In addition to a decreased areal bone mineral density (aBMD) and reduced bone resorption long-standing, well-controlled type 1 diabetes (T1DM) was found to be linked with a cortical bone deficit at the ultradistal tibia with decreased bone strength and stiffness. Diabetic neuropathy is a determinant of cortical bone structure as well as bone strength at the tibia potentially contributing to the elevated non-vertebral fracture risk.

• In this study with 59 patients with T1DM and 77 non-diabetic controls, experts evaluated areal and volumetric bone mineral density (vBMD), bone microarchitecture, bone turnover and estimated bone strength in cases of long-standing T1DM, defined as disease duration >25 years.

• Lower aBMD at the hip, distal radius, lumbar spine and femoral neck were detected in patients with T1DM vs controls.

• In patients with T1DM, significantly lower CTX (a marker of bone resorption) was identified.

• No significant differences in vBMD and bone microarchitecture, at the distal radius, were found between both groups.

• Lower cortical thickness and lower cortical vBMD at the ultradistal tibia were present in T1DM cases.

• T1DM patients had significantly decreased bone strength and bone stiffness at the tibia than controls.

• Both the altered cortical microarchitecture and reduced bone strength and stiffness were identified to be dependent on the presence of diabetic peripheral neuropathy.