MON-352 Contributions of Skeletal Microarchitecture and Fall Risk to Fractures in Adults with Long-standing Type 1 Diabetes Mellitus

Abstract L.A. Marion: None. A.I. Fremaint: None. F. Johannesdottir: None. E. Cagliero: None. V.R. Aroda: None. M.L. Bouxsein: None. E.W. Yu: Grant Recipient; Self; Amgen Inc. Introduction: Type 1 diabetes mellitus (T1D) is associated with a marked increase in fracture risk, a phenomenon not entirely explained by lower DXA-measured BMD. Recent studies suggest that T1D may lead to deficits in bone microarchitecture, but results are inconsistent. Whether the heightened fracture risk in T1D is driven by mechanisms primarily intrinsic to bone or extrinsic remains unknown. Thus, our objective was to assess fracture history, falls and bone microarchitecture in adults with long-standing T1D. Methods: We recruited 97 individuals with T1D and 53 non-diabetic controls aged ≥50 years as part of the T1D Bone Health Connection (BEACON) Study, an ongoing prospective observational cohort study enrolling from the greater Boston area. We measured DXA-BMD of the spine, femoral neck, and total hip, as well as volumetric BMD (vBMD), bone microarchitecture and estimated bone strength by high-resolution peripheral quantitative computed tomography (HRpQCT) at the 4% distal radius (R4), 7% distal tibia (T7) and 30% diaphyseal tibia (T30). We also assessed self-reported prevalent fractures and recent falls. We used linear regression models with adjustments for age, sex, height and weight to analyze group differences in bone parameters as well as multivariate logistic regression to assess independent associations between variables of interest and binary outcomes. RESULTS: Mean age of the full cohort (n=150) was 64±7 years; 51% were women. T1D and control groups were similar in age (p=0.20) and sex distribution (p=0.46), though T1D subjects had a higher mean BMI (27.9±5.0 vs 26.0±4.9 kg/m2, p=0.03). T1D subjects (mean disease duration 46±10 years, HbA1c 7.1±1.0%) reported a higher prevalence of fractures compared to controls (39% vs 6%, p<0.001). DXA-BMD did not differ between the two groups at any site, though T1D participants had lower cortical vBMD at T7 (-5.5%, p <0.001) and lower cortical area (-5.4%, p=0.008) and thickness (-4.9%, p=0.02) at T30. Unexpectedly, T1D subjects had higher trabecular thickness at T7 (+3.5%, p=0.008). Failure loads at T7 and R4 were similar between T1D and controls. While there were no intergroup differences in the proportion of individuals who had ≥1 fall in the past year (19% vs 13%, p=0.40), among those who fell, T1D subjects reported a higher fall frequency than controls (median 2 vs 1 fall/person, p=0.045). A fall in the past year was associated with higher odds of prevalent fracture [OR 4.9 (95% CI 1.8-13.8)]. Conclusion: This study highlights the increased fracture risk in adults ≥50 years with T1D. Differences in fall risk and deficits in cortical microarchitecture may contribute to fractures in T1D. Although we observed minor differences in bone microarchitecture in our cohort, these did not impact peripheral bone strength. Further studies are needed to elucidate the precise mechanisms for the increased fracture susceptibility in this population. Monday, June 3, 2024