Abstract

The purpose of this study was (a) to evaluate the cytocompatibility of three resorbable and nonresorbable membranes in fibroblast and osteoblast-like cell cultures and (b) to observe the growth of those cells on the various barriers by scanning electron microscopy (SEM). Primary human periodontal ligament fibroblasts (HPLF) and human osteoblast-like cells (SAOS-2) were incubated with nonresorbable polytetrafluoroethylene (ePTFE) barriers and resorbable polylactic acid as well as collagen membranes. Cytotoxic effects were determined by XTT (mitochondrial metabolic activity) and sulforhodamine B assays (cellular protein content). In addition, HPLF and SAOS-2 grown for 21 days on the investigated barriers were evaluated by SEM. Data were analyzed statistically by ANOVA using the Wilcoxon-Mann-Whitney test (P < 0.05). No changes were established in the periodontal ligament fibroblasts and human osteoblast-like cells after incubation with the collagen membrane. Cytotoxic effects, however, were induced by the polylactic acid barrier which slightly inhibited cell metabolism of the periodontal fibroblasts (XTT: 90.1% +/- 3.6 of control value). Moderate cytotoxic reactions were caused by the nonresorbable ePTFE membrane in HPLF-cultures (XTT: 82.7% +/- 3.5) and osteoblast-like cell monolayers (XTT: 80.0% +/- 0.6%). Mitochondrial activity in both cell cultures was significantly reduced by ePTFE barriers in comparison to non-incubated control cells (P = 0.028). SEM analysis of cell behavior on barriers demonstrated the differences between these materials: collagen barriers were densely populated with HPLF and SAOS-2, whereas only few or no cells were seen to adhere to the ePTFE and polylactic acid membranes. Our findings indicate that the collagen barrier investigated is very cytocompatible and may be integrated into connective tissue well. On the contrary, the ePTFE and polylactic acid membranes induced slight to moderate cytotoxic reactions which may reduce cellular adhesion. Thus, gap formation between the barrier surface and the connective tissue may be promoted which may facilitate epithelial downgrowth and microbial accumulation. Consequently, these effects may reduce the potential gain in periodontal attachment.

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