Diabetes increases the rate of fibroblast apoptosis stimulated by a bacteria-induced wound, and the higher level of apoptosis contributes to an impaired wound-healing response.(48) There is also evidence of increased apoptosis of pericytes and endothelial cells in retinas of diabetic animals, which was found to be a contributing factor to diabetic retinopathy and caused in part by increased levels of TNF.(49–52) Thus TNF dysregulation caused by diabetes may affect a number of different tissues, including cartilage, during fracture healing. This evidence concerns the gene TNF and diabetic retinopathy.