![]() ![]() Answers to these questions will be critical to further our understanding of osteoporosis in this patient population and key to developing effective screening tools and treatment options. As life expectancy continues to increase for those living with DM1, a further increase in the number of fractures occurring in this population is expected in the future.Īlthough we are now beginning to understand some of the genetic and molecular pathways underlying the association between DM1 and bone fragility, many questions remain. DM1 accounts for approximately 5% of all cases of diabetes in the USA and is associated with a 6.4–6.9-fold increase in the relative risk of hip fracture compared to individuals without diabetes. While both type 1 (DM1) and type 2 (DM2) diabetes have been found to increase fracture risk, the link is far more profound with DM1. Diabetes, although identified more than half a century ago as being associated with bone frailty, has come to the forefront only within the last decade as an important osteoporosis risk factor. Over time, a number of risk factors have been associated with osteoporosis and are useful when used in screening tools and treatment algorithms. Approximately 30% of all postmenopausal women are affected and up to 40% will develop a fragility fracture within their lifetime. Osteoporosis is the most common bone disease known, affecting an estimated 200 million people worldwide. Together, our current understanding of bone fragility in DM1 calls for an update of diabetes guidelines, better screening tools, and further research into the use of therapeutic strategies in this patient population. There is also a lack of data regarding the efficacy of therapeutic strategies to treat osteoporosis in this patient population. Despite this increased fracture risk, bone fragility remains an underappreciated complication of DM1 and is not addressed in most diabetes guidelines. As a result, patients with DM1 have a 6.9-fold increased incidence of hip fracture compared to controls. Other contributing factors include an accumulation of advanced glycation end products (AGEs) and the development of diabetes complications (such as neuropathy and hypoglycemia), which cause further decline in bone mineral density (BMD), worsening geometric properties within bone, and increased fall risk. While a number of cellular mechanisms have been postulated to mediate this association, it is now established that defects in osteoblast differentiation and activity are the main culprits underlying bone fragility in DM1. The link between type 1 diabetes mellitus (DM1) and osteoporosis, identified decades ago, has gained attention in recent years. ![]()
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