The development of scarring following accidental injury or surgery is an important clinical problem, often resulting in adverse effects on frowth and function, as well as an undersirable cosmetic appearance. Adult wound healing and scar formation are characterised by acute inflammation, wound contraction and disordered collagen deposition. Similar processes may also be involved in the progression of fibrotic disease states such as pulmonary fibrosis and hepatic cirrhosis. A major clinical objective is therefore, the reduction, and ideally the prevention, of scarring. The embryo and early fetus respond to injury in a way that is fundamentally different from the adult. In general, the early fetus heals rapidly, without scar formation. Extracellular matrix deposition in the fetal wound is rapid and organised in its structure, much more similar in appearance to unwounded skin, whilst, in the adult, matrix deposition is disordered. The inflammatory response, charasterisitic of the early phase of adult wound healing, is absent, or highly limited, in the fetus and the levels of cytokines are generally greatly reduced. Research into fundamental cellular and molecular differences between adult and fetal wound healing have revealed a number o targets in the adult wound which can be manipulated to more closely resemble the fetal wound environment and hence result in the reduction of adult scarring.
Mast Cells Contribute to Scar Formation during Fetal Wound Healing
