[P1-2-18] Oral-bacterial metabolites may have a potential to increase bone mineralization and delay onset of inflammation at the blood-clot-losing socket wall surface after tooth extraction
Keywords:短鎖脂肪酸、骨、マクロファージ
When the blood clot is removed from the socket cavity, the surface of the cavity wall appears, and food remnant impaction occurs in the cavity. Bacteria resident in the surface of the cavity ferment the food remnant and produce high concentrations of short-chain fatty acids (SCFAs). In this study, we examined the effects of SCFA-treatment on macrophages, osteoblasts, and osteoclasts, which are residence in the cavity surfaces. Although LPS-treated Raw264.7 cells, a murine macrophage cell line, induced production of iNOS, a M1 macrophage marker, bacterial culture supernatants of Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn) reduced LPS-induced iNOS production. Then, each SCFA concentrations in the bacterial culture supernatants are measured, and SCFA-mixtures were prepared as mimics of bacterial culture supernatants. Treatments of cells with Pg or Fn mimic also reduced LPS-induced iNOS production. These results indicate that SCFAs, which are contained in the Pg- or Fn- culture supernatant, suppresses LPS-induced M1-macrophage formation. In addition, treatment with Pg or Fn mimics of bacterial culture supernatant increased murine preosteoblast MC3T3-E1 cell mineralization and decreased RANKL-induced osteoclast-like cell formation. Taken together, SCFAs produced by Pg or Fn may increase mineralization of the socket wall and delay onset of inflammation of the clot-losing cavity surface.