Contributors to impaired bone health in type 2 diabetes

Type 2 diabetes (T2D) is associated with numerous complications, including in-creased risk of fragility fractures, despite seemingly protective factors [e.g., normal bone mineral density and increased body mass index(BMI)]. However, fracture risk in T2D is underestimated by current fracture risk calculators. Importantly, post-fracture mortality is worse in T2D following any fracture, highlighting the importance of identifying high-risk patients that may benefit from targeted man-agement. Several diabetes-related factors are associated with increased fracture risk, including exogenous insulin therapy, vascular complications, and poor glycaemic control, although detailed comprehensive studies to identify the inde-pendent contributions of these factors are lacking. The underlying pathophysiologi-cal mechanisms are complex and multifactorial, with different factors contributing during the course of T2D disease. These include obesity, hyperinsulinaemia, hyperglycaemia, accumulation of advanced glycation end products, and vascular supply affecting bone-cell function and survival and bone-matrix composition. This review summarises the current understanding of the contributors to impaired bone health in T2D, and proposes an updated approach to managing these patients.

Automated summary

Type 2 diabetes is associated with an increased risk of fragility fractures, even in individuals with normal bone mineral density and higher body mass index. Current fracture risk calculators underestimate fracture risk in individuals with type 2 diabetes. Several diabetes-related factors, such as insulin therapy, vascular complications, and poor glycemic control, contribute to increased fracture risk, but their independent contributions are not well-studied. Understanding the complex mechanisms underlying impaired bone health in type 2 diabetes is crucial for effective management of these patients.