Non-healing chronic wounds present a major biological, psychological, social, and financial burden on both individual patients and the broader health system. Pathologically extensive inflammation plays a major role in the disruption of the normal healing cascade. The causes of chronic wounds (venous, arterial, pressure, and diabetic ulcers) can be examined through a juxtaposition of normal healing and the rogue inflammatory response created by the common components within chronic wounds (ageing, hypoxia, ischaemia-reperfusion injury, and bacterial colonisation). Wound bed care through debridement, dressings, and antibiotics currently form the basic mode of treatment. Despite recent setbacks, pharmaceutical adjuncts form an interesting area of research.
The skin forms an important and effective barrier against the environment. It plays a vital role in protection against insults such as bacteria, xenobiotics and dehydration. When a cutaneous injury occurs, the body initiates a series of complex events to re-establish this protection. Wound healing can be roughly divided into four continuous and overlapping phases: (1) haemostasis; (2) an immediate inflammatory response defined by an infiltration of cytokine-releasing leukocytes with antimicrobial functions; (3) these cytokines kick off a proliferative phase where new epithelium, blood vessels, and extracellular matrix (ECM) are laid down; (4) over a period of weeks to months, the wound contracts as the ECM is remodelled [1]. These highly regulated cellular, humoral and molecular processes have been described as an orchestral performance—a potential flawless interplay can lead to perfect regeneration; however, human adult wounds undergo a repair process that leads to scarring, and, in some cases, non-healing chronic wounds …. read more