[P-032] 歯石により誘導されるHSC-2口腔上皮細胞の細胞死において結晶構造および菌体成分が果たす役割
The role of crystalline structures and microbial components in HSC-2 oral epithelial cell death induced by dental calculus
研修コード：2504
キーワード：歯石、細胞死、結晶構造
Objective: Previously, we found that dental calculus could induce cell death via NLRP3 inflammasome in HSC-2 oral epithelial cells. Dental calculus contains both crystalline structures and microbial components, however, the relative importance of these components in HSC-2 cell death has not been investigated. This study aimed to determine which component of dental calculus plays an important role in HSC-2 cell death.
Materials and methods: To inactivate microbial components, dental calculus samples from five periodontitis patients were treated at 250ﾟC for 1 hour（baked）or left untreated（unbaked）. HSC-2 cells were exposed to 500 μg/ml of unbaked or baked calculus. The cells were also exposed to synthetic hydroxyapatite（HA）crystals, which contain no microbial components, in the presence or absence of LPS or Pam3CSK4. After 24 hours, cytotoxicity was quantified by measuring lactate dehydrogenase release in the culture supernatants.
Results: Unbaked and baked calculus induced a similar level of cell death in HSC-2 cells. HA crystals also induced cell death in HSC-2 cells and addition of LPS or Pam 3CSK 4 did not change its cytotoxicity.
Conclusion: Crystalline structures play a major role in the HSC-2 cell death induced by dental calculus. The non-significant contribution of microbial products to cell death might be due to the low sensitivity of HSC-2 cells to microbial ligands.
Materials and methods: To inactivate microbial components, dental calculus samples from five periodontitis patients were treated at 250ﾟC for 1 hour（baked）or left untreated（unbaked）. HSC-2 cells were exposed to 500 μg/ml of unbaked or baked calculus. The cells were also exposed to synthetic hydroxyapatite（HA）crystals, which contain no microbial components, in the presence or absence of LPS or Pam3CSK4. After 24 hours, cytotoxicity was quantified by measuring lactate dehydrogenase release in the culture supernatants.
Results: Unbaked and baked calculus induced a similar level of cell death in HSC-2 cells. HA crystals also induced cell death in HSC-2 cells and addition of LPS or Pam 3CSK 4 did not change its cytotoxicity.
Conclusion: Crystalline structures play a major role in the HSC-2 cell death induced by dental calculus. The non-significant contribution of microbial products to cell death might be due to the low sensitivity of HSC-2 cells to microbial ligands.