ABSTRACT
Recent advances in the molecular and cellular biology of fetal wound healing and the fetal phenotype of scarless healing have opened up new avenues in our understanding of the mechanisms for preventing/controlling scarring following postnatal injury. Fetal wounds heal rapidly, without formation of a scab, with reduced inflammatory and angiogenic responses, with different extracellular matrix composition, with enhanced regeneration of epithelial and mesenchymal tissues, and with a different growth factor profile compared with adult wounds (13). Over the last decade, the role of growth factors in wound healing has been studied extensively. Whitby and Ferguson (2) used immunolocalization techniques to compare the differences among the growth factor profiles of healing upper lip wounds in fetal, neonatal, and adult mice. While platelet-derived growth factor (PDGF) was detected in fetal, neonatal, and adult wounds, transforming growth factor-β1,2 (TGF-β1,2) was only detected in neonatal and adult wounds, which heal with scar formation, and not in the fetal wounds, which heal without scar formation (2). Using in situ hybridization and immunolocalization techniques, Martin et al. (4) reported a rapid but transient expression of TGF-β1 in fetal wounds compared with adult wounds in which the expression of TGF-β1 appeared much slower and was sustained for a longer period of time. Moreover, Krummel et al. (5), Adolph et al. (6), Houghton et al. (7), and Haynes et al. (8) have demonstrated that fetal wounds can be made to heal with scar formation
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by exogenous addition of TGF-β or PDGF. This suggests that growth factors not only play a crucial role in wound healing, but also appear to influence the quality of healing.
