An inflammatory molecule called TNF-a may contribute to delayed bone fracture healing in diabetics, according to a study.

A research article on the study, published in the American Journal of Pathology, describes diabetes as a condition where the body either does not produce enough, or respond to, insulin.

The report says that long-term complications of diabetes include cardiovascular disease, chronic renal failure, retinal damage that may lead to blindness, nerve damage, and blood vessel damage, which may cause erectile dysfunction and poor wound healing.

It further points out that diabetic patients often experience low bone density, which is associated with increased risk of bone fractures and delayed fracture repair.

With a view to determining how diabetes affects bone, Dr. Dana Graves and colleagues of the University of Medicine and Dentistry of New Jersey and the Boston University School of Medicine explored bone repair in a mouse model of diabetes.

The researchers observed increased levels of inflammatory molecules, including TNF-a during fracture healing.

They revealed that the diabetic animals had rapid loss of cartilage in the healing bones, which was due to increased numbers of osteoclasts, cells that remove bone and cartilage.

They further said that factors that stimulate osteoclast formation were regulated by both TNF-a and a downstream mediator, FOXO1.

According to the researchers, these results suggest that diabetes-mediated increases in TNF-a and FOXO1 may underlie the impaired healing of diabetic fractures.

The researchers say: "TNF-a dysregulation plays a prominent role in the recently identified catabolic events associated with diabetic fracture healing." In future studies, Dr. Graves and colleagues plan to "examine the effect of FOXO1 on mineralized tissue to examine how it may regulate factors that control bone resorption and osteoclastogenesis, in addition to effects it may have on osteoblastic cells."