You can read part 6 of most common disease before reading part 7.
Saliva and Dental Caries
The immediate environment of the teeth is bacterial plaque, but saliva is the medium in which plaque develops and works. Though saliva inevitably plays some part in the process of caries, it is a complex secretion whose rates of flow, composition and properties are not easy to determine.
Effects of Desalivation
Salivary flow is highly important in clearing cariogenic foods from the mouth. In animals, removal or inactivation of major salivary glands leads to increased caries activity roughly in proportion to the reduction in saliva production. Dental caries may also become rampant in humans with xerostomia due to salivary gland disease.
Rate of Flow and Buffering Power
The buffering power of saliva depends mainly on its bicarbonate content and is increased at high rates of flow. The buffering power of the saliva affects the buffering power of dental plaque to some degree and helps to prevent the pH from falling to very low levels. A rapid flow rate, with greater salivary buffering power that is associated, has been found to be associated with low caries activity. In Down’s syndrome, caries activity is low in spite of gross accumulation of plaque and immunodeficiencies possibly because of the high rate of salivation with greater buffering power. Whilst a rapid flow of saliva of low viscosity assists clearance of foodstuffs from the mouth, other physical properties of different salivas have not been shown to have a significant relationship to caries activity.
Other Factors
Inorganic Components and Enamel Maturation
Radioactive isotope studies suggest that there is some exchange of calcium and phosphate ions between enamel surface and saliva. In particular enamel undergoes post-eruptive changes. Clinical observations suggest that newly erupted teeth are more susceptible to caries than adult teeth and radioactive tracer studies show that newly erupted teeth can incorporate 10 to 20 times as much inorganic material in ionic form as adult teeth. More important is that saliva is a vehicle for fluoride which can enter plaque from the saliva and affect caries activity.
Enzymic Activity
Salivary amylase breaks down polysaccharides such as starch. This contribution to digestion is small, and its main value is to make food residues on the teeth more soluble to assist their clearance. The breakdown of polysaccharides leads to production of sugars, but the amounts and their contribution to caries are small and are only likely to be seen with experimental sucrose-deficient diets. Usually, the amount of sucrose present in the diet overwhelms that produced by amylase activity. In general, therefore, amylase activity and caries prevalence are not closely related.
Antibacterial Activities
Saliva contains thiocyanates, a lysozyme-like substance and other theoretically antibacterial substances. Nevertheless the mouth teems with bacteria, and there is no evidence that nonspecific antibacterial substances in saliva have any significant effect on caries activity.
Immunological Defences
IgA is secreted in saliva but small amounts of IgG enter the mouth from the gingival crevice. Persons who suffer from defects in non-specific host defences (complement and neutrophils) or specific immunological defences (IgA deficiency, Down’s syndrome or AIDS) do not appear to suffer an excess of dental caries. Nevertheless, an immunological host resistance to dental caries is detectable experimentally in man and appears to act by reducing the number of S. mutans in plaque. The effect does not appear to be very potent and is easily overwhelmed if the diet is high in sucrose or if low levels of the relevant antibody are produced.
Immunological defences against S. mutans could be mediated by salivary IgA or serum IgG from the crevicular fluid. Although salivary IgA is capable of preventing caries in experimental animals it appears to play no significant role in humans. Immunization of monkeys against S. mutans generates specific serum IgG which protects them against caries. Serum IgG also appears to protect against S. mutans in humans but the response varies widely between individuals.
It has been shown that dripping a solution of monoclonal antibody against S. mutans onto the teeth prevents recolonization by S. mutans in humans. However, plaque must be removed before treatment by using chlorohexidine and effective oral hygiene. This effect of antibody lasts for several months after applications and this ‘passive immunization’ may reduce caries activity significantly.
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