Neutralization and buffering of acids
Although while the effect of saliva in facilitating sugar clearance can partly explain why saliva reduces formation of plaque acids and therefore caries, the neutralizing and buffering actions of saliva are more dramatic. These are due predominantly to salivary bicarbonate, originating mainly from the parotid gland. In unstimulated saliva, the bicarbonate level is low; at the greater secretion rates of stimulated saliva, the concentration is higher, the pH rises, and the buffering power of saliva increases dramatically. There are also other less important buffering systems in saliva, such as macromolecular proteins.
Ingestion of sugar causes a drop in plaque pH. When saliva is experimentally prevented from entering the mouth (by cannulating the excretory ducts and discharging the saliva extraorally), the fall in plaque pH after ingestion of sugar is greater and more prolonged than when salivary access is normal. If, after ingestion of sugar, flow is stimulated by chewing of paraffin or cheese, the plaque exhibits an immediate and dramatic rise in pH and a fall in lactic acid concentration, accompanied by a change in its amino acid spectrum. Similar effects are seen with sugar-free chewing gum and even with sucrose-sweetened gum, provided that this is chewed for longer than the time it takes for the sugar to be dissolved.
Although the plaque of caries-resistant patients and the plaque of caries-susceptible patients respond similarly to a sugar challenge, the levels at which these responses occur are quite different. In the plaque from a caries-resistant person, the presugar pH is higher and the fall in pH after the sugar challenge is smaller. Studies have also shown that the capacity to buffer plaque acids is greater in caries-resistant patients than it is in caries-susceptible patients.
The buffering effects of saliva are mostly measured in vitro by laboratory methods or chairside methods. In the laboratory, 1.0 mL of saliva is mixed with 3.0 mL of hydrochloric acid (0.0033 M for resting saliva; 0.005 M for stimulated saliva). A stream of air is then passed through the mixture for 20 minutes and the pH (the “final pH”), is measured. If the air stream step, which removes carbon dioxide, is excluded, about the same results are obtained for saliva with low buffering effect, final pH 5 or lower.
Chairside tests are available, allowing the clinician to evaluate the salivary buffering effect directly after sampling and to discuss the results with the patient. In the Dentobuff Strip system (Fig 98a to 98c), one drop of stimulated saliva is placed on a test strip containing an acid and a pH indicator. After the reaction between saliva and acid, the color of the test pad is compared to a chart, and the final pH value is obtained. This test is highly simplified and will discriminate among low, medium, and high buffering capacities. The method is particularly useful for identifying individuals with risk values, that is, low buffering capacity (final pH of 4 or less). As with secretion rates, there is a normal range of buffer capacity, with no apparent relation to caries risk. However, below a threshold value (final pH less than 4), the carious process seems to be facilitated.
Figure 99 shows the frequency distribution of the buffering effects in males and females, taken from the previously described salivary study in adults by Heinze et al (1983); more females had low values (pH less than 4.0) for both resting and stimulated saliva. Notably, other studies have shown a dramatic reduction in salivary buffering effects during the last months of pregnancy, which may explain in part why caries incidence seems to increase during pregnancy.
On a population basis, there is a positive correlation between SSR and buffering
effect, but there are many individual exceptions. A low SSR combined with a low or
moderate buffering effect clearly indicates poor salivary resistance to microbial
attack: Clearance of microorganisms is slow, and the residual saliva, ranging in
various individuals from 0.5 to 1.0 mL, is spread as a thin film on the oral surfaces.
Fermentable carbohydrates dissolved in this small volume of saliva would be
neutralized only slowly, because of the low buffering effect.
The interpretation of salivary buffering tests in isolation is questionable. In most
investigations, there is little or no correlation with variables measuring different
aspects of dental caries. One important explanation is that the decisive events in a
carious attack take place in the plaque and below the enamel surface. In these loci, the
buffering mechanisms are very different from those found in saliva. It is unlikely that
salivary buffering substances could significantly influence pH changes in the depth of
the plaque, particularly in areas of limited accessibility, for example, the approximal
surfaces of the molars. The buffering capacity of the plaque may have greater
relevance, but test methods are as yet unavailable. On more accessible mandibular
lingual surfaces covered with only a thin plaque, the salivary buffering effect may
play a more significant role as a modifying factor in lesion development.
The human mouth is quite frequently exposed to agents that have a pH different from
that of saliva (6.5 to 7.5) and are potentially damaging to the teeth (erosion) or to the
mucosa. Under these conditions, the role of the buffering agents in saliva is to restore
the pH to the normal range as quickly as possible.
