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Background: Lipopolysaccharide (LPS) is one of the leading causes of pulpitis. The differences in establishing an in vitro pulpitis model by using different lipopolysaccharides (LPSs) are unknown. This study aimed to determine the discrepancy in the ability to induce the expression of inflammatory cytokines and the underlying mechanism between Escherichia coli (E. coli) and Porphyromonas gingivalis (P. gingivalis) LPSs in human dental pulp stem cells (hDPSCs). Material and methods: Quantitative real-time polymerase chain reaction (QRT-PCR) was used to evaluate the mRNA levels of inflammatory cytokines including IL-6, IL-8, COX-2, IL-1β, and TNF-α expressed by hDPSCs at each time point. ELISA was used to assess the interleukin-6 (IL-6) protein level. The role of toll-like receptors (TLR)2 and TLR4 in the inflammatory response in hDPSCs initiated by LPSs was assessed by QRT-PCR and flow cytometry. Results: The E. coli LPS significantly enhanced the mRNA expression of inflammatory cytokines and the production of the IL-6 protein (p < 0.05) in hDPSCs. The peaks of all observed inflammation mediators’ expression in hDPSCs were reached 3–12 h after stimulation by 1 μg/mL E. coli LPS. E. coli LPS enhanced the TLR4 expression (p < 0.05) but not TLR2 in hDPSCs, whereas P. gingivalis LPS did not affect TLR2 or TLR4 expression in hDPSCs. The TLR4 inhibitor pretreatment significantly inhibited the gene expression of inflammatory cytokines upregulated by E. coli LPS (p < 0.05). Conclusion: Under the condition of this study, E. coli LPS but not P. gingivalis LPS is effective in promoting the expression of inflammatory cytokines by hDPSCs. E. coli LPS increases the TLR4 expression in hDPSCs. P. gingivalis LPS has no effect on TLR2 or TLR4 expression in hDPSCs. [ABSTRACT FROM AUTHOR]

Aim: To investigate the impact of chronic apical periodontitis (CAP) on atherosclerosis and gut microbiota by establishing a Porphyromonas gingivalis (P. gingivalis)‐induced CAP in an apolipoprotein E‐deficient (apoE−/−) mice model. Methodology: Twenty‐eight male apoE−/− mice were divided into two groups with 14 in each: CAP group and control group. In the CAP group, sterile cotton wool containing 108 colony‐forming units of P. gingivalis was placed into the pulp chamber after pulp exposure followed by coronal resin filling in bilateral maxillary first and second molars. The mice were fed with a chow diet to induce atherosclerosis. Animals were euthanized 16 weeks after the operation, and the periapical lesions of bilateral maxillary first and second molars were assessed by micro‐CT. After collection of aortic arches, atherosclerotic lesions were measured by Oil Red O staining. Serum levels of high‐density lipoprotein cholesterol (HDL‐C), low‐density lipoprotein cholesterol (LDL‐C), total cholesterol (TC), and triglycerides (TG) were measured. Stools were collected to detect alterations in gut microbiota by 16S rRNA gene sequencing. Independent samples t‐test was used to calculate the difference between the two groups. Results: CAP was observed in 98.2% of molars. A significant increase in atherosclerotic plaque formation in the aortic arches was found in the CAP groups (CAP: 2.001% ± 0.27%, control: 0.927% ± 0.22%, p =.005). No significant difference was observed between sevum level of HDL‐C (CAP: 2.295 ± 0.31 mmol/L, Control: 3.037 ± 0.55 mmol/L, p =.264) or LDL‐C (CAP: 17.066 ± 3.95 mmol/L, Control: 10.948 ± 1.69 mmol/L, p =.177) in CAP group and Control group. There were no significant differences in TG (CAP: 1.076 ± 0.08 mmol/L, control: 1.034 ± 0.13 mmol/L, p =.794) or TC (CAP: 6.372 ± 0.98 mmol/L, control: 6.679 ± 0.75 mmol/L, p =.72) levels between the two groups (p >.05). The alpha diversity was elevated in the CAP group. In terms of beta diversity, the CAP and control groups were clearly distinguished by the microbial community. Conclusion: In a mouse experimental model, pulp infection with P. gingivalis ‐induced CAP, thus aggravating the development of atherosclerosis. Meanwhile, CAP increased alpha diversity and altered the beta diversity of the gut microbiota. [ABSTRACT FROM AUTHOR]

Mechanical debridement supplemented with antibacterial agents effectively eradicates subgingival biofilms formed in the periodontal pockets of severe periodontitis patients. However, the available antimicrobial agents have limited penetrating ability to kill the bacteria encased in the deep layers of biofilms. This study aimed to fabricate a novel magnetic nanoparticle (MNP) loaded with rhamnolipid (RL) and vancomycin (Vanc, Vanc/RL-Ag@Fe 3 O 4) to combat subgingival biofilms. The multispecies subgingival biofilm was formed by periodontal pathogens, including Streptococcus oralis (S. oralis), Streptococcus sanguinis (S. sanguinis), Actinomyces naeslundii (A. naeslundii), Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum). Scanning electron microscope (SEM), confocal laser scanning microscopy (CLSM), and quantitative real-time polymerase chain reaction (qRT-PCR) were used to determine the anti-biofilm efficacy of Vanc/RL-Ag@Fe 3 O 4 with or without a magnetic field on multispecies subgingival biofilms. The minimal inhibitory concentration (MIC) values of Vanc/RL-Ag@Fe 3 O 4 on S. oralis , S. sanguinis , A. naeslundii , P. gingivalis , and F. nucleatum were 25, 50, 100, 50, and 25 μg/mL, respectively. Vanc/RL-Ag@Fe 3 O 4 (200 μg/mL) reduced the 7-d biofilm thickness from 22 to 13 µm by degrading extracellular polymeric substance (EPS) and killing most bacteria except for tolerant F. nucleatum. A magnetic field enhanced the anti-biofilm effect of Vanc/RL-Ag@Fe 3 O 4 by facilitating its penetration into the bottom layers of biofilms and killing tolerant F. nucleatum. Vanc/RL-Ag@Fe 3 O 4 MNPs can release RL, Vanc, and Ag and eradicate subgingival biofilms by disrupting EPS and killing bacteria. Vanc/RL-Ag@Fe 3 O 4 combined with a magnetic force is a promising approach for combating periodontal infection. [Display omitted] [ABSTRACT FROM AUTHOR]