[Molecular mechanisms of wound scarring]

A few years ago, the discovery of growth factors, their pharmaceutical obtention at a purified grade, their powerful effects on cells in vitro, resulted in demeasured hopes that they could be applied easily and successfully to the treatment of wounds. Now, the process of healing is still uncompletely understood. The interplay of epithelial and matrix cells, the multiplicity of cell types involved, the huge number of growth factors implicated and the difficulties in describing the specific timing of their action on the cells present in wounds, explain why therapy of wound has not yet been revolutioned. An important distinction must be made between normal healing, which leads to a solid functional, reparation tissue, and scarring which opposes any functional healing by making extensive granulation tissue or even keloids. Recent studies pointed out the necessity of a convenient balance between the concentrations of growth factors present in the wound during the different stages of healing. Excess connective tissue production (scarring) would be more particularly due to an excess of TGF beta 1, whereas predominance of TGF beta 3 conducts to harmonious healing.