(PR133) Protective Role of Bitter Taste Signaling Cascade in Modulating Pulpitis

Objectives: This study aims to investigate the protective and immune-modulating roles of the bitter taste signaling pathway during dental pulp injury (DPI). The comparison focuses on wild-type (WT) mice and knockout (KO) mice lacking key elements of the taste signaling cascade, specifically SKN1a/Pou2f3, GNAT3, and TRPM5.

Methods: Mechanical DPI was induced in the upper first molar of both WT and KO mice. SKN1a/Pou2f3, a transcription factor essential for the differentiation of cells involved in taste signaling, and GNAT3, a G-protein critical for bitter, sweet, and umami taste transduction, along with TRPM5, an ion channel needed for taste signal transmission, were examined in their roles related to protective immune responses. Histological analysis was performed at intervals up to 14 days post-intervention to assess immune cell infiltration, inflammatory progression, and tissue damage in the pulp.

Results: Significant differences were observed, particularly between the WT and SKN1a knockout (KO) groups. Wild-type (WT) mice exhibited less pulpal necrosis, which was limited to the upper coronal area, and showed more substantial immune cell infiltration throughout the root and part of the coronal pulp. In contrast, SKN1a KO mice displayed more severe pulpal necrosis, with immune cells confined to the root pulpal area. These findings suggest that bitter taste signaling pathway in WT mice plays a protective role by modulating immune responses and reducing tissue damage during pulpitis.

Conclusions: These findings suggest that the bitter taste signaling pathway plays a protective role as an immune modulator during dental pulpitis, potentially influencing the inflammation resolution process.