Clinical aspects of diabetic bone disease: An update

Abstract

Older adults with type 2 diabetes have a higher risk of fracture but do not have decrements in bone density. The reasons for greater bone fragility in diabetes are still not clearly understood, but progress has been made in identifying potential contributors. With new imaging techniques, increased cortical porosity has been identified as a possible contributing factor to bone fragility. Cortical porosity may be especially detrimental to bone strength in the presence of higher levels of advanced glycation end products. Initial results have reported higher levels of marrow adiposity in diabetic men, suggesting that diabetes may contribute to marrow stem-cell lineage allocation toward adipocytes rather than osteoblasts. Higher levels of sclerostin have also been observed in diabetic patients, indicating that osteocyte function may play a role in diabetic bone. An important clinical question, "How to best predict fracture in diabetic patients?" has been addressed with studies demonstrating that BMD T-score and FRAX score predict fractures but underestimate absolute risk in diabetic patients. For prevention of fractures, there is now evidence from a clinical trial that intensive glycemic control does not increase fracture or fall risk but also does not reduce these outcomes. The pursuit of these new findings promises to provide insights into the reasons for greater fragility of diabetic bone and the best methods for fracture prevention in this population. © 2012 Springer Science+Business Media, LLC.