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Keywords:

  • endodontic sealer;
  • enzyme-linked immunosorbent assay;
  • fibroblasts;
  • macrophages;
  • prostaglandin;
  • viability

Abstract

Aim  To determine whether commonly used endodontic sealers could either induce or increase the release of prostaglandin E2 (PGE2) when in contact with cell types found in the periapical tissues.

Methodology  Freshly mixed samples of Roth 801 sealer, Sealapex® and ProRoot® mineral trioxide aggregate (MTA) were placed in contact with cultured macrophages and fibroblasts for 24 h. The supernatant from the cultures was assayed for PGE2 using enzyme-linked immunosorbent assay. Cell viability counts were made. As a positive control, similar cultures were also exposed to lipopolysaccharide and the supernatant analysed for PGE2. Data were compared by anova.

Results  The three materials examined in these experiments did not stimulate increased PGE2 release from either of the cell lines. In control cultures, lipolysaccharide increased PGE2 release from macrophages but not from fibroblasts. Viability counts revealed that, whilst Roth 801 sealer caused some cell death in both fibroblasts and macrophages, Sealapex® led to cell death only in the macrophage cultures. ProRoot® MTA did not lead to statistically significant cell death in either culture.

Conclusions  Under 24-h culture conditions, the three freshly mixed test materials did not increase directly either production or release of PGE2 from either macrophages or gingival fibroblasts. Roth 801 decreased cell viability counts for both fibroblasts and macrophages. Sealapex® decreases macrophage viability. ProRoot® MTA did not affect viability in either cell line.