Neurovascular factors in wound healing in the foot skin of Type 2 diabetic subjects

Abstract

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.

Objective: Research Design and Methods

Objective: 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) 1α expression.

Objective: Results

Objective: 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-1α and dermal blood vessel density between control subjects and diabetic patients.

Objective: Conclusion

Objective: 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.