Esomeprazole 20 mg was superior to placebo for on-demand treatment of GORD; a higher dose did not confer additional clinical benefit. Over 90% of patients were willing to continue on-demand treatment with esomeprazole 20 mg over a 6-month period.

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Initial attachment of the cariogenic Streptococcus mutans onto dental enamel is largely promoted by the adsorption of specific salivary proteins on enamel surface. Some phosphorylated salivary proteins were found to reduce S. mutans adhesion by competitively inhibiting the adsorption of S. mutans-binding salivary glycoproteins to hydroxyapatite (HA). The aim of this study was to develop antiadherence compounds for preventing dental biofilm development. We synthesized phosphorylated polyethylene glycol (PEG) derivatives and examined the possibility of surface pretreatment with them for preventing S. mutans adhesion in vitro and dental biofilm formation in vivo. Pretreatment of the HA surface with methacryloyloxydecyl phosphate (MDP)-PEG prior to saliva incubation hydrophilized the surface and thereby reduced salivary protein adsorption and saliva-promoted bacterial attachment to HA. However, when MDP-PEG was added to the saliva-pretreated HA (S-HA) surface, its inhibitory effect on bacterial binding was completely diminished. S. mutans adhesion onto S-HA was successfully reduced by treatment of the surface with pyrophosphate (PP), which desorbs salivary components from S-HA. Treatment of S-HA surfaces with MDP-PEG plus PP completely inhibited salivapromoted S. mutans adhesion even when followed by additional saliva treatment. Finally, mouthwash with MDP-PEG plus PP prevented de novo biofilm development after thorough teeth cleaning in humans compared to either water or PP alone. We conclude that MDP-PEG plus PP has the potential for use as an antiadherence agent that prevents dental biofilm development.Dental plaque, a complex microbial biofilm, is the primary etiologic factor in dental caries. Colonization of enamel surfaces by the cariogenic bacterium Streptococcus mutans is thought to be initiated by attachment to a saliva-derived conditioning film, the acquired enamel pellicle (9). The acquired enamel pellicle is formed largely by adsorption of heterogeneous salivary proteins (1, 18) onto dental enamel (ϳ98% [wt/wt] hydroxyapatite [HA]) and promotes the adhesion of S. mutans by specific (2, 17) and nonspecific (4) mechanisms.Saliva contains a multitude of proteins that contribute to oral microbial ecology and biofilm formation (6,16,32). A variety of salivary proteins have been shown to modulate bacterial adhesion onto HA surfaces in vitro. Adsorption of specific salivary proteins, such as acidic proline-rich proteins (8) and agglutinin (3), promotes the adhesion of S. mutans onto HA surfaces by providing ligands for bacterial attachment. Many studies thus far have suggested that an initial bacterial adhesion promoted by salivary protein adsorption onto the enamel surface contributes to facilitate dental biofilm development.Recently, we reported the clinical relevance of saliva-promoted S. mutans adhesion in both de novo dental biofilm development and caries experience (29). Dental biofilm formation after thorough teeth cleaning was positively correlated with both salivary glycoprotein content and S. mutans a...