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Wound Healing

The process by which tissue repair takes place is termed wound healing and is comprised of a continuous sequence of inflammation and repair, in which epithelial, endothelial, inflammatory cells, platelets and fibroblasts briefly come together outside their normal domains, interact to restore a semblance of their usual discipline and having done so resume their normal function.

The process of wound repair differs little from one kind of tissue to another and is generally independent of the form of injury. Although the different elements of the wound healing process occur in a continuous, integrated manner, it is convenient to divide the overall process into three overlapping phases and several natural components for descriptive purposes.

Fig. 1. Phases of wound repair. Wound healing has been arbitrarily divided into three phases: inflammation, proliferation and maturation


Inflammatory Phase (Day 0-5)

The healing response is initiated at the moment of injury. Surgical or traumatic wounds disrupt the tissue architecture and cause haemorrhage. Initially, blood fills the wound defect and exposure of this blood to collagen in the wound leads to platelet degranulation and activation of Hageman factor [1]. This in turn sets into motion a number of biological amplification systems including the complement kinin and clotting cascades and plasmin generation. These serve to amplify the original injury signal and lead not only to clot formation, which unites the wound edges, but also to the accumulation of a number of mitogens and chemoattractants at the site of wounding [2].

Production of both kinins and prostaglandins leads to vasodilatation and increased small vessel permeability in the region of the wound [3]. This results in oedema in the area of the injury and is responsible for the pain and swelling which occurs early after injury. Within 6 h, circulating immune cells start to appear in the wound. Polymorphonuclear leucocytes (PMN) are the first blood leucocytes to enter the wound site. They initially appear in the wound shortly after injury and subsequently their numbers increase steadily, peaking at 24-48 h [4]. Their main function appears to be phagocytosis of the bacteria which have been introduced into the wound during injury. The presence of PMN in the wound following injury does not appear to be essential in order for normal wound healing to take place [5, 6], with healing proceeding normally in their absence provided that bacterial contamination has not occurred. In the absence of infection, PMN have a relatively short life span in the wound and their numbers decrease rapidly after the third day [7].

The next cellular, immune element to enter the wound are macrophages. These cells are derived from circulating monocytes by a combination of migration and chemotaxis. They first appear within 48-96 h post-injury and reach a peak around the third day post-injury [4]. These macrophages have a much longer life span than the PMN and persist in the wound until healing is complete. Their appearance is followed somewhat later by T lymphocytes, which appear in significant numbers around the fifth day post-injury, with peak numbers occurring about the seventh day after injury. In contrast to PMN, the presence and activation of both macrophages and lymphocytes in the wound is critical to the progress of the normal healing process [8, 9].

Macrophages just like neutrophils phagocytose and digest pathological organisms and tissue debris. In addition, macrophages release a plethora of biologically active substances. Many of these substances facilitate the recruitment of additional inflammatory cells and aid the macrophage in tissue decontamination and debridement; in addition growth factors and other substances are also released which are necessary for the initiation and propagation of granulation tissue formation. These intercellular transmitters are known collectively as cytokines.



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