Abstract
Purpose of review We describe relationships between microvascular complications and bone fragility fracture in the context of diabetes. We highlight gaps in knowledge and suggest areas of further study. Recent findings Evidence in type 1 diabetes (T1D) demonstrates that low bone mineral density (BMD) is associated with microvascular complications and linked to increased fracture risk. Of note, the low BMD does not solely explain bone fragility. Microvascular disease also has been linked to compromised bone microarchitecture and poorer bone quality. Moreover, microvascular complications may indirectly increase the rate of fragility fracture through increasing fall propensity; however, to date no conclusive studies have assessed microvascular disease and fracture risk independent of falls. In the other hand, individuals with type 2 diabetes (T2D) have increased fracture risk despite high BMD. Data suggest microvascular disease mediates microarchitectural changes by increasing cortical porosity and is associated with lower bone turnover. There is no direct evidence linking microangiopathy to fracture incidence. Taken together present evidence suggests associations between diabetic bone disease, fragility fracture, and microvascular disease. Data are more convincing for T1D than T2D. Further studies are required to confirm whether microvascular disease is itself causative of fracture or merely a contributory factor to fragility fracture for persons with diabetes.