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Cleft palate patients often show mid-facial growth impairment after surgical closure of the defect. This is a consequence of palatal wound healing, and more specifically of wound contraction and scar tissue formation. Cells of the fibroblast lineage are responsible for these processes and they display different phenotypes in the course of the wound healing process. The aim of this study was to analyze the in vitro adhesion and migration of wound fibroblasts, isolated during the palatal wound healing process in the rat. Additionally, we analyzed the expression of beta1 integrins and vinculin, the key players in adhesion and migration. Palatal fibroblasts from age-matched controls were analyzed to measure the effects of normal aging. Palatal fibroblasts from unwounded tissue showed a low migratory behavior (<25 microm), a strong capability to adhere (>80%) and a low expression of beta1 integrins and vinculin. In contrast, fibroblasts obtained from healing palatal wounds were highly migratory (>200 microm) coupled to a weak capability to adhere (<65%) and a high expression of vinculin and beta1 integrins. These data show that the palatal wound healing process induces a change in fibroblast phenotype from "quiescent" to "activated," which persists in vitro.

Wound healing after cleft palate surgery is often associated with impairment of maxillary growth and dento-alveolar development. Wound contraction and scar tissue formation contribute strongly to these effects. In vitro studies have revealed that fibroblasts isolated during different phases of palatal wound healing show phenotypical differences. They change from a quiescent to an activated state and then partly back to a quiescent state. In this study, we evaluated the existence of fibroblast phenotypes at several time-points during palatal wound healing in the rat. Based on cytoskeletal changes (alpha-sma, vimentin, vinculin), integrin expression (alpha1, alpha2, alpha(v) and beta1) and changes in cellularity, we conclude that phenotypically different fibroblast populations are also present during in vivo wound healing. Alpha-sma and the integrin subunits alpha1 and alpha(v) were significantly up-regulated, and vinculin was significantly down-regulated, at early time-points compared to late time-points in wound healing. These changes point to an activated fibroblast state early in wound healing. Later in wound healing, these activated fibroblasts return only partially to the unwounded situation. These results strongly support the idea that different fibroblast populations with specific phenotypes occur in the course of palatal wound healing.

Background: Wound contraction and scar formation after cleft palate repair impair the growth of the maxilla. The implantation of a growth factor-loaded scaffold might solve these problems. Methods: The tissue response to fibroblast growth factor (FGF)-2 loaded collagen scaffolds was evaluated after implantation in the palate of rats. Scaffolds, with and without FGF-2, were implanted submucoperiosteally in the palate of 25 rats and evaluated after up to 16 weeks. On hematoxylin and eosin (H&E)-stained sections, the cell density and the number of giant cells within the scaffolds were quantified. Infiltration of inflammatory cells, myofibroblasts, and the number of blood vessels were quantified after immunohistochemistry. Results: The cell density was significantly higher in the FGF-2 group up to 4 weeks after implantation (102% at 2 weeks, P < 0.001). The number of blood vessels was also significantly higher in the FGF-2 group at 1 and 2 weeks (316% at 1 week, P = 0.003), but the myofibroblast score was lower (100% at 2 weeks, P = 0.008). A comparable mild and rapidly subsiding inflammatory response and foreign body reaction were found in both groups. Conclusion: FGF-2-loaded scaffolds displayed a faster influx of host cells, an increased rate of vascularization, and a reduced differentiation of myofibroblasts. These scaffolds might therefore be highly suitable for intra-oral reconstructions, such as cleft palate repair. [ABSTRACT FROM AUTHOR]

Abstract: The biomechanical character of the periodontal ligament (PDL) is crucial in its response to functional and orthodontic forces. Collagen has been the primary subject of investigations in this field. Several studies, however, indicate that oxytalan fibres, which belong to the elastic fibre family, also contribute to the biomechanical character and behaviour of the PDL. In order to elucidate this, we have evaluated the available literature on the oxytalan fibre network within the PDL and supra-alveolar tissues with respect to development, morphology and distribution, and response to mechanical stimulation. To this end, we have combined the classical histological studies with more recent in vitro studies. Oxytalan fibres develop simultaneously with the root and the vascular system within the PDL. A close association between oxytalan fibres and the vascular system also remains later in life, suggesting a role in vascular support. Mechanical loading of the PDL, through orthodontic force application, appears to induce an increase in the number, size, and length of oxytalan fibres. In line with this, in vitro stretching of PDL fibroblasts (PDLFs) results in an increased production of fibrillin, a major structural component of the microfibrils that make up oxytalan fibres. The available data suggest a mechanical function for oxytalan, but to date experimental data are limited. Further research is required to clarify their exact mechanical function and possible role in orthodontic tooth movement. [Copyright &y& Elsevier]