The inflammatory process is a "biological emergency" response as there is a latent stage of about 12 hours before any obvious healing begins (Silver 1994). Once an injury has been sustained by the body, platelets are released from the blood vessel, which initiate haemostasis and coagulation of blood leaking from damaged, inflamed and dilated blood vessels ( Golsen 1987, Kerstein 1997). At the same time, a biochemical cascade occurs that liberates thrombokinase and this is converted to thrombin. The clots are from fibrinogen, converted to fibrin, which covers the wound, and brings the wound edges together. A series of elaborate messages are initiated which cause blood cells to commute to the site of the injury bringing extra oxygen to the wound along with phagocytes to clear tissue debris. There is also release of growth factors and several cytokines which include regulatory peptides and glycopeptides (Hopkinson 1992).
On injury, damaged cells release inflammatory mediators such as prostaglandins and histamine from mast cells. Serotonin may also be released from the basophils (also known as mast cells) which causes vasodilatation from the existing blood vessels and results in increased cell permeability for the neutrophils and monocytes and other white blood cells (T and B lymphocytes) thus improving the blood supply to the wound. Wound cleansing is commenced by the macrophages by the process of phagocytosis. Macrophages and neutrophils are essential for the transition from the inflammatory to proliferative phase of healing (Silver 1992a).
Erythema occurs as a result of the blood vessels expanding and increasing the blood supply. The endothelial cells become more permeable and this fluid may leak into the surrounding area (extravasation). The combination of these processes results in oedema, which may last for up to three days after injury (Tortora & Anagnostaks 1987, Seton Health Care 1993, Collier 1996).
The literature demonstrates that the regeneration phase ranges from 3 to 24 days and can be divided into two phases:
Granulation occurs in deep dermal wounds (Chen & Hutchinson 1998). Macrophages signal to the dermal fibroblasts to lay fibrils of reticulin across the wound. This is later converted to collagen. The next stage is angiogenesis. New granulation tissue is vascular due to capillary loops, which give its classic red appearance. New tissue is composed of macrophages, fibroblasts, capillary buds and loops in a matrix of fibronectin, collagen and hyaluronic acid (Dealey 1994). Prolonged lack of oxygen will reduce the mobility of the fibroblasts and delay healing.
As new tissue is laid down, the wound edges contract, which is when the growth factors signal to the mediator cells to cause the myosin bundles to bring together the wound edges.
The final stage of wound healing is epithelization, which occurs in shallow superficial wounds above the dermis and happens faster in small wounds and slower in wounds healed by secondary intention. Following the frantic activity from the growth factor cocktail, macrophages and fibroblasts continue to produce new dermis rich in collagen, hyaluronan, fibronectin, keratinocytes, hair follicles, and sebaceous glands. Epithelization is achieved by squamous cells migrating across the wound surface until the deficit is resolved (Dealey 1994, Chen & Hutchinson 1998). The survival of this very delicate tissue is dependent on a moist environment (Winter 1962). The new epithelial tissue is pinkish white which gives a translucent appearance and can be seen in granulating wounds (Flanagan 1997a).
