Individuals with type 2 diabetes mellitus show dimorphic and heterogeneous patterns of loss in femoral bone quality

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Individuals with type 2 diabetes mellitus show dimorphic and heterogeneous patterns of loss in femoral bone quality. / Wölfel, Eva M; Jähn-Rickert, Katharina; Schmidt, Felix N; Wulff, Birgit; Mushumba, Herbert; Sroga, Grazyna E; Püschel, Klaus; Milovanovic, Petar; Amling, Michael; Campbell, Graeme M; Vashishth, Deepak; Busse, Björn.

In: BONE, Vol. 140, 11.2020, p. 115556.

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@article{629463c11492419b838fad6228c4c3e7,
title = "Individuals with type 2 diabetes mellitus show dimorphic and heterogeneous patterns of loss in femoral bone quality",
abstract = "Type 2 diabetes mellitus (T2DM), a metabolic disease on the rise, is associated with substantial increase in bone fracture risk. Because individuals with T2DM have normal or high bone mineral density (BMD), osteodensitometric measurements of BMD do not predict fracture risk with T2DM. Here, we aim to identify the underlying mechanism of the diabetes-induced fracture risk using a high-resolution multi-scale analysis of human cortical bone with special emphasis on osseous cellular activity. Specifically, we show increased cortical porosity in a subgroup of T2DM individuals accompanied by changed mineralization patterns and glycoxidative damage to bone protein, caused by non-enzymatic glycation of bone by reducing sugar. Furthermore, the high porosity T2DM subgroup presents with higher regional mineralization heterogeneity and lower mineral maturity, whereas in the T2DM subgroup regional higher mineral-to-matrix ratio was observed. Both T2DM groups show significantly higher carboxymethyl-lysine accumulation. Our results show a dimorphic pattern of cortical bone reorganization in individuals afflicted with T2DM and hence provide new insight into the diabetic bone disease leading to increased fracture risk.",
author = "W{\"o}lfel, {Eva M} and Katharina J{\"a}hn-Rickert and Schmidt, {Felix N} and Birgit Wulff and Herbert Mushumba and Sroga, {Grazyna E} and Klaus P{\"u}schel and Petar Milovanovic and Michael Amling and Campbell, {Graeme M} and Deepak Vashishth and Bj{\"o}rn Busse",
year = "2020",
month = nov,
doi = "10.1016/j.bone.2020.115556",
language = "English",
volume = "140",
pages = "115556",
journal = "BONE",
issn = "8756-3282",
publisher = "Elsevier Inc.",

}

RIS

TY - JOUR

T1 - Individuals with type 2 diabetes mellitus show dimorphic and heterogeneous patterns of loss in femoral bone quality

AU - Wölfel, Eva M

AU - Jähn-Rickert, Katharina

AU - Schmidt, Felix N

AU - Wulff, Birgit

AU - Mushumba, Herbert

AU - Sroga, Grazyna E

AU - Püschel, Klaus

AU - Milovanovic, Petar

AU - Amling, Michael

AU - Campbell, Graeme M

AU - Vashishth, Deepak

AU - Busse, Björn

PY - 2020/11

Y1 - 2020/11

N2 - Type 2 diabetes mellitus (T2DM), a metabolic disease on the rise, is associated with substantial increase in bone fracture risk. Because individuals with T2DM have normal or high bone mineral density (BMD), osteodensitometric measurements of BMD do not predict fracture risk with T2DM. Here, we aim to identify the underlying mechanism of the diabetes-induced fracture risk using a high-resolution multi-scale analysis of human cortical bone with special emphasis on osseous cellular activity. Specifically, we show increased cortical porosity in a subgroup of T2DM individuals accompanied by changed mineralization patterns and glycoxidative damage to bone protein, caused by non-enzymatic glycation of bone by reducing sugar. Furthermore, the high porosity T2DM subgroup presents with higher regional mineralization heterogeneity and lower mineral maturity, whereas in the T2DM subgroup regional higher mineral-to-matrix ratio was observed. Both T2DM groups show significantly higher carboxymethyl-lysine accumulation. Our results show a dimorphic pattern of cortical bone reorganization in individuals afflicted with T2DM and hence provide new insight into the diabetic bone disease leading to increased fracture risk.

AB - Type 2 diabetes mellitus (T2DM), a metabolic disease on the rise, is associated with substantial increase in bone fracture risk. Because individuals with T2DM have normal or high bone mineral density (BMD), osteodensitometric measurements of BMD do not predict fracture risk with T2DM. Here, we aim to identify the underlying mechanism of the diabetes-induced fracture risk using a high-resolution multi-scale analysis of human cortical bone with special emphasis on osseous cellular activity. Specifically, we show increased cortical porosity in a subgroup of T2DM individuals accompanied by changed mineralization patterns and glycoxidative damage to bone protein, caused by non-enzymatic glycation of bone by reducing sugar. Furthermore, the high porosity T2DM subgroup presents with higher regional mineralization heterogeneity and lower mineral maturity, whereas in the T2DM subgroup regional higher mineral-to-matrix ratio was observed. Both T2DM groups show significantly higher carboxymethyl-lysine accumulation. Our results show a dimorphic pattern of cortical bone reorganization in individuals afflicted with T2DM and hence provide new insight into the diabetic bone disease leading to increased fracture risk.

U2 - 10.1016/j.bone.2020.115556

DO - 10.1016/j.bone.2020.115556

M3 - SCORING: Journal article

C2 - 32730921

VL - 140

SP - 115556

JO - BONE

JF - BONE

SN - 8756-3282

ER -