日本歯周病学会60周年記念京都大会

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一般演題ポスター

微生物

一般演題ポスター
微生物

2017年12月16日(土) 09:00 〜 17:00 ポスター会場 (さくら)

P-031~P-034
(ポスター討論:11:40~12:30)

[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

SM Ziauddin1,吉村 篤利1,Jorge Luis Montenegro Raudales1,尾崎 幸生1,樋口 賀奈子1,金子 高士2,原 宜興1/SM Ziauddin1,Atsutoshi Yoshimura1,Jorge Luis Montenegro Raudales1,Yukio Ozaki1,Kanako Higuchi1,Takashi Kaneko2,Yoshitaka Hara1 (長崎大学大学院医歯薬学総合研究科 歯周病学分野1,福岡歯科大学口腔医療センター2/Department of Periodontology, Nagasaki University Graduate School of Biomedical Scieces1,Center for Oral Diseases, Fukuoka Dental College2)

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.