Detrimental dermal wound healing: what can we learn from the oral mucosa?

Wound Repair Regen. Sep-Oct 2013;21(5):648-60. doi: 10.1111/wrr.12072. Epub 2013 Aug 8.

Abstract

Wounds in adults are frequently accompanied by scar formation. This scar can become fibrotic due to an imbalance between extracellular matrix (ECM) synthesis and ECM degradation. Oral mucosal wounds, however, heal in an accelerated fashion, displaying minimal scar formation. The exact mechanisms of scarless oral healing are yet to be revealed. This review highlights possible mechanisms involved in the difference between scar-forming dermal vs. scarless oral mucosal wound healing. Differences were found in expression of ECM components, such as procollagen I and tenascin-C. Oral wounds contained fewer immune mediators, blood vessels, and profibrotic mediators but had more bone marrow-derived cells, a higher reepithelialization rate, and faster proliferation of fibroblasts compared with dermal wounds. These results form a basis for further research that should be focused on the relations among ECM, immune cells, growth factors, and fibroblast phenotypes, as understanding scarless oral mucosal healing may ultimately lead to novel therapeutic strategies to prevent fibrotic scars.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Actins / metabolism
  • Animals
  • Cicatrix / immunology
  • Cicatrix / pathology
  • Cicatrix / physiopathology*
  • Collagen Type I / metabolism
  • Endothelial Cells / metabolism
  • Extracellular Matrix / metabolism*
  • Fibroblasts / metabolism
  • Humans
  • Inflammation / immunology
  • Inflammation / physiopathology
  • Keratinocytes / metabolism
  • Mice
  • Mouth Mucosa / immunology
  • Mouth Mucosa / pathology
  • Mouth Mucosa / physiopathology*
  • Saliva / immunology*
  • Skin / immunology
  • Skin / pathology*
  • Tenascin / metabolism
  • Transforming Growth Factor beta / metabolism
  • Wound Healing* / immunology
  • Wounds and Injuries / immunology
  • Wounds and Injuries / pathology
  • Wounds and Injuries / physiopathology*

Substances

  • Acta2 protein, mouse
  • Actins
  • Collagen Type I
  • Tenascin
  • Transforming Growth Factor beta
  • collagen type I, alpha 1 chain