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The fibroblasts are activated to divide and produce collagen by processes initiated by the macrophages (Timmons 2006). Newly synthesized collagen creates a ‘healing ridge’ below an intact suture line, thus giving an indication of how primary wound healing is progressing. Wound healing by secondary intention will also have a healing rim around it as the wound contracts. This mechanism is dependent on the presence of iron, vitamin C and oxygen. Vitamin C (ascorbic acid) and lactate are stimulants for fibroblast activity (Hampton and Collins 2004). Fibroblasts are also dependent on the local oxygen supply (Dealey 2005). The wound surface and the oxygen tension within encourage the macrophages to instigate the process of angiogenesis, forming new blood cell vessels (Dealey 2005, Hampton and Collins 2004). These vessels branch and join other vessels, forming loops. The fragile capillary loops are held within a framework of collagen. This complex is known as granulation tissue. At this stage, the wound will appear pink and moist with raised red bumps (Hampton and Collins 2004).

The process of wound contraction can significantly reduce the size of the wound and the area that new tissue must cover. It is extremely important and only observable in open wounds healing by secondary intention. There is debate about the exact method by which wound contraction occurs (Tejero-Trujeque 2001).

Re-epithelialization of the wound usually begins within 24 hours of injury (Calvin 1998, Garrett 1997). Macrophages produce a number of growth factors including keratinocyte growth factor (KGF) which stimulates a proliferation of cells within the wound bed (Timmons 2006). Epithelial cells (keratinocytes) may migrate from hair follicles and sweat glands within the wound or from the perimeter of the wound (Moore and Foster 1998). Endothelial buds grow and the fibroblasts continue the process of repair by laying down fibrous tissue (Hampton and Collins 2004). Epithelial cells will burrow under contaminated debris and unwanted material (Waldorf and Fewkes 1995) while also secreting an enzyme that separates the scab from underlying tissue. Dissolving dry eschar requires nearly 50% of the cell’s metabolic energy (Dealey 2005). Through a mechanism called contact inhibition, epithelial cells will cease migrating when they come into contact with other epithelial cells (Garrett 1997).

Epithelialization (migration, mitosis and differentiation) occurs at an increased rate in a moist wound environment, as do the synthesis of collagen and formation of new capillaries (Flanagan 1999). Wound contraction is a function of myofibroblasts, which are prominent in granulating tissue. The extent of wound contraction is dependent on the number of myofibroblasts present and it is maintained by collagen deposition and cross-linking (Giele and Cassell 2008). The rate of epithelialization is influenced by growth factors (Timmons 2006) but little is known about the reality of growth factor activity in chronic wounds (Hampton and Collins 2004).

Maturation phase (21 days onward)

This stage begins at around 21 days following the initial injury (Figure 15.4). Maturation or remodelling of the healed wound may last for more than a year. Collagen is reorganized, the fibres becoming enlarged and orientated along the lines of tension in the wound (at right angles to the wound margin) (Silver 1994). This occurs via a process of lysis and resynthesis. Intermolecular cross-linking aids the tensile strength of the wound. During this reorganization fibroblasts may constrict the neighbouring collagen fibres surrounding them, causing contraction of the tissue and reduction of blood vessels within the scar (Cho and Hunt 2001). Maximum strength is reached in approximately 3 months, although the scar will only achieve about 70–80% of normal skin strength (Calvin 1998, Ehrlich 1998). At the end of the maturation phase, the delicate granulation tissue of the wound will have been replaced by stronger avascular scar tissue. Rationalization of the blood vessels