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Press Release

Date: 10-06-09
Name: Terri Guess
Phone: 973-972-7265
Email: guesstp@umdnj.edu

UMDNJ Research Links Diabetes with Slow Recovery From Bone Fractures

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NEWARK, N. J.—A study led by UMDNJ researchers finds that an inflammatory molecule triggered by diabetes may inhibit the healing of bone fractures in people who have the disease. The report, “High Levels of TNF-a Contribute to Accelerated Loss of Cartilage in Diabetic Fracture Healing” appears in the October 2009 issue of The American Journal of Pathology.

Diabetes, which affects at least 171 million people worldwide, is a condition where the body either does not produce enough insulin or cannot use insulin effectively, thereby leaving the body with excess blood sugar.. Patients often experience low bone density, which is associated with increased risk of bone fractures and delayed fracture repair. To examine how diabetes might cause low bone density, Dana Graves, DDS, chair of the Department of Periodontics at UMDNJ-New Jersey Dental School and his colleagues from UMDNJ, and Drs. Thomas A. Einhorn and Louis Gerstenfeld at Boston University School of Medicine, explored bone regeneration in a mouse model of diabetes. Their research suggests that the inflammatory molecule TNF-a may contribute to delayed bone fracture healing in diabetics.

“Diabetes enhances inflammation, which is related to diabetic complications, including periodontal diseases, osteopenia and impaired fracture healing,” explained Graves. “These disorders affect bone, which explains the connection to both dental and orthopedic complications of diabetes.”

The research team observed increased levels of inflammatory molecules, including TNF-aduring fracture repair. In the diabetic group there were more osteoclasts, cells that remove bone and cartilage and are important for the transition from cartilage to bone during fracture healing. In these mice, increased osteoclast numbers were due to greater production of TNF-a TNF-a regulated the expression of molecules that stimulate osteoclast formation through a downstream mediator, FOXO1, which was elevated in diabetic fracture healing. These results suggest that diabetes-mediated increases in TNF-a and FOXO1 may underlie the delayed healing of diabetic fractures.

In future studies, Dr. Graves and his colleagues plan to examine the transcription factor of FOXO1 which is activated in a number of diabetic complications. “We think that FOXO1 is related to higher levels of inflammation in cell death that occurs with diabetic complications that might occur in fracture healings, impaired wound healing and diabetic retinopathy,” he said.

The University of Medicine and Dentistry of New Jersey (UMDNJ) is the nation's largest free-standing public health sciences university with more than 5,500 students attending the state's three medical schools, its only dental school, a graduate school of biomedical sciences, a school of health related professions, a school of nursing and its only school of public health, on five campuses. Annually, there are more than two million patient visits at UMDNJ facilities and faculty practices at campuses in Newark, New Brunswick/Piscataway, Scotch Plains, Camden and Stratford. UMDNJ operates University Hospital, a Level I Trauma Center in Newark, and University Behavioral HealthCare, a mental health and addiction services network.

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