Abstract
Fracture risk is increased in type 1 diabetes (T1D). Diabetic neuropathy might contribute to this increased risk directly through effects on bone turnover and indirectly through effects on balance, muscle strength, and gait. We compared patients with T1D with (T1DN+, n=20) and without (T1DN-, n=20) distal symmetric sensorimotor polyneuropathy and controls (n=20). We assessed areal bone mineral density (aBMD) and appendicular muscle mass by dual-energy X-ray absorptiometry, microarchitecture by high-resolution peripheral quantitative tomography at the standard ultra-distal site and at an exploratory 14% bone length site at the tibia and radius, bone turnover markers, and muscle strength, gait, and balance by Short Physical Performance Battery (SPPB). At the standard ultra-distal site, tibial cortical porosity was 56% higher in T1DN+ compared with T1DN- (p=.009) and correlated positively with the severity of neuropathy (Toronto Clinical Neuropathy Score; r=0.347, p=.028) and negatively with nerve conduction amplitude and velocity (r=-0.386, p=.015 and r=-0.358, p=.025, respectively). Similar negative correlations were also observed at the radius (r=-0.484, p=.006 and r=-0.446, p=.012, respectively). At the exploratory 14% offset site (less distal), we found higher trabecular volumetric BMD (tibia 25%, p=.024; radius 46%, p=.017), trabecular bone volume (tibia 25%, p=.023; radius 46%, p=.017), and trabecular number (tibia 22%, p=.014; radius 30%, p=.010) in T1DN- compared with controls. Both CTX and PINP were lower in participants with TD1 compared with controls. No difference was found in aBMD and appendicular muscle mass. T1DN+ had worse performance in the SPPB compared with T1DN- and control. In summary, neuropathy was associated with cortical porosity and worse performance in physical tests. Our findings suggest that bone structure does not fully explain the rate of fractures in T1D. We conclude that the increase in the risk of fractures in T1D is multifactorial with both skeletal and non-skeletal contributions. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).
Highlights
Diabetes is a chronic disease characterized by hyperglycemia
In type 1 diabetes (T1D), the hyperglycemia is caused by β-cells autoimmune destruction, leading to insulin deficiency.[1]. Juvenile onset is considered typical of T1D, but people of any age can be affected and up to 50% of cases start in adulthood.[1]. Most people living with T1D are adults.[1]. Diabetic neuropathy is a result of nerve damage and leads to sensory abnormalities.[2]. Diabetic neuropathy can cause negative symptoms such as impaired touch, vibration, pinprick, hot and cold sensation, or positive symptoms such as paradoxical pain and hypersensitivity.[2]. Distal symmetrical sensorimotor polyneuropathy (DSPN) is the most common form of diabetic neuropathy and has a stocking–glove distribution.[2]
Dual-energy X-ray absorptiometry (DXA) can predict fractures in diabetes.[12]. Overall, bone mineral density (BMD) is decreased in people with T1D,(5) but the small decrease in BMD does not explain the magnitude of the increase in the risk of fractures.[5]. Several studies have investigated bone microarchitecture in diabetes using high-resolution peripheral quantitative computed tomography (HR-pQCT).(13–19) Most of the studies have addressed type 2 diabetes (T2D)(14–20) and data on T1D are scarce.[13]. Results are conflicting, and the most common finding was an increase in the cortical porosity reported in T2D(14–18,20) but not in T1D.(13)
Summary
Diabetes is a chronic disease characterized by hyperglycemia. In type 1 diabetes (T1D), the hyperglycemia is caused by β-cells autoimmune destruction, leading to insulin deficiency.[1]. Dual-energy X-ray absorptiometry (DXA) can predict fractures in diabetes.[12] Overall, bone mineral density (BMD) is decreased in people with T1D,(5) but the small decrease in BMD does not explain the magnitude of the increase in the risk of fractures.[5] Several studies have investigated bone microarchitecture in diabetes using high-resolution peripheral quantitative computed tomography (HR-pQCT).(13–19) Most of the studies have addressed T2D(14–20) and data on T1D are scarce.[13] Results are conflicting, and the most common finding was an increase in the cortical porosity reported in T2D(14–18,20) but not in T1D.(13). Some studies have reported differences in microarchitecture associated with diabetic microvascular disease (MVD).(13,14) neuronal regulation of bone metabolism has been described,(21,22) no study has investigated the effect of diabetic neuropathy on the skeleton. The aim of this study is to compare bone structural and biochemical analysis, appendicular muscle mass, and physical function test between adults with T1D diabetes with and without DSPN and controls
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