Fractures in women with type 2 diabetes are associated with marked deficits in cortical parameters and trabecular plates.

The basis for increased fracture risk in type 2 diabetes (T2DM) is not well understood. In this multi-ethnic, population-based study (n = 565), we investigated bone microstructure, trabecular plate/rod morphology and mineralization in women with T2DM (n = 175) with and without fracture using a second-generation HRpQCT and individual trabecula segmentation and mineralization (ITS; ITM). Covariate-adjusted aBMD was 3.0-6.5% higher at all sites (all p < 0.005) in T2DM versus controls. By HRpQCT, T2DM had higher covariate-adjusted trabecular vBMD (5.3-6.4%) and number (3.8-5.1%) and greater cortical area at the radius and tibia. Covariate-adjusted cortical porosity was 10.0% higher at the tibia only in T2DM versus controls, but failure load did not differ. Among women with T2DM, those with adult atraumatic fracture (n = 59) had 5.2-8.5% lower adjusted aBMD at all sites by DXA compared to those without fracture (n = 103). By HRpQCT, those with fracture had lower adjusted total vBMD and smaller cortical area (10.2-16.1%), lower cortical thickness (10.5-15.8%) and lower cortical vBMD associated with 18.1% and 17.2% lower failure load at the radius and tibia respectively (all p < 0.05); plate volume and thickness were 5.7% and 4.7% lower respectively (p < 0.05) while rod volume fraction was 12.8% higher in the fracture group at the tibia only. Sodium glucose cotransporter 2 inhibitor users (SGLT2i; n = 19), tended to have lower radial rod tissue mineral density by ITS (p = 0.06). GLP1 agonist users (n = 19) had trabecular deficits at both sites and higher cortical porosity and larger pores at the distal tibia. In summary, T2DM is associated with increased cortical porosity while those with T2DM and fracture have more marked cortical deficits and fewer trabecular plates associated with lower failure load.