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A well defined sequence of events follows dermal injury and with normal healing there is a controlled progression to re-epithelialisation, scarring and restoration of an intact epidermis. In contrast compromised wounds such as diabetic ulcers, varicose ulcers and decubitus ulcers fail to heal and if not given appropriate care will enlarge and may persist for many months or even years. Our knowledge of healing has grown significantly since the pioneering demonstration by Winter (Winter, 1962) that maintenance of a moist wound environment would assist healing. This observation stimulated development of wound dressings with physical properties designed to maintain an optimum level of wound moisture whilst still removing excess exudate and acting as a barrier to infection. Understanding of the cell biology and biochemistry of healing and non-healing wounds gained over the following 4 decades has allowed characterisation of the healing process and the defects that develop in compromised wounds. This growing body of knowledge is leading to the rational design of treatments for chronic wounds that interact with the cellular environment to modulate the healing process with the intention of stimulating healing.

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