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Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

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Keloid scars are a result of an imbalance in wound healing physiology with an excessive deposition of collagenous connective tissue. There is excessive production of collagen, reduced degradation or both processes occurring concurrently. A variety of theories have been put forward to explain this:

  • excessive inflammation:
    • fibroproliferative scars have many features of ongoing inflammation
    • mammalian wounds in utero have a blunted inflammatory response and less tendency to scarring
    • addition of anti-TGF beta-1 or 2 to wounds (profibrogenic, inflammatory molecules) reduces scarring in adult rodent wounds, the same is true for the addition of exogenous TGF beta-3 (antifibrogenic)
    • other suggested pro-fibrogenic, inflammatory molecules suggested to be increased in keloid wounds include FGF, EGF, PDGF, IGF-1 and IL-4
    • anti-fibrogenic molecules include TNF-alpha, interferon gamma, and IL-1
    • the balance of these molecules is suggested to attract an excessive number of fibroblasts which secrete increased amounts of collagen
  • fibroblast abnormality:
    • cultured fibroblasts from keloids demonstrate increased procollagen production with elevated levels of type I to type III collagen
    • keloid, as opposed to normal, fibroblasts:
      • secrete other extracellular matrix elements at increased concentration including fibronectin, elastin and proteoglycans
      • secrete such molecules at an increased rate in response to cues such as increased tension across a collagenous scaffold in which they are seeded and the application of cytokines
    • there may be an intrinsic failure of myofibroblasts to undergo a normal wave of apoptosis at the end of the proliferative phase of wound healing
  • aberrant remodelling:
    • reduced activity of the enzymes which remodel collagen in the late stages of scar production
    • alpha-1-antitrypsin and alpha-2-macroglobulin are raised at this time and both are inhibitors of collagenases
    • TIMP molecules may have a similar action
  • microvascular hypoxia:
    • electron micrographic studies suggest that although there are increased numbers of vessels in the keloid scar, they may be occluded due to endothelial cell division
    • the subsequent hypoxia is thought to be a stimulus to fibroblast growth
  • immune dysregulation:
    • both humoral and cell-mediated immunity seem to be aberrant in keloidal scarring
    • increased levels of histamine and immunoglobulins have been identified
    • a specific anti-nuclear antibody to keloidal cells has been noted; this may act as a stimulant
    • antigen-presenting cells may downregulate the T cell response to injury by reducing levels of the antifibrogenic cytokine IL-1
  • miscellaneous theories:
    • excessive responsiveness to hormonal fluxes
    • excess neuronal re-innervation
    • increased levels of wound nitric oxide or free radicals
    • altered lipid environment of the wound
    • reduced barrier function of the epidermis

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