People with type 1 diabetes (T1D) have a six- to eight-fold higher risk for hip fractures compared to people without diabetes. Hip fractures are associated with significant morbidity, mortality, loss of independence, and financial burden. Moreover, hip fracture mortality is higher in patients with diabetes compared to subjects without diabetes. Dual x-ray absorptiometry (DXA), the most common test to assess bone health, underestimates fracture risk in patients with T1D. Altered geometry in young-onset T1D (T1D diagnosis before age 20), and reduced bone mechanical and material qualities are implicated in bone fragility in T1D. Chronic hyper- and hypoglycemia is postulated to suppress bone turnover leading to accumulation of microdamage and advanced glycation endproducts (AGE) resulting in compromised bone material properties in T1D. Despite higher fracture risk, the effect of T1D on bone structural and material properties and diabetes-related factors affecting bone health are unknown. Considering the knowledge gap, we propose to evaluate baseline skeletal phenotype using validated quantitative computed tomography (QCT), finite element (FE) based bone strength, and OsteoProbe- measured in vivo bone material strength index (BMSi), and changes in these measures over 3 years in a large cohort of adults with and without T1D from the ongoing ?Coronary Artery Calcification in Type 1 Diabetes? (CACTI) study. We will also determine the role of acute hyper- and hypoglycemia on bone turnover and its long-term impact on bone material properties. With improved care, people with T1D are living longer and there is no specific approach for prevention and treatment of osteoporosis for older adults with T1D. Therefore, this research project will help to characterize bone phenotype and the effect of long-term hyperglycemia on bone changes over a period of three years; and therefore, it will allow for future clinical trials to improve bone health and reduce facture risk among adults with T1D.
Hip fracture risk is six- to eight-fold higher in adults with type 1 diabetes and occurs at a relatively young age. Bone mineral density alone does not explain the higher fracture risk in this population. However, little is known about bone quality in adults with type 1 diabetes. This study proposes to explore bone quality and strength at the hip in adults with long-standing type 1 diabetes compared to age-, gender-, and body mass index-matched controls without diabetes over a period of 3 years. Characterizing bone phenotype and understanding the effect of glycemic control on bone health will help us understand the mechanisms of bone fragility; and thus plan future interventions to improve bone health in this population.
