Consideration of salivary factors in caries models rarely extends beyond viewing saliva as a sink or diluent for plaque metabolic products, or as a source of buffering, for neutralizing plaque acids. In reality, saliva has a complex chemistry and a wide range of biochemical activities that may significantly affect plaque chemistry and microbiology. Thus, saliva is a major source of microbial nutrients, without which bacterial acid production is diminished. Buffering by salivary bicarbonate, and base production from urea and basic amino acids and peptides, significantly affect Stephan curves. Saliva is supersaturated with respect to basic calcium phosphate salts and contains novel inhibitors of calcium phosphate precipitation, while specific salivary proteins bind calcium. It seems important to consider if this system is reflected in plaque. Saliva, with contributions from serum and bacterial constituents, provides most of the precursors for the acquired enamel pellicle, which acts to slow demineralization during caries attack. Pellicle constituents appear to influence initial bacterial colonization of tooth surfaces and, therefore, may affect the microbial composition of plaque, but their detailed effects on plaque are poorly understood. Microbial adaptations to the anti-bacterial systems also seem important but are poorly investigated. Thus, saliva possesses an array of activities that have substantial actual or potential impact on plaque and, therefore, merit consideration for inclusion in systems intended to model dental caries.
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