Bone deterioration alone does not explain the higher fracture risk in older adults with type 2 diabetes

A new study published in Diabetes Care reveals that bone deterioration alone cannot account for the higher fracture risk seen in some older adults with type 2 diabetes. The research, titled "Type 2 Diabetes and Longitudinal Changes in Cortical and Trabecular Bone Density, Microarchitecture, and Strength: The Framingham Study," aimed to unravel the mystery behind why individuals with type 2 diabetes are more prone to fractures.

Lead author Alyssa B. Dufour, Ph.D., from the Hinda and Arthur Marcus Institute for Aging Research, Hebrew SeniorLife, and Harvard Medical School, explained that the team utilized a cutting-edge bone imaging device to examine two specific bone compartments: cortical bone (the hard outer layer) and trabecular bone (the spongy inner layer).

Despite anticipating more significant changes in bone microstructure and strength among those with type 2 diabetes, the findings showed that bone loss was comparable between the two groups.

Senior author and project principal investigator, Elizabeth (Lisa) Samelson, Ph.D., highlighted that while people with type 2 diabetes often exhibit denser bones, they still experience a higher likelihood of fractures. This apparent contradiction suggests that bone density alone is insufficient to explain the increased fracture risk, emphasizing the need to explore other factors that impact bone strength and fracture susceptibility.

The study, involving Alyssa B. Dufour et al., demonstrated that older adults with type 2 diabetes experienced longitudinal reductions in cortical and trabecular bone density, microarchitecture, and estimated strength, similar to those without diabetes. Consequently, the elevated fracture risk associated with type 2 diabetes likely stems from factors beyond bone loss and density.