Wound Healing

The third phase of transgress better is granulation phase, which takes lay to repair the damaged carrels by regenerating new cells. This phase consists of different subphases, which can last up to 4 weeks in the clean and uncontaminated injury. These sub phases do not happen in discrete term frames but constitute an overall and ongoing bring. The sub phases are fibroplasia, hyaloplasm deposition, angiogenesis and re-epithelialization (Cho & Lo, 1998). The first sub phase of granulation process is fibroplasia.In eld 5-7, fibroblasts have migrated into the aggravate, laying down new collagen of the subtypes I and III. In shape wound healing, early type III collagen predominates but is later re attituded by type I collagen. Tropocollagen, which is the precursor of all collagen types, is then transformed within the cells rough endoplasmic reticulum, where proline and lysine are hydroxylated. by and by tropocollagen transformation, disulfide bonds are established, allowing 3 tropocollagen strands to form a triple left-handed triple helix, termed procollagen.As the procollagen is secreted into the extracellular space, peptidases in the cell wall cleave terminal peptide chains, creating true collagen fibrils, which mark the hallmark of fibroplasia. After fibroplasia, matrix deposition takes place. In matrix deposition, the wound is first suffused with GAGs and fibronectin produced by fibroblasts. These GAGs include he space-reflection symmetryn sulfate, hyaluronic acid, chondroitin sulfate, keratan sulfate, and proteoglycans. Then, proteoglycans bond covalently to a protein core and this contributes to matrix deposition.Later, angiogenesis takes place. Angiogenesis is the product of enhance vessel offshoots which is known as new vasculature. The formation of new vasculature requires extracellular matrix and basement membrane degradation followed by migration, mitosis, and maturation of endothelial cells. Basic FGF and vascular endothelial ingathering factor are withal involved in the modulating angiogenesis. Finally, re-epithelization occurs with the migration of cells from the periphery of the wound and adnexal structures.This process commences with the bedspread of cells within 24 hours. Leter, division of peripheral cells occurs in hours 48-72, resulting in a thin epithelial cell layer, which bridges the wound. In addtition, epidermal growth factors play a key role in this aspect of wound healing (Lynch, Colvin, Antoniades, 1989). The last phase of wound healing is remodeling. Remodeling process takes place after the third week, whereby the wound is altered constantly. Constant alteration of wound can last for years after the initial injury occurred.In remodeling, collagen is degraded and deposited in an equilibrium-producing fashion, resulting in no change in the touchstone of collagen deposited in the wound. In normal wound healing, the collagen deposition reaches a circus tent by the third week after the wound is crea ted. Then, contraction of the wound takes place following collagen deposition. Wound contraction is an ongoing process resulting in part from the proliferation of the specialized fibroblasts termed myofibroblasts, which resemble contractile smooth muscle cells (Deodhar Rana, 1997, para 3).Wound contraction occurs to a greater extent with secondary healing than with primary healing, whereby it leaves a scar in socondary healing. By the 12th week, maximal tensile strength of the wound is achieved although the ultimate resultant scar has just now 80% of the tensile strength of the original skin that it has replaced (Brunner Suddarth, 2008, p. 38). In brief, the process of wound healing constitutes an array of interrelated and concomitant events of hemostasis, inflammation, granulation and remodeling.