Impairment of the microcirculation of diabetic patients may contribute to secondary complications in the lower extremity, such as foot infections and ulcerations. These microcirculatory changes, which are mainly functional rather than structural, are responsible for the impaired ability of the microvasculature to vasodilate in response to injury. Dysfunction of vascular endothelial cells and vascular smooth muscle cells both contribute to the reduction in vasodilation that is observed in diabetic patients. Nerve-axon reflex related microvascular vasodilation is also impaired in the diabetic population, and there is a growing belief that both the failure of the vessels to dilate and the impairment of the nerve axon reflex are major causes for impaired wound healing in diabetic patients. Further studies are necessary to clarify the precise etiology of endothelial and smooth muscle dysfunction in diabetic patients so that potential therapeutic interventions may be identified.