With the increasing worldwide prevalence of diabetes the resulting complications, their consequences and treatment will lead to a greater social and financial burden on society. One of the many organs to be affected is bone. Loss of bone is observed in type 1 diabetes, in extreme cases mirroring osteoporosis, thus a greater risk of fracture. In the case of type 2 diabetes, both a loss and an increase of bone has been observed, although in both cases the quality of the bone overall was poorer, again leading to a greater risk of fracture. Once a fracture has occurred, healing is delayed in diabetes, including nonunion. The reasons leading to such changes in the state of the bone and fracture healing in diabetes is under investigation, including at the cellular and the molecular levels. In comparison with our knowledge of events in normal bone homeostasis and fracture healing, that for diabetes is much more limited, particularly in patients. However, progress is being made, especially with the use of animal models for both diabetes types. Identifying the molecular and cellular changes in the bone in diabetes and understanding how they arise will allow for targeted intervention to improve diabetic bone, thus helping to counter conditions such as Charcot foot as well as preventing fracture and accelerating healing when a fracture does occur.
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