Aggregatibacter actinomycetemcomitans is considered to be a major etiological agent of aggressive periodontitis and includes serotype a to g strains. We herein report the first complete genome sequence of A. actinomycetemcomitans serotype g strain NUM4039. The genome is 2,382,853 bp in length with a G+C content of 44.34%.

The purpose of this study was to assess the antibacterial efficacy of incorporating catechins into 4-META/MMA-TBB resin against Streptococcus mutans and to measure the shear bond strength of a metal bracket bonded to enamel using catechin-incorporated with 5% 4-methacryloyloxyethyl trimellitate anhydride (4-META)/methyl methacrylate (MMA)-tri-n-butyl borane (TBB) resin (catechin-resin). Catechin-resin disks were incubated with the bacterial suspension at 37 °C for 24 h. The bacterial counts (colony forming units) of the disk and the suspension were determined separately. Catechin release from catechin-resin was monitored. The catechin-containing composites were used to bond metal brackets to human premolars pretreated with self-etching primer. After the bonded samples were immersed in water at 37 °C for 24 h, shear bond strength was measured.The most significant antibacterial activity was observed in (-)-epigallocatechin gallate-resin disk and (-)-epigallocatechin gallate-resin-treated bacterial suspension when compared with the control. Catechin was released from catechin-resin during 6 week immersion in deionized water. (-)-Epicatechin gallate, (-)-epigallocatechin and (-)-epigallocatechin gallate showed a large amount of catechin release. Only significant differences was detected in bond strength between the control and (-)-epigallocatechin gallate. The addition of (-)-epigallocatechin gallate to 4-META/MMA-TBB resin confers an antibacterial effect while retaining sufficient bond strength.

Individuals with Down syndrome (DS) are prone to periodontitis. No studies have focused on mRNA expression of a proinflammatory cytokine, IL -1β and an antiinflammatory cytokine, IL -37 in gingival fibroblasts (GFs) derived from individuals with DS (DGFs) . We cultured GFs derived from non -DS individuals (NGFs) and DGFs with outer membrane vesicles from Porphyromonas gingivalis (P -OMVs) . IL -1β and IL -37 mRNA expression was quantified using realtime PCR. Extracellular signalregulated kinase (ERK) 1/2 phosphorylation was performed by western blotting. We also analyzed the effect of an ERK1/2 inhibitor on IL -1β and IL -37 mRNA expression in GFs. Furthermore, we examined the influence of recombinant IL -37 (rIL -37) on the cellular response of GFs. We quantified mRNA expression of IL -8 using realtime PCR and measured IL -8 productions in culture medium by an enzymelinked immunosorbent assay.IL -1β mRNA expression and phosphorylated -ERK1/2 expression were significantly higher in P -OMVsstimulated DGFs than in NGFs. In contrast, IL -37 mRNA expression was significantly lower in P -OMVstimulated DGFs than in NGFs. P -OMVsinduced IL -1β and IL -37 mRNA expression in NGFs was reduced by an ERK1/2 inhibitor, while P -OMVsinduced IL -37 mRNA expression was not reduced by an ERK1/2 inhibitor in DGFs. P -OMVsinduced IL -8 mRNA expression and protein production were decreased by rIL -37 in both NGF and DGFs. It is considered that the imbalance of proand antiinflammatory responses via ERK1/2 in DGFs may cause severe periodontal inflammation in DS. In addition, IL -37 may be a key mediator of the antiinflammatory response in DGFs. These results provide insights into the therapeutic potential of targeting antiinflammatory factors for severe periodontal inflammation in DS.