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Objective: Delayed wound healing in diabetic patients without large vessel disease has been attributed to microvascular dysfunction, neuropathy, and abnormal cellular and inflammatory responses. The role of these abnormalities has been examined mainly in animal models. Few studies have been undertaken in diabetic patients and those that have are limited due to analysis in wounds from chronic ulcers. In this study, we quantified the rate of wound healing in relation to skin neurovascular function and structure following a dorsal foot skin biopsy in Type 2 diabetes.
Research Design and Methods Twelve healthy controls (C) and 12 Type 2 subjects with neuropathy (D) but without macrovascular disease were studied. We quantified rate of wound healing and related it to skin microvascular function (LDImax), blood vessel density (BVD), small nerve fiber function (LDIflare) and density (NFD), VEGF and its receptor (FLK1) and hypoxia inducible factor (HIF) 1alpha expression.
Results The rate of wound closure was identical between control subjects and diabetic patients despite a significant reduction in maximum hyperemia (LDImax), epidermal and dermal VEGF-A and epidermal and dermal blood vessel VEGFR-2 expression as well as the neurogenic flare response (LDIflare) and dermal nerve fiber density. There was no significant difference in HIF-1alpha and dermal blood vessel density between control subjects and diabetic patients.
Conclusion In conclusion, the results of this study suggest that wound closure in subjects with type 2 diabetes is not delayed despite significant alterations in neurovascular function and structure.
Neurovascular status did not affect wound closure rate
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