Abstract
Chronic leg ulcers are typically wounds that do not heal at a normal rate. Impaired healing appears to be due to primary microvascular changes and it is aggravated by ongoing bacteria-driven vasculitis. The various cytokines identified in experimental wounds are also present in leg ulcers. VEGF is strongly implicated as a promoter of blood vessel growth in patients with venous disease. In addition, there is good evidence of increased expression of bFGF, TGF-beta1, and PDGF in lipodermatosclerosis. All of these growth factors are involved in wound healing. Upregulated TGF-beta1 is probably one of the main causes of the fibrosis observed in lipodermatosclerosis. In leg ulcers, cytokines appear to be trapped in the perivascular fibrinoid deposits. It is not the nature and amount of cytokines that are inadequate in leg ulcers, but rather their spatial distribution. Dermal dendrocytes (DD) are resident factor XIIIa-enriched macrophages. They likely play a role in tissue repair when boosted adequately. New therapies aiming at helping the release of cytokines by DD apparently promote and improve the healing phase.
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