thus, in male with T1DM, a statistically significant increase in the level of b-CTx (P < 0.05) was observed in comparison with the control group, which indicates an increased bone resorption in this group. Similar results were obtained in number of other authors' studies [4,6]. The propensity to low-traumatic fractures in diabetes is associated with changes in the quality of the organic component of bone tissue, under the influence of glycosylation processes of proteins acting on the metabolism of bone tissue and its strength, changing the processes of osteoblastogenesis and osteoclastogenesis [9,10].…”

Section: Discussionsupporting

confidence: 82%

“…A number of studies have also demonstrated a divergence in the processes of bone formation in diabetes [4,6]. One possible explanation for this discrepancy may be that different markers of bone formation reflect different stages of osteoblast differentiation.…”

Section: Discussionmentioning

confidence: 99%

“…Additional factors for diabetic osteopenia may be an abnormality of blood circulation in the bone with micro-and macroangiopathy and a decrease in the mechanical stress on the bone associated with polyneuropathy and myopathy [6]. Another cause of diabetic osteopenia in type 1 diabetes mellitus (T1DM) is the accumulation of low peak bone mass during puberty, in part due to osteoblast dysfunction, partly related to the need for diet and physical activity.…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of Bone Turnover in Patients With Type 1 Diabetes Mellitus

Safarova¹

2018

J Endocrinol Metab

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Evaluation of Bone Turnover in Patients With Type 1 Diabetes Mellitus

Safarova¹

2018

J Endocrinol Metab

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confidence: 99%

Diabetes and Bone

Ferrari

2017

Calcif Tissue Int

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only begin to be understood and have not yet been fully integrated [1,2]. In particular, the relative contribution of altered bone microstructure and material properties versus bone mass in diabetes-related fractures has not yet been unequivocably proven. An intriguing question is whether there is really increased cortical porosity in diabetes, and if so, what are the mechanisms involved in consideration of the fact that poor glucose control has been associated with lower, rather than higher, bone turnover. Even more intriguing are recent reports suggesting that the bone alterations in diabetes are more prominent among subjects with microvascular complications, suggesting that impairment of vascularization to the skeleton, in particular osteoblasts and osteocytes, could play an important role in the pathophysiology of bone fragility in diabetes. The relative paucity of bone biopsy studies in this area certainly does not help clarify whether bone fragility in diabetes is the expression of alterations that mirror those found in common osteoporosis, albeit perhaps in different proportions (bone quality changes disproportionately greater than bone mineral mass changes)-in which case we could qualify this bone fragility as "diabetoporosis (DIO)," by analogy to "GIOP," or whether specific alterations in the bone/bone marrow of diabetic patients occur that are not found in common osteoporosis, in which case we should call this type of bone fragility "diabetic bone disease (DBD)," by analogy to CKD-MBD. Another key question is regarding the role of osteocytes in this disorder, as they are involved in both the control of bone modeling and remodeling and in glucose homeostasis.From a clinical standpoint, there are many challenges as well. Both aBMD and FRAX underestimate fracture prediction in diabetic patients, particularly with type 2, and the addition of TBS brings only a marginal improvement to this evaluation. Hence, new clinical tools and adjusted Diabetes and osteoporosis are two of the most common chronic disorders which prevalence increases worldwide, eventually affecting hundreds of millions of people. The environmental, primarily nutritional, conditions that predispose to diabetes and osteoporosis, respectively, appear quite different, but there may be some common genetic factors predisposing to both disorders. Although the morphotype of subjects developing type 2 diabetes as a consequence of overweight and the metabolic syndrome seems protective against fractures, and is certainly far from the image of the frail elderly with bone fragility, type 2 diabetes is increasingly recognized as an independent risk factor for fractures-at least in the bone community, although not yet broadly recognized as a complication of glucose impairment in the diabetes community. The risk of fragility fractures is even higher among the leaner patients with type 1 diabetes, whose long-standing disease is associated with an up to fivefold higher hip fracture risk, which incidence starts to rise 10-15 years before the exponential rise...

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“…BMP-2 is composed of two peptides, including the 147 amino acids. One of the main biological activities of BMP-2 is to regulate embryonic development and induce osteogenesis [11]. In addition, BMP-2 can affect the fracture repair ability [12].…”

Section: Discussionmentioning

confidence: 99%

Angelica facilitates fracture healing by promoting juvenile rat bone marrow stem cells proliferation

Zheng¹,

Zhou²,

Liu³

2018

biomedicalresearch

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Objective: To investigate the impact of Angelica on promoting juvenile rat fracture healing and Bone Marrow Stem Cells (BMSCs) proliferation. Patients and methods: A total of 30 juvenile rats were selected to establish bilateral tibia fracture model and then randomly divided into Angelica group and the control. The rats in Angelica group were fixed with plaster and received Angelica lavage every day. X-ray was used to observe tibia fracture. Bone Morphogenetic Protein 2 (BMP-2) expression at the fracture was tested by in situ hybridization. BMSCs were separated upon density gradient method and divided into Angelica group and the control group.Cell proliferation was evaluated by MTT assay. Supernatant VEGF protein concentration was detected by ELSIA assay. Results: At the first week after modeling, callus formation was found in Angelica group but not control. At the second week, the fracture in Angelica group was completely filled by callus. At the fourth week, the fracture exhibited cortical bone reconstruction and the medullary cavity recanalization in Angelica group. X-ray macroscopic observation score in Angelica group was higher than control. BMP-2 mRNA level significantly increased in Angelica group compared with control. In addition, BMSCs proliferation in Angelica group was obviously higher than that in control. VEGF protein concentration in the supernatant markedly elevated in Angelica group compared with control. Conclusions: Angelica can facilitate juvenile rat fracture healing by stimulating BMSCs proliferation and upregulating VEGF protein expression.

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MECHANISMS IN ENDOCRINOLOGY: Mechanisms and evaluation of bone fragility in type 1 diabetes mellitus

Cited by 127 publications

References 122 publications

Evaluation of Bone Turnover in Patients With Type 1 Diabetes Mellitus

Evaluation of Bone Turnover in Patients With Type 1 Diabetes Mellitus

Diabetes and Bone

Angelica facilitates fracture healing by promoting juvenile rat bone marrow stem cells proliferation

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