Diabetic foot: Which one comes first, the ulcer or the contracture?

Abstract

Diabetic foot is among the most common complications of patients with diabetes. One of the known causes of foot ulceration is ankle equinus, which increases the pressure on the plantar surface during ambulation. Conversely, equinus contracture can be caused by a complicated wound, and it may be due to prolonged immobilization. In this paper, we reviewed the pathogenesis of both conditions and their clinical considerations. Poor glycemic control in patients with diabetes may result in angiopathy and neuropathy as an underlying condition. An ulcer can be precipitated by an injury, improper foot care, or increased biomechanical loading as seen in elevated plantar pressure following equinus contracture. Equinus contracture may be a direct effect of hyperglycemia or can arise in combination with another pathway, for example, involving the activation of transforming growth factor β. Static positioning resulting from any prior foot wound may develop fibrotic changes leading to contracture. Wound healing promoting factors can also result in overhealing outcomes such as hypertrophic scarring and fibrosis. The body's repair mechanism during the healing cascade activates repair cells and myofibroblasts, which also serve as the main producers and organizers of the extracellular matrix. Considering this intricate pathogenesis, appropriate interventions are essential for breaking the vicious cycle that may disturb wound healing.

Keywords: Contracture; Diabetes; Intervention; Pathogenesis; Ulcer; Vicious cycle.

Figure 1

Schematic diagram indicating how a vicious cycle can occur between equinus contracture and foot ulceration in patients with diabetes. TGF-β: Transforming growth factor β; AGEs: Advanced glycation end-products; RAAS: Renin angiotensin aldosterone system; ECM: Extracellular matrix.