(117) Lipopolysaccharide but not lipoteichoic acid induces inflammation and sensitization of nerve ending in the dental pulp

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Painful pulpitis is an inflammation of the dental pulp caused by bacterial proliferation near the pulp after tooth damage or caries. Previous data show that toxins produced by bacteria are particularly important in the induction of inflammation, and the toxin lipopolysaccharide can directly activate sensory neurons. In this study we evaluated the effects of the bacterial toxins lipopolysaccharide (LPS) from E. coli and lipoteichoic acid (LTA) from Bacillus subtilis on neuronal sensitization and cytokine production in an ex vivo model using human tooth slices. Healthy 3rd molars were collected and sectioned to obtain 2-3 slices, 1mm thick, per tooth. Tooth slices were treated with either LPS (1 and 100ug/ml), LTA (1 and 100ug/ml) or control media culture for 3 or 24h. After incubation with LPS or vehicle, calcitonin gene related peptide (CGRP) release from peripheral sensory nerve endings was stimulated with capsaicin (6 mM), and the supernatent was collected, concentrated and CGRP was quantified by ELISA. The release of the cytokines (IFNγ, IL10, IL12p70, IL13, IL1β IL2, IL4, IL6, IL8 and TNFα) in the culture media was quantified with an MSD multiplex assay kit. Although 3h treatment with LPS did not induce changes in CGRP or cytokine release compared to control tooth slices, 24h treatment with LPS (100μg/ml) increased the release of CGRP from sensory nerve endings, pro-inflammatory cytokines, IFNγ, IL1β and TNFα and the anti-inflammatory cytokine IL10 from the dental pulp. In contrast, 24h treatment with LTA (1 and 100 μg/ml) did not affect the level of CGRP or cytokine release compared to control tooth slices. In conclusion, LPS is a more important toxin than LTA in producing neuronal sensitization and inflammation that contribute to painful pulpitis.