Increased cortical porosity in type 2 diabetic postmenopausal women with fragility fractures
Janina M. Patsch,Andrew J. Burghardt,Samuel P. Yap,Thomas Baum,Ann V. Schwartz,Gabby B. Joseph,Thomas M. Link +6 more
TLDR
It is suggested that severe deficits in cortical bone quality are responsible for fragility fractures in postmenopausal diabetic women.Abstract:
The primary goal of this study was to assess peripheral bone microarchitecture and strength in postmenopausal women with type 2 diabetes with fragility fractures (DMFx) and to compare them with postmenopausal women with type 2 diabetics without fractures (DM). Secondary goals were to assess differences in nondiabetic postmenopausal women with fragility fractures (Fx) and nondiabetic postmenopausal women without fragility fractures (Co), and in DM and Co women. Eighty women (mean age 61.3 ± 5.7 years) were recruited into these four groups (DMFx, DM, Fx, and Co; n = 20 per group). Participants underwent dual-energy X-ray absorptiometry (DXA) and high-resolution peripheral quantitative computed tomography (HR-pQCT) of the ultradistal and distal radius and tibia. In the HR-pQCT images volumetric bone mineral density and cortical and trabecular structure measures, including cortical porosity, were calculated. Bone strength was estimated using micro–finite element analysis (µFEA). Differential strength estimates were obtained with and without open cortical pores. At the ultradistal and distal tibia, DMFx had greater intracortical pore volume (+52.6%, p = 0.009; +95.4%, p = 0.020), relative porosity (+58.1%, p = 0.005; +87.9%, p = 0.011) and endocortical bone surface (+10.9%, p = 0.031; +11.5%, p = 0.019) than DM. At the distal radius DMFx had 4.7-fold greater relative porosity (p < 0.0001) than DM. At the ultradistal radius, intracortical pore volume was significantly higher in DMFx than DM (+67.8%, p = 0.018). DMFx also displayed larger trabecular heterogeneity (ultradistal radius: +36.8%, p = 0.035), and lower total and cortical BMD (ultradistal tibia: −12.6%, p = 0.031; −6.8%, p = 0.011) than DM. DMFx exhibited significantly higher pore-related deficits in stiffness, failure load, and cortical load fraction at the ultradistal and distal tibia, and the distal radius than DM. Comparing nondiabetic Fx and Co, we only found a nonsignificant trend with increase in pore volume (+38.9%, p = 0.060) at the ultradistal radius. The results of our study suggest that severe deficits in cortical bone quality are responsible for fragility fractures in postmenopausal diabetic women. © 2013 American Society for Bone and Mineral Researchread more
Citations
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Mechanisms of diabetes mellitus-induced bone fragility
TL;DR: Factors including treatment-induced hypoglycaemia, certain antidiabetic medications with a direct effect on bone and mineral metabolism, as well as an increased propensity for falls, all contribute to the increased fracture risk in patients with diabetes mellitus.
Journal ArticleDOI
In vivo assessment of bone quality in postmenopausal women with type 2 diabetes.
Joshua N. Farr,Matthew M Drake,Shreyasee Amin,L. Joseph Melton,Louise K. McCready,Sundeep Khosla +5 more
TL;DR: In vivo microindentation testing of the tibia is performed to directly measure bone microarchitecture in 60 postmenopausal women to represent the first demonstration of compromised BMS in patients with T2D and highlight the potential detrimental effects of prolonged hyperglycemia on bone quality.
Journal ArticleDOI
Establishing biomechanical mechanisms in mouse models: practical guidelines for systematically evaluating phenotypic changes in the diaphyses of long bones.
Karl J. Jepsen,Matthew J. Silva,Deepak Vashishth,X. Edward Guo,Marjolein C. H. van der Meulen +4 more
TL;DR: A comprehensive framework is presented using real data, and several examples from the literature are reviewed to illustrate how to synthesize morphological, tissue‐level, and whole‐bone mechanical properties of mouse long bones.
Journal ArticleDOI
Diagnosis and management of bone fragility in diabetes: an emerging challenge
Serge Ferrari,Bo Abrahamsen,Nicola Napoli,Nicola Napoli,Kristina Åkesson,Manju Chandran,R. Eastell,G. El-Hajj Fuleihan,Robert G. Josse,Robert G. Josse,David L. Kendler,Marius E. Kraenzlin,Atsushi Suzuki,D. D. Pierroz,Ann V. Schwartz,William D. Leslie +15 more
TL;DR: An algorithm is proposed for the identification and management of diabetic patients at increased fracture risk and the impact of diabetes drugs on bone as well as the efficacy of osteoporosis treatments in this population of adults with diabetes.
Journal ArticleDOI
The bone–fat interface: basic and clinical implications of marrow adiposity
TL;DR: Understanding of the relationship between bone and fat cells that arise from the same progenitor within the bone marrow niche provides insight into the pathophysiology of age-related osteoporosis, diabetes, and obesity.
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