๐ ็ธฝ็ฎ้ ๏ฝ ๐ ่ฑๆๅๆ๏ผๆฌ็ฏ๏ผ ๏ฝ ๐ ๅฎๆด็ฟป่ญฏ ๏ฝ โญ ็ฒพ่ฏ็ญ่จ
Importance
Importance
Debridement enhances wound healing in various ways, including the removal of nonviable or infected tissue. Left in wounds, necrotic tissue may serve as a nidus for the proliferation of bacteria and subsequent infection.8 Bacteria produce biofilms as a means of protection from the host inflammatory response during the wound healing process.9 The establishment of a biofilm within a wound hinders wound healing by creating a physical barrier to reepithelialization and through the release of waste products that induce a state of chronic inflammation.10 Once reaching critical level of colonization, local tissue damage ensues due to elevated levels of toxins and inflammatory cytokines.11 A bacterial concentration of greater than 105 bacteria per gram of tissue has been shown to reduce skin graft adherence and graft success.12,13
Debridement also facilitates the growth of a nonhealing wound edge via removal of senescent fibroblasts from the wound base and nonmigratory keratinocytes from the wound edge.6,7 Abnormal nuclear expression of ฮฒ-catenin in keratinocytes at the wound edge leads to the expression of c-myc, resulting in impaired keratinocyte function (differentiation, growth, and migration).14 In addition, microarray analysis of the wound edge of nonhealing ulcers showed a reduction in epidermal growth factor receptors, diminishing the response of keratinocytes to epidermal growth factor itself. Fibroblasts grown from the base of chronic wounds have also been shown to migrate slower than those from adjacent, intact skin and are less responsive to growth promoting factors.15 The removal of these senescent cells through debridement makes way for new keratinocytes and fibroblasts to promote reepithelialization and wound closure.7
Finally, debridement creates a new wound, and platelets recruited to the site of injury function not only to control hemorrhage, but also to initiate the first phase of wound healing. Platelets release multiple growth factors, including platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) which mediate the inflammatory phase of wound healing.8