Objectives: Endodontic sealers are in intimate contact with apical tissues for long periods, yet the biological impact of many new endodontic sealers is not well understood. We assessed the cellular metabolic and inflammatory responses of monocytes to several contemporary endodontic sealers.
Methods: AH-Plus, Pulp Canal Sealer, Epiphany, Endo-Rez, and experimental Endo-Rez were mixed according to manufacturer's directions and formed into discs (n = 6), then aged in buffered-saline for 12 weeks. After aging, specimens were placed in direct contact with THP-1 monocytes for 72 h, after which the mitochondrial response (MTT) relative to Teflonâ (Tf) controls was measured. Other THP-1 cells were exposed to the aged materials to assess activation or suppression of activation when cells were exposed to lipopolysaccharide (LPS). Monocyte activation was estimated by TNFa, IL-1b and IL-6 secretion (ELISA). Cellular responses were compared ANOVA with Tukey post-hoc analysis (a = 0.05).
Results: Two of the five sealers, Epiphany and Pulp Canal Sealer, suppressed cell mitochondrial activity to < 30% of Tf controls at 12 weeks. Other sealers exhibited little mitochondrial suppression vs. Tf (p > 0.05). No sealer alone activated monocytic TNFa, IL-1b or IL-6 secretion (p > 0.05 vs. +LPS controls). However, when THP-1 were activated by LPS, differential suppression of TNFa, IL-1b and IL-6 secretion was significant for (Epiphany and Pulp Canal Sealer (p < 0.05) and suggested for two others (Endo-Rez and experimental version). There was poor correlation between suppression of mitochondrial activity and suppressed activation of cytokine secretion
Conclusion: The current results suggest that by themselves, common endodontic sealers do not activate monocytic TNFa, IL-1b and IL-6 secretion, but that the cytotoxicity of several aged sealers is sufficient to suppress activation of monocytes by LPS. Such suppression suggests a chronically elevated risk of impaired periapical healing.