Diabetes Weakens Bones

Current research suggests that the inflammatory molecule tumor ne­cro­­sis factor-α (TNF-α) may contribute to delayed bone fracture healing in people with diabetes. Dia­betes affects at least 171 million people worldwide, a figure that is likely to double by 2030. Patients with diabetes often experience low bone density, which is associated with in­creased risk of bone fractures and delayed fracture repair. To ex­amine how diabetes affects bone, re­search­ers at the Uni­versity of Med­icine and Den­tistry of New Jer­sey and Boston Uni­versity School of Med­icine explored bone repair in a mouse model of diabetes. They observed in­creased levels of inflammatory molecules, including TNF-α, during fracture healing. The diabetic animals had rapid loss of cartilage in the healing bones, which was due to increased numbers of osteoclasts. Factors that stimulate osteoclast formation were regulated by both TNF-α and a downstream mediator forkhead box O1 (FOXO1). These re­sults suggest that diabetes-mediated increases in TNF-α and FOXO1 may underlie the im­paired healing of fractures. The re­searchers plan to examine the effect of FOXO1 on mineralized tissue and how it may regulate factors that control bone resorption and osteoclastogenesis, in addition to effects it may have on osteoblastic cells. This work was supported by grants from the National Institutes of Health. 

The original study by Alblowi et al, entitled, “High Levels of Tumor Necrosis Factor-α Contribute to Ac­celerated Loss of Car­tilage in Diabetic Fracture Heal­ing” appeared in the American Journal of Pathology (October 2009, Volume 175).