Wound Dressing

Figure:Hand abrasion, 30 minutes after injury.
Any injury results in disruption of blood vessels leading to haemorrhage which is controlled by clot formation which contains fibrin mesh with aggregated platelets embedded in it. Fibrin is the end product of coagulation pathway and besides causing heamostasis it is also the primary component of the provisional tissue matrix seen in the early phases of wound healing. It provides a scaffold for the migration of inflammatory and mesenchymal cells. Platelet aggregation is a vicious cycle and leads to release of cytokines, which includes PDGF, TGF-a, FGFb, PDEGF. These cytokines influence wound healing directly or indirectly. The processes of clot formation and platelet aggregation terminate when stimuli for clot formation dissipate. Lysis of clot starts along with clot formation and is mediated by plasminogen activator, which converts plasminogen to plasmin.

Figure 2 : 2 days after injury.
Tissue trauma stimulates the inflammatory response. Immediately after injury intense local vasoconstriction occurs, mediated by circulating catecholeamines and prostaglandins released by injured cells. This is followed by vasodilatation and increased capillary permeability resulting in local edema. This is mediated by histamine, kinins, prostaglandins, leukotrienes, and endothelial cell products. Neutrophils are the first leukocytes to be found in wounded tissues. They phagocytose damaged tissue or bacteria. Neutrophils themselves are phagocytosed by macrophages. Pain in the area of injury is due to changes in pH due to break down of tissues and bacteria along with swelling and decreased tissue oxygenation due to disruption of blood vessels. Neutrophil count of the wound increases for 24-48 hrs and then declines unless wound contamination has occurred.
Monocytes transform into macrophages as they migrate from capillaries into extra vascular space. Macrocytes phagocytose bacteria and tissue debris and secrete enzymes (collagenase and elastase) responsible for breaking down damaged matrix. They also cytokines, P.G.s, oxygren free radicals and other regulators of wound healing.
Lymphocytes produce various factors like HB-EGF(Heparin binding epidermal growth factor), basic fibroblast growth factor and they are also involved in cellular and humoral immunity. Initially for 24-48 hrs neutrophils dominate but 48-72hrs later they are outnumbered by macrophages which persist for few days. After 5-7 days fibroblasts are the predominant cell type.

Figure 2 : 2 days after injury.
Epithelialization alone is enough to provide total healing in partial thickness wounds. Incisional wounds are usually completely re-epithelized in 24-48 hrs.
Epithelialization can be divided into separate cellular events including cell dedifferentiation, mitosis, migration and proliferation, which begin within hours of injury and results in resurfacing any denuded area. Thickening of the basal cell layer at the wound edge is the earliest aspect of epithelialization process. The marginal basal cell layer then elongates and detaches from the basement membrane with subsequent migration into the wound. These cells migrate as a single layer in a leap frog fashion and usually orient themselves along collagen fibres exhibiting contact guidance till they meet similar cell types when adhesions occur the entire process reverts to a resting stage, the phenomenon called contact inhibition. Cells of the mono-layer then differentiate into multi-layer. A new basement membrane is generated beginning at the wound edge. Cellular proliferation continues as a multi-layered epithelium is re-established. Subsequently new surface cells begin to keratinize. Cytokines are involved in all aspects of epithelialization and they include EGF, TGF-a, HB-EGF, IGF and members of FGF. Unfortunately regenerated epithelium does not retain all the functional advantages of normal epithelium. These include fewer basal cells, abnormal interface between dermis and epidermis and thin epithelium in the mid portion of the re-epithelized wound.