Prostaglandin E 2 production and viability of cells cultured in contact with freshly mixed endodontic materials K. K. Melegari, T. M. Botero & G. R. Holland Department of Cariology, Restorative Sciences, and Endodontics, University of Michigan, School of Dentistry, Ann Arbor, MI, USA Abstract Melegari KK, Botero TM, Holland GR. Prostaglandin E 2 production and viability of cells cultured in contact with freshly mixed endodontic materials. International Endodontic Journal, 39, 357–362, 2006. Aim To determine whether commonly used endodon- tic sealers could either induce or increase the release of prostaglandin E 2 (PGE 2 ) when in contact with cell types found in the periapical tissues. Methodology Freshly mixed samples of Roth 801 sealer, Sealapex Ò and ProRoot Ò mineral trioxide aggre- gate (MTA) were placed in contact with cultured macrophages and fibroblasts for 24 h. The supernatant from the cultures was assayed for PGE 2 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 PGE 2 . Data were compared by anova. Results The three materials examined in these experiments did not stimulate increased PGE 2 release from either of the cell lines. In control cultures, lipolysaccharide increased PGE 2 release from macroph- ages but not from fibroblasts. Viability counts revealed that, whilst Roth 801 sealer caused some cell death in both fibroblasts and macrophages, Sealapex Ò led to cell death only in the macrophage cultures. ProRoot Ò 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 PGE 2 from either macrophages or gingival fibroblasts. Roth 801 decreased cell viability counts for both fibroblasts and macrophages. Sealapex Ò decreases macrophage viability. ProRoot Ò MTA did not affect viability in either cell line. Keywords: endodontic sealer, enzyme-linked immu- nosorbent assay, fibroblasts, macrophages, prostaglan- din, viability. Received 26 April 2005; accepted 11 October 2005 Introduction Following root canal treatment, discomfort occurs in a proportion of endodontic patients (Harrison et al. 1983, Genet et al. 1986). The painful response is inflamma- tory in origin either as the continuation of a preoper- ative condition and/or as a response to new irritation. One possible source of new or additional irritation is the endodontic sealer used to enhance the apical seal. The effect of these materials in their set condition has been examined in vitro (Willershausen et al. 2000, Pistorius et al. 2003), but there are few data on the effect of these materials when freshly mixed which may be more relevant to the immediate post-filling period. The principal mediators of inflammatory pain are products of the arachadonic acid pathway most notice- ably prostaglandin E 2 (PGE 2 ) (Juan 1978, Cohen et al. 1985, Samad et al. 2002). This has been found in inflamed periapical tissue (McNicholas et al. 1991, Takayama et al. 1996, Shimauchi et al. 1997) and is released from mouse macrophages when exposed to gutta-percha particles (Sjo ¨gren et al. 1998) and from Correspondence: G. R. Holland, Cariology, Restorative Sci- ences & Endodontics, University of Michigan, School of Dentistry, 1011 North University, Ann Arbor, MI, 48109- 1078, USA (Tel.: +1 734 763 3703; fax: +1 734 936 1597; e-mail: rholland@umich.edu). ª 2006 International Endodontic Journal International Endodontic Journal, 39, 357–362, 2006 doi: 10.1111/j.1365-2591.2006.01070.x 357