Individuals with diabetes mellitus type 2 (T2DM) have an increased risk of hip fracture, especially if vascular complications are present. However, microstructural origins of increased bone fragility in T2DM are still controversial. DXA measurement of the contralateral hip and three-dimensional microCT analyses of femoral neck trabecular microarchitecture were performed in 32 individuals (26 women and 6 men, 78 ± 7 years). The specimens were divided to two groups: T2DM individuals with hip fracture (DMFx, n = 18) and healthy controls (CTL, n = 14). DMFx group consisted of individuals with vascular complications (DMFx_VD, n = 8) and those without vascular complications (DMFx_NVD, n = 10). T-score was significantly lower in DMFx_VD and DMFx_NVD than in controls (p < 0.001). BV/TV, Tb.N, Tb.Sp, SMI, and FD varied among DMFx_NVD, DMFx_VD, and CTL groups (p = 0.023, p = 0.004, p = 0.008, p = 0.001, p = 0.007, respectively). Specifically, BV/TV of DMFx_VD was significantly lower than that of DMFx_NVD group (p = 0.020); DMFx_NVD group had higher Tb.N and lower Tb.Sp compared with DMFx_VD (p = 0.006, p = 0.012, respectively) and CTL (p = 0.026, p = 0.035, respectively). DMFx group and healthy controls showed similar BV/TV, Tb.Th, Tb.N, Tb.Sp, Conn.D, DA, and FD (p = 0.771, p = 0.503, p = 0.285, p = 0.266, p = 0.208, p = 0.235, p = 0.688, respectively), while SMI was significantly higher in controls (p = 0.005). Two distinct phenotypes of bone fragility were identified in T2DM patients: patients with vascular complications showed impaired trabecular microarchitecture, whereas bone fragility in the group without vascular complications was independent on trabecular microarchitecture pattern. Such heterogeneity among T2DM patients may explain contradicting literature data and may set a basis for further studies to evaluate fracture risk related to T2DM.

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Individuals with diabetes mellitus type 2 (T2DM) have approximately 30% increased risk of hip fracture; however, the main cause of the elevated fracture risk in those subjects remains unclear. Moreover, micromechanical and microarchitectural properties of the superolateral femoral neck—the common fracture-initiating site—are still unknown. We collected proximal femora of 16 men (eight with T2DM and eight controls; age: 61 ± 10 years) at autopsy. After performing post-mortem bone densitometry (DXA), the superolateral neck was excised and scanned with microcomputed tomography (microCT). We also conducted Vickers microindentation testing. T2DM and control subjects did not differ in age ( p = 0.605), body mass index ( p = 0.114), and femoral neck bone mineral density (BMD) ( p = 0.841). Cortical porosity (Ct.Po) was higher and cortical thickness (Ct.Th) was lower in T2DM ( p = 0.044, p = 0.007, respectively). Of trabecular microarchitectural parameters, only structure model index ( p = 0.022) was significantly different between T2DM subjects and controls. Control group showed higher cortical ( p = 0.002) and trabecular bone microhardness ( p = 0.005). Increased Ct.Po and decreased Ct.Th in T2DM subjects increase the propensity to femoral neck fracture. Apart from the deteriorated cortical microarchitecture, decreased cortical and trabecular microhardness suggests altered bone composition of the superolateral femoral neck cortex and trabeculae in T2DM. Significantly deteriorated cortical microarchitecture of the superolateral femoral neck is not recognized by standard DXA measurement of the femoral neck.

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