This review updates the surgeon about the cellular, matrix, and growth factor components of scarless fetal wound repair.Summary Background Data
Fetal skin wound healing is characterized by the absence of scar tissue formation. This unique repair process is not dependent on the sterile, aqueous intrauterine environment. The differences between fetal and adult skin wound healing appear to reflect processes intrinsic to fetal tissue, such as the unique fetal fibroblasts, a more rapid and ordered deposition and turnover of tissue components, and, particularly, a markedly reduced inflammatory infiltrate and cytokine profile. Scarless fetal wounds are relatively deficient in the inflammatory cytokine, transforming growth factor β (TGF-β). In contrast, the fibrosis characteristic of adult wound repair may be associated with TGF-β excess. Recent experimental studies suggest that specific anti-TGF-β therapeutic strategies can ameliorate scar formation in adult wound repair and fibrotic diseases. Inhibitors of TGF-β may be important future drugs to control scar.Conclusions
Based on the scarless fetal wound repair model, a number of ways in which the matrix and cellular response of the healing adult wound might be manipulated to reduce scarring are reviewed.