Bone loss alone doesn’t explain fractures in older type 2 diabetics

A new study in Diabetes Care is challenging a widely held assumption about fractures in older adults with type 2 diabetes. Although diabetes is associated with a higher risk of broken bones, researchers found that the increased risk cannot be explained simply by faster bone loss or greater deterioration in the internal structure of bone. The findings point to a more complex relationship between diabetes, skeletal strength, and the factors that determine whether a fall results in a fracture.

The study, titled “Type 2 Diabetes and Longitudinal Changes in Cortical and Trabecular Bone Density, Microarchitecture, and Strength: The Framingham Study,” examined how the skeleton changes over time in older adults with and without type 2 diabetes. The research team used advanced bone imaging to measure not only bone density, but also the architecture and mechanical properties of two distinct parts of bone: cortical bone, the hard outer shell, and trabecular bone, the porous, lattice-like tissue inside.

“Bone density alone does not tell the whole story,” said senior author Elizabeth J. Samelson, PhD, principal investigator of the National Institutes of Health-funded project. People with type 2 diabetes often have bones that appear denser when measured using conventional techniques, yet they experience more fractures than people without diabetes. This apparent contradiction, sometimes called the diabetes bone paradox, has led scientists to investigate whether changes in the quality and organization of bone may be more important than bone mass alone.

The researchers initially expected adults with type 2 diabetes to show greater losses in bone density, microarchitecture, and strength during follow-up. Instead, the longitudinal analysis found that changes in bone were broadly similar between older adults with and without the disease. The result suggests that the elevated fracture risk associated with type 2 diabetes may emerge through pathways that are not captured by conventional measures of bone loss or by changes in the structural properties assessed in this study.

The imaging approach allowed the scientists to analyze cortical and trabecular bone separately. Cortical bone provides much of the skeleton’s resistance to bending and impact, while trabecular bone helps distribute forces through the spine, hips, and other load-bearing regions. Microarchitecture refers to features such as the thickness, spacing, and connectivity of these structures. Even subtle changes can affect how efficiently bone absorbs energy, but the study did not find a diabetes-related pattern of accelerated deterioration in these measures over time.

The study’s findings do not mean that bone health is irrelevant for people with type 2 diabetes. Rather, they indicate that fracture susceptibility may depend on a broader combination of skeletal and non-skeletal factors. Diabetes can affect vision, balance, muscle function, nerve sensation, and reaction time, all of which may increase the likelihood of falling. In addition, complications such as peripheral neuropathy can reduce awareness of foot position and uneven surfaces, potentially making falls more frequent or more severe.

The mechanical behavior of bone may also be influenced by properties that are difficult to measure with standard imaging. Long-term exposure to elevated blood glucose can promote the formation of advanced glycation end products, chemical compounds that accumulate in tissues and may alter the flexibility of collagen. Bone is a composite material made from mineral crystals embedded in a collagen-rich matrix, and changes to that matrix could affect how bone resists cracks even when bone density remains normal or high. The present study underscores the need to investigate these material-level properties more closely.

Alyssa B. Dufour, PhD, lead author and associate scientist at the Hinda and Arthur Marcus Institute for Aging Research at Hebrew SeniorLife, said the team expected to observe greater changes in bone microstructure and strength among participants with type 2 diabetes. Instead, the similar rates of bone loss in the two groups suggest that clinicians and researchers should avoid treating bone density as a complete measure of fracture risk in diabetes. A person may have relatively dense bones while remaining vulnerable because of impaired balance, falls, altered bone material quality, or other disease-related factors.

The work was conducted by investigators from Hebrew SeniorLife, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston University, the University of Calgary, and Cardiovascular Engineering, Inc., using data from the Framingham Heart Study. Funding came from the National Institute on Aging, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, and the National Heart, Lung, and Blood Institute. By showing that similar longitudinal bone changes can coexist with different fracture risks, the study adds an important piece to the growing scientific picture of diabetes-related skeletal fragility and may encourage more comprehensive approaches to fracture prevention in older adults.

News Publication Date: 5-Aug-2026

Web References: Diabetes Care article: https://diabetesjournals.org/care/article-abstract/doi/10.2337/dc26-0846/172304/Type-2-Diabetes-and-Longitudinal-Changes-in?redirectedFrom=fulltext

References: DOI: 10.2337/dc26-0846