The Physiology Of Wound Healing

The Physiology Of Wound Healing

• It occurs in a clean Incised wound or surgical wound.
• Wound edges are approximated with sutures. There is more epithelial regeneration than firosis. Wound heals rapidly with complete closure.
• Scar will be linear, smooth and supple.

• It occurs in a wound with extensive soft tissue loss like in major trauma, bums and wound with sepsis.
• It heals slowly with firosis.
• It leads into a wide scar, often hypertrophied and contracted.
• It may lead into disability.
• Re-epithelialization occurs from remaining dermal elements or wound margins.

• In primary healing of wound, edges are approximated by surgical sutures.
• In the initial phase, there will be formation of blood clot,which helps to hold the parts of the wound together.
• Within 10 to 15 minutes of injury vasodilatation occur and there is increased capillary permeability mediated by vasoactive substances released by damage cells and clot breakdown.
• The tissue becomes edematous and an inflammatory process starts, with the infitration of polymorphonuclear neutrophils (PMN) and lymphocytes into the area.
• The tissue debris collected in the wound are cleared either by the process of phagocytosis or by their lysis with the help of proteolytic enzymes, liberated by the inflmmatory cells.
• Once the tissue debris are cleared, granulation tissue forms that replaces the blood clot in the wound, and it usually consists of young blood capillaries, proliferating firoblasts, PMN and other leukocytes.
• The epithelium at the edge of the wound starts to proliferate and gradually, it covers the entire wound surface.
• Finally, the healing process is complete with invasion of wound area by firoblast on 3rd day, progressive increase in the amount of dense collagen bundles on 5th day and formation of scar tissue with scanty cellular and vascular elements, some inflammatory cells and epithelialized surface by 4th week.

• When the opposing margins of the wound cannot be approximated together by suturing, the wound fils in from the base with the formation of a larger amount of granulation tissue, such type of healing of the open wound is known as healing by “secondary intention” or “secondary healing”.
• The secondary healing occurs essentially by the same process as seen in the primary healing, the only diffrence is that a more severe inflmmatory reaction and an exuberant firoblastic and endothelial cell proliferation occur in the later.
• In secondary healing, once the blood clot is removed, proliferation starts, the granulation tissue fils up the entire area, contraction ofwound occur and the epithelium begins to grow over it, until the wound surface is completely epithelized.
• Later on, the inflmmatory exudates disappear slowly and the firoblasts produce large amounts of collagen.
  Most of the healing processes occurring due to secondary intention,result in scar formation at the healing site.
  However, in the oral cavity scars are very rare.

• It begins at the time of injury and lasts 2–4 days.
• This phase is characterized by hemostasis and inflmmation.
• First hemostasis occurs and there is formation of the platelet plug.
• Injury to vascular tissue initiates the extrinsic coagulation pathway by releasing intracellular calcium and tissue factor that activate factor VII. Resulting firin plug leads to hemostasis which is aided by reflx vasoconstriction.
• Now this plug acts as a lattce for aggregation of platelets,this is the indication of early inflmmatory phase.
• In inflammatory phase, both bacteria and debris are phagocytosed and removed, now the factors are released that cause the migration and division of cells involved in the proliferative phase.

“Steps to explain the physiology of wound healing: Stages vs factors vs complications: Q&A guide”

• Collagen which were exposed at the time of wound formation causes activation of the clottng cascade (both the intrinsic and extrinsic pathways), initiating the inflmmatory phase.
• Injured tissues, via activated phospholipase A, catalyze arachidonic acids to produce potent vasoconstrictors thromboxane A2 and prostaglandin 2-alpha, which is collectively known as eicosanoids.
  This initial response limits hemorrhage.
• After a short period of time capillary vasodilatation occurs which is due to local histamine release, and the cells of inflmmation migrate to the wound bed.
• Chemical mediators, i.e. platelets release platelet-derived growth factor (PDGF) and and transforming growth factor beta (TGF-β) from their alpha-granules attact neutrophils and macrophages.
• Now, neutrophils scavenge for bacteria and foreign debris and macrophages continue to release growth factors to attact firoblasts and enter in the next phase of wound healing.

• It starts from day 3 and last for 3 to 6 weeks. It overlaps with the inflammatory phase.
  This phase is characterized by angiogenesis, collagen deposition, granulation tissue formation, and epithelialization.
• Fibroblasts initiate angiogenesis, epithelialization, and collagen formation. Fibroblasts migrate inside from wound margins over the firinous matrix which is established during this phase.
• During fist week, firoblasts begin secreting glycosaminoglycans and proteoglycans, the ground substance for granulation tissue, as well as collagen, in response to macrophage-synthesized FGF and TGF-β, as well as PDGF.
• Fibroblasts grow and form a new, provisional extracellular matrix (ECM) by excreting collagen and fironectin.
• There is re-epithelialization of the epidermis, in which epithelial cells proliferate and reaches to the wound bed,providing cover for the new tissue.
  This process starts from the basement membrane, if the basement membrane remains intact, otherwise the process initiates from the wound edges.
• Fibroblasts produce mainly type III collagen in this phase.
• As firin clot and provisional matrix degrades, there is deposition of granulation tissue (ground substance, collagen, capillaries), which continues until the wound is covered.
  Granulation tissue formed during this phase, is important in secondary wound healing.

• Remodeling continues for 6–12 months after injury.
• In this, there is maturation of collagen by cross linking and realignment of collagen fiers along the line of tension which is responsible for tensile strength ofscar. Vascularity of wound reduces.
  Fibroblast and myofiroblast leads to wound contraction.
  Here Type III collagen is replaced by Type I collagen causing maturity of collagen.
  Ratio of Type I collagen to Type III collagen is 4:1.
• Early extracellular matrix consists of fironectin and collagen Type III; eventually it consists of glycosaminoglycans and proteoglycans; fial matrix consists of Type I collagen.
• Strength of scar is 3% in one week, 20% in 3 weeks, 80% in 12 weeks. Finally, matured scar is acellular and avascular.