Wound contraction and subsequent scar tissue formation is thought to be a main cause of the maxillary and dento-alveolar growth inhibition observed after cleft palate surgery. A reduction in wound contraction and scar tissue formation might prevent these iatrogenic effects. To achieve this, different approaches have been chosen in the past. Nowadays, a main approach is to interfere with fibroblast activity, since these cells play a key role during wound contraction and scar tissue formation. First, wound fibroblasts have to be characterized. Therefore, tissue samples were taken from different phases of the wound healing process in rats. The tissues were used to analyze the expression of different integrins and cytoskeletal markers in vivo and in vitro. Furthermore, the functional activity of fibroblast phenotypes was determined by comparing adhesion and migration of fibroblasts from early and late phases of wound healing with age-matched cells from unwounded palates. From the studies we can conclude that heterogeneous populations of fibroblasts are present in the course of palatal wound healing. These different subpopulations can be isolated and cultured, and maintain their characteristics up to seven passages. We distinguished two main fibroblast phenotypes both during palatal wound healing in vivo, and in vitro: an early activated phenotype and a late more quiescent phenotype. These fibroblast phenotypes were also observed in the functional assays for adhesion and migration. The modulation of activity of these specific fibroblast phenotypes might offer a good starting point for the control of wound contraction and scar formation. Ultimately, this will lead to an improved wound healing process after cleft palate repair