Compromised wound healing: a scientific approach to healing
 
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Differences between normally healing and compromised wounds (1)

Normal wound healing

Haemostasis is promoted rapidly after injury when platelets released from blood at the wound site bind to freshly exposed tissue components. These cells contain many chemicals that act as messenger molecules responsible for initiating blood coagulation, inflammation and wound healing. For healing one of the most important molecules released is Platelet Derived Growth Factor (PDGF) which attracts neutrophils and monocytes from the blood and fibroblasts from adjacent dermis into the wound site by a process known as chemotaxis. These cells then initiate the healing process. The importance of PDGF is emphasised by the fact that it was one of the first pharmaceutical products developed as a wound treatment from our knowledge of the healing process and is now available for topical application to enhance wound healing (Nagai, 2002).

Inflammation following injury is a normal part of healing but it rapidly resolves and is followed by a cell proliferation phase. Fibroblasts at the wound site are stimulated by PDGF and other growth factors to proliferate and produce extracellular matrix (ECM) as a component of granulation tissue. The presence of functional ECM is required to allow keratinocyte migration from the wound edge and re-epithelialise the wound surface with eventual scar formation.

Many growth factors and other proteins known as cytokines are involved in regulating the healing process (Moore, 2001). They are synthesised by all cell types present and once released in an active form bind to receptors on other cells to control their activity. This raises the possibility that they may be used for therapeutic interventions as demonstrated for PDGF. Conversely, because they act in complex networks any disruption to the network may delay healing.

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