Abstract
The goal of our study was to investigate interactions between sex and type 2 diabetes mellitus (T2DM) with regard to morphology of the peripheral skeleton. We recruited 85 subjects (mean age, 57±11.4 years): women with and without T2DM (n = 17; n = 16); and men with and without T2DM (n = 26; n = 26). All patients underwent high-resolution, peripheral, quantitative, computed tomography (HR-pQCT) imaging of the ultradistal radius (UR) and tibia (UT). Local bone geometry, bone mineral density (BMD), and bone microarchitecture were obtained by quantitative analysis of HR-pQCT images. To reduce the amount of data and avoid multi-collinearity, we performed a factor-analysis of HR-pQCT parameters. Based on factor weight, trabecular BMD, trabecular number, cortical thickness, cortical BMD, and total area were chosen for post-hoc analyses. At the radius and tibia, diabetic men and women exhibited trabecular hypertrophy, with a significant positive main effect of T2DM on trabecular number. At the radius, cortical thickness was higher in diabetic subjects (+20.1%, p = 0.003). Interestingly, there was a statistical trend that suggested attenuation of tibial cortical hypertrophy in diabetic men (cortical thickness, pinteraction = 0.052). Moreover, we found an expected sexual dichotomy, with higher trabecular BMD, Tb.N, cortical BMD, Ct.Th, and total area in men than in women (p≤ 0.003) at both measurement sites. Our results suggest that skeletal hypertrophy associated with T2DM is present in men and women, but appears attenuated at the tibial cortex in men.
Highlights
Fragility fractures are increasingly recognized as a skeletal secondary complication of type 2 diabetes mellitus (T2DM) [1,2,3,4]
As determined from visual assessment of HR-pQCT scans by a board-certified radiologist (JMP), there were no significant differences between lower leg vascular calcification frequencies in diabetic men (50% with calcifications) and women (42.4% with calcifications, p = 0.607)
We found a trend toward higher cortical bone mineral density (BMD) in subjects with T2DM (+3.6%, p = 0.076)
Summary
Fragility fractures are increasingly recognized as a skeletal secondary complication of type 2 diabetes mellitus (T2DM) [1,2,3,4]. The pathogenesis of diabetic bone disease and associated fragility fractures is not sufficiently understood. Bone mineral density (BMD)—as measured by dual-energy, x-ray absorptiometry (DXA) or quantitative computed tomography (QCT)—is typically high to normal or only mildly reduced in patients with T2DM [6]. Potential explanations for the paradoxical positive association of high BMD and fragility fractures include microarchitectural and matrix-based causes, such as cortical porosity [7, 8], and deposition of advanced glycation end products (AGEs) [9]. Diabetic bone disease is characterized by low bone turnover [10, 11], and there are numerous suggestions of a significant imbalance of the WNT/SOST/PTH pathway, possibly through osteocyte dysfunction [12, 13]
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