Wound debridement

Like any other moist wound dressing, honey facilitates the debridement of wounds by the autolytic action of tissue proteases. Unlike other wound dressings, honey creates a moist environment by drawing out lymph fluid from the wound tissues through its strong osmotic action. This provides a constantly replenished supply of proteases at the interface of the wound bed and the overlying necrotic tissue, which may, in part, explain the rapid debridement brought about by honey. This osmotic action also washes the surface of the wound bed from beneath. This explains the frequent observation of honey dressings removing debris such as foreign bodies (eg. dirt, grit) with the dressing (Molan, 2002). It also helps explain the painless lifting off of slough and necrotic tissue that is observed (Efem, 1988 and 1993; Hejase et al, 1996; Subrahmanyam, 1993 and 1998). Another possible explanation for the observed rapid debridement is activation of the proteases by hydrogen peroxide liberated by honey. The proteases in wound tissues are normally in an inactive state but can be activated by oxidation. The matrix metalloproteases of connective tissue, normally present in a catalytically inactive conformation, may be activated by the hydrogen peroxide (Peppin and Weiss, 1986; Weiss et al, 1985). High protease activity is strongly associated with impaired wound healing, which may suggest that activation of proteases by honey would be harmful rather than beneficial. However, a causal effect has never been proved (Ashcroft et al, 2000); possibly, the association is the result of both impaired healing and high protease activity together caused by the same factor — excessive, uncontrolled inflammation (Agren et al, 2000). Excessive inflammation prevents healing and the attraction of inflammatory leukocytes gives rise to high levels of proteolytic enzyme activity at the site of the inflammation (Ashcroft et al, 2000; Agren et al, 2000). The potent anti-inflammatory action of honey (see below) would resolve such a situation and prevent excessive proteolytic activity. It also has been suggested that high levels of proteolytic activity and high levels of inflammation are both caused by a lack of secretory leukocyte protease inhibitor, which is an inhibitor both of serine proteases and the production of TGF-ß, a potent chemoattractant of inflammatory cells. Yet, proteolysis in wound tissues is a normal part of the healing process and responsible for autolytic debridement.

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