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Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/87

Title: Effect of Some Antiplaque Agents on the Activity of Glucosyltransferases of Streptococcus mutans Adsorbed onto Saliva-Coated Hydroxyapatite and in Solution
Authors: Vacca-Smith, Anne M.
Bowen, William H.
Keywords: Anti-plaque, mouthrinse, glucosyltransferase, glucan, streptococci, plaque
Issue Date: Sep-1996
Publisher: Biostrategy Associates
Citation: Biofilm Journal 1(1)
Abstract: The bulk of dental plaque is composed of bacterial-derived extracellular polysaccharide known as glucan, which is synthesized by streptococcal glucosyltransferase (Gtf) enzymes. At least three Gtf gene products of Streptococcus mutans have been identified. GtfB synthesizes a polymer of insoluble alpha1,3-linked glucan, GtfC produces a mixture of insoluble alpha1,3-linked glucan and soluble alpha1,6-linked glucan, and GtfD synthesizes an alpha1,6-linked soluble glucan. Polysaccharides are important in the development of plaque and in the pathogenesis of dental caries, so we therefore decided to explore the effects of putative antiplaque agents on the activities of streptococcal Gtf enzymes in solution and on the surface of parotid-saliva-coated hydroxyapatite (SHA) beads. Most of the agents tested, particularly cetylpyridinium chloride, hexylresorcinol, alexidine dihydrochloride and triclosan, inhibited the activity of GtfB in solution and on the surface of SHA beads. The agents moderately reduced the glucan-forming activity of GtfD in solution and on the surface of SHA beads, and had no effect on the activity of GtfC in solution or on the SHA surfaces. Several commercial mouthrinses were also evaluated for their effects on reducing Gtf activity; only Plax(R) (European formulation) significantly reduced Gtf activity, and its effect was limited to GtfB in solution. These data suggest that some mouthrinses are highly inhibitory towards GtfB enzymes only, and are with low effect on GtfC and GtfD. This lack of effect may in part explain the comparative poor clinical efficacy of some antiplaque agents.
URI: http://hdl.handle.net/1807/87
Appears in Collections:Bioline International Legacy Collection

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