Bone deterioration alone does not explain the higher fracture risk in older adults with type 2 diabetes
A new study published in Diabetes Care finds that bone loss alone does not explain the increased fracture risk observed in some older adults with type 2 diabetes.
The article, “Type 2 Diabetes and Longitudinal Changes in Cortical and Trabecular Bone Density, Microarchitecture, and Strength: The Framingham Study,” sought to better understand why people with type 2 diabetes are at greater risk of fractures.
Lead author Alyssa B Dufour, PhD, Associate Scientist, Hinda and Arthur Marcus Institute for Aging Research, Hebrew SeniorLife, and Instructor in Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, explained, “We used a novel bone imaging device to look closely at two compartments of bone: the hard outer layer (cortical bone) and the spongy inner layer (trabecular bone). We expected to see greater changes in bone microstructure and strength in people with type 2 diabetes. However, we found that bone loss was similar in older adults with and without type 2 diabetes.”
Senior author and Principal Investigator (PI) of the NIH-funded project, Elizabeth (Lisa) Samelson, PhD, explained, “Although people with type 2 diabetes often have denser bones, they are still more likely to suffer fractures. This paradox suggests that bone density alone does not tell the whole story and highlights the importance of understanding other factors that influence bone strength and fracture risk.”
In addition to Dufour, other coauthors include Douglas P. Kiel, Hinda and Arthur Marcus Institute for Aging Research, Hebrew SeniorLife, and Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School; Chandler Da Cruz, Hinda and Arthur Marcus Institute for Aging Research, Hebrew SeniorLife; Laiji Yang, Hinda and Arthur Marcus Institute for Aging Research, Hebrew SeniorLife; Elizabeth J. Samelson (Principal Investigator), Hinda and Arthur Marcus Institute for Aging Research, Hebrew SeniorLife, and Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School; Mary L. Bouxsein, Department of Orthopedic Surgery, Harvard Medical School and Center for Advanced Orthopedic Studies, Beth Israel Deaconess Medical Center; Musong Gao, Department of Biostatistics, School of Public Health Boston University; Ching-Ti Liu, Department of Biostatistics, School of Public Health Boston University; Steven K. Boyd, McCaig Institute for Bone and Joint Health, University of Calgary; and Gary F. Mitchell, Cardiovascular Engineering, Inc.
Funding was provided by the National Institute on Aging (grant R01 AG065299); National Institute of Arthritis and Musculoskeletal and Skin Diseases (grant R01AR061445); and the Framingham Heart Study of the National Heart Lung and Blood Institute (NHLBI) of the National Institutes of Health (NIH) and Boston University School of Medicine. This project has been funded in whole or in part with federal funds from the NHLBI, NIH, Department of Health and Human Services, under contract 75N92019D00031.
