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Biofilm formation on dental implant surfaces can cause peri-implant mucositis and peri-implantitis. Lectins are involved in interactions between bacteria or between bacteria and their hosts. Disrupting these interactions via specific sugars can result in reduced adhesion and biofilm formation. The purpose of this study was to identify sugars that function as antiadhesion or antibiofilm agents on titanium discs. Of the sugars tested, the sugars that did not affect the planktonic growth of Streptococcus oralis , Fusobacterium nucleatum , and Porphyromonas gingivalis were selected. The selected sugars were assessed for their ability to inhibit biofilm formation of bacteria in single and consortium species by crystal violet staining, confocal laser scanning microscopy after live/dead staining, and scanning electron microscopy. The sugars were evaluated for their ability to inhibit activity of the quorum sensing molecule autoinducer 2 (AI-2) by bioluminescence assay. Biofilm formation of single bacteria or consortia of S. oralis , F. nucleatum , and P. gingivalis on titanium discs was significantly inhibited in the presence of d -arabinose. Pretreating titanium discs with d -arabinose for 3 min inhibited biofilm formation at a level comparable to that observed when d -arabinose was present over the entire period, suggesting that d -arabinose had initial anti-adhesive activity. In addition, d -arabinose inhibited the activity of AI-2. d -Arabinose may be a good candidate for application as an antibiofilm agent and AI-2 inhibitor. • d -Arabinose inhibited biofilm formation of S. oralis , F. nucleatum , and P. gingivalis on titanium discs. • Pretreatment of titanium discs with d -arabinose for 3 min resulted in significantly reduced biofilm formation. • d -Arabinose inhibited the activity of autoinducer 2, a quorum sensing molecule. [ABSTRACT FROM AUTHOR]

Abstract: Autoinducer 2 (AI-2) is a quorum sensing molecule and plays an important role in dental biofilm formation, mediating interspecies communication and virulence expression of oral bacteria. Fusobacterium nucleatum connects early colonizing commensals and late colonizing periodontopathogens. F. nucleatum AI-2 and quorum sensing inhibitors (QSIs) can manipulate dental biofilm formation. In this study, we evaluated the effect of F. nucleatum AI-2 and QSIs on biofilm formation of Streptococcus gordonii and Streptococcus oralis, which are initial colonizers in dental biofilm. F. nucleatum AI-2 significantly enhanced biofilm growth of S. gordonii and attachment of F. nucleatum to preformed S. gordonii biofilms. By contrast, F. nucleatum AI-2 reduced biofilm growth of S. oralis and attachment of F. nucleatum to preformed S. oralis biofilms. The QSIs, (5Z)-4-bromo-5-(bromomethylene)-2(5H)-furanone and d-ribose, reversed the stimulatory and inhibitory effects of AI-2 on S. gordonii and S. oralis, respectively. In addition, co-culture using a two-compartment system showed that secreted molecules of F. nucleatum had the same effect on biofilm growth of the streptococci as AI-2. Our results demonstrate that early colonizing bacteria can influence the accretion of F. nucleatum, a secondary colonizer, which ultimately influences the binding of periodontopathogens. [Copyright &y& Elsevier]

Abstract: Periodontitis is initiated by bacteria in subgingival biofilms, which are composed mostly of Gram-negative anaerobes. Autoinducer 2 (AI-2) is a universal quorum sensing (QS) molecule that mediates intergeneric signalling in multispecies bacterial communities and may induce biofilm formation. As Fusobacterium nucleatum is the major coaggregation bridge organism that links early colonising commensals and late pathogenic colonisers in dental biofilms via the accretion of periodontopathogens, we hypothesised that AI-2 of F. nucleatum contributes to this interspecies interaction, and interruption of this signalling could result in the inhibition of biofilm formation of periodontopathogens. To test this hypothesis, we evaluated the effect of partially purified F. nucleatum AI-2 on monospecies biofilm as well as mutualistic interactions between F. nucleatum and the so-called ‘red complex’ (Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia). Then we tested the effect of two QS inhibitors (QSIs), (5Z)-4-bromo-5-(bromomethylene)-2(5H)-furanone (furanone compound) and d-ribose, on AI-2-induced biofilm formation and coaggregation. F. nucleatum AI-2 remarkably induced biofilm growth of single and dual species and coaggregation between F. nucleatum and each species of the ‘red complex’, all of which were inhibited by the QSIs. F. nucleatum AI-2 induced the expression of the representative adhesion molecules of the periodontopathogens, which were inhibited by the QSIs. Our results demonstrate that F. nucleatum AI-2 plays an important role in inter- and intraspecies interactions between periodontopathogens via enhanced expression of adhesion molecules and may be a target for the inhibition of pathogenic dental biofilm formation. [Copyright &y& Elsevier]

• d -Galactose reduced biofilm formation of Streptococcus mutans. • d -Galactose increased biofilm formation of commensal oral streptococci. • d -Galactose inhibited the gene expression of S. mutans glucosyltransferases. • d -Galactose can be a valuable candidate substance for the development of oral hygiene products to prevent caries. In the oral microbial community, commensals can compete with pathogens and reduce their colonization in the oral cavity. A substance that can inhibit harmful bacteria and enrich beneficial bacteria is required to maintain oral health. The purpose of this study was to examine the effect of d -galactose on the biofilm formation of the cariogenic bacteria Streptococcus mutans and oral commensal streptococci and to evaluate their use in solution and in paste form. Biofilms of S. mutans , Streptococcus oralis , and Streptococcus mitis were formed on saliva-coated glass slips in the absence or presence of d -galactose and evaluated by staining with 1 % crystal violet. d -Galactose significantly inhibited the biofilm formation of S. mutans at concentrations ranging from 2 μM to 200 mM but increased the biofilm formation of S. oralis and S. mitis at concentrations of 2–200 mM. d -Galactose significantly inhibited three glucosyltransferase genes, gtfB , gtfC , and gtfD. The effect of d -galactose in the form of solution and paste was evaluated using bovine teeth. Pretreatment with 100 mM d -galactose on bovine teeth resulted in significantly reduced S. mutans biofilm formation. Our results suggest that d -galactose can be a candidate substance for the development of oral hygiene products to prevent caries by inhibiting the biofilm formation of S. mutans and simultaneously increasing the biofilm formation of commensal oral streptococci. [ABSTRACT FROM AUTHOR]