Influence of artificial saliva contamination on adhesion in class V restorations.

This study aimed to evaluate the effects of artificial saliva contamination on a glass ionomer cement (GIC), a resin-modified GIC (RMGIC), and a composite resin (CR) that was used with two different etching adhesive systems. Three surface conditions were created on bovine teeth using artificial saliva: control (group I), mild saliva contamination (group II), and severe saliva contamination (group III). The microtensile bond strength (µTBS) of CR with dentin was significantly lower in group III than in group I. However, the µTBS of GIC and RMGIC with both enamel and dentin showed no significant intergroup differences. Moreover, CR exhibited significantly greater microleakage on cementum in group III than in group I, whereas both GIC and RMGIC showed no significant differences for both enamel and cementum. Thus, GIC and RMGIC may be suitable for preventing secondary caries after class V restorative treatments when contamination by saliva cannot be avoided.

Contribution of Streptococcus gordonii Hsa Adhesin to Biofilm Formation.

Adhesion of oral mitis group streptococci, such as Streptococcus gordonii, to acquired pellicle on the tooth surface is the first step in oral biofilm formation. S. gordonii strain DL1 possesses an Hsa adhesin, which recognizes the terminal sialic acid of host sialoglycoconjugates. The aim of the present study was to investigate the role of the Hsa adhesin in biofilm formation. The biofilm-forming ability of a S. gordonii hsa mutant on microtiter plates pre-coated with saliva, fetuin, or mucin was significantly lower than that of wild-type strain DL1. In contrast, no significant difference in biofilm-forming ability was observed in plates pre-coated with bovine serum albumin, which does not contain sialic acid. The biofilm-forming ability of strain DL1 in saliva-coated microtiter plates was also significantly reduced when the plate was pre-treated with neuraminidase. The sialic acid-dependent biofilm-forming ability of different wild-type S. gordonii strains varied. However, Southern and western blot analyses showed that all the tested wild-type strains possessed and expressed hsa homologs, respectively. These results indicate that the binding of Hsa adhesin to sialoglycoconjugates is associated with biofilm formation of S. gordonii DL1, and imply variation in the contribution of Hsa and its homologs to S. gordonii biofilm formation.

Correction: Two Arginine Residues of Streptococcus gordonii Sialic Acid-Binding Adhesin Hsa Are Essential for Interaction to Host Cell Receptors.

[This corrects the article DOI: 10.1371/journal.pone.0154098.].

Two Arginine Residues of Streptococcus gordonii Sialic Acid-Binding Adhesin Hsa Are Essential for Interaction to Host Cell Receptors.

Hsa is a large, serine-rich protein of Streptococcus gordonii DL1 that mediates binding to α2-3-linked sialic acid termini of glycoproteins, including platelet glycoprotein Ibα, and erythrocyte membrane protein glycophorin A, and band 3. The binding of Hsa to platelet glycoprotein Ibα contributes to the pathogenesis of infective endocarditis. This interaction appears to be mediated by a second non-repetitive region (NR2) of Hsa. However, the molecular details of the interaction between the Hsa NR2 region and these glycoproteins are not well understood. In the present study, we identified the amino acid residues of the Hsa NR2 region that are involved in sialic acid recognition. To identify the sialic acid-binding site of Hsa NR2 region, we prepared various mutants of Hsa NR2 fused with glutathione transferase. Fusion proteins harboring Arg340 to Asn (R340N) or Arg365 to Asn (R365N) substitutions in the NR2 domain exhibited significantly reduced binding to human erythrocytes and platelets. A sugar-binding assay showed that these mutant proteins abolished binding to α2-3-linked sialic acid. Furthermore, we established S. gordonii DL1 derivatives that encoded the corresponding Hsa mutant protein. In whole-cell assays, these mutant strains showed significant reductions in hemagglutination, in platelet aggregation, and in adhesion to human leukocytes. These results indicate that the Arg340 and Arg365 residues of Hsa play an important role in the binding of Hsa to α2-3-linked sialic acid-containing glycoproteins.

Effects of surface reaction-type pre-reacted glass ionomer on oral biofilm formation of Streptococcus gordonii.

Streptococcus gordonii, a bacterium involved in the initial colonization of tooth surfaces, contributes to dental biofilm formation and is an important cause of infective endocarditis. This study aimed to investigate the influence of surface reaction-type pre-reacted glass ionomer (S-PRG) filler on oral bacterial growth and aggregation of S. gordonii. The effect of various concentrations of S-PRG eluate on the growth and the biofilm formation of S. gordonii and other oral microorganisms (Streptococcus mutans, Streptococcus oralis, Lactobacillus acidophilus, and Candida albicans) was assessed. In addition, the effect of S-PRG eluate on coaggregation of S. gordonii with both S. oralis and Fusobacterium nucleatum was assessed. The effect of S-PRG eluate treatment on autoaggregation of S. gordonii was also evaluated. Our results indicate that S-PRG eluate treatment reduced both for the growth and for biofilm of all organisms in a dose-dependent manner. Coaggregation of S. gordonii with both S. oralis and F. nucleatum was inhibited by S-PRG eluate, whereas autoaggregation of S. gordonii increased at certain concentrations of S-PRG eluate. These results indicate that the S-PRG filler possesses antimicrobial activity that is mediated by inhibiting growth and biofilm of oral microorganisms, and by suppressing coaggregation of S. gordonii. In addition, these findings indicate that coaggregation of S. gordonii with other bacteria is inhibited by increased autoaggregation of S. gordonii.