The factors most frequently responsible for slowing down phlebostatic ulcer healing comprise, in addition to a deficit in cicatrization, microbial contamination of the breached skin with proliferation of pathogenic organisms and changes in the microenvironment (oxygenation, temperature, humidity), associated with loss of electrolytes and poor stimulation of granular tissue.¹ These are a direct result of the functional breakdown of the skin, which prevents it from exercising its normal protective functions.

    Until now, the numerous attempts to use human skin substitutes for the treatment of ulcers have given contradictory results because none of them showed the characteristics of an "ideal skin substitute".^{2 5}

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