6.5. Caries

In the groups with the sucrose diet, there was the smallest quantity of dentinal caries in metabolic alkalosis. There was also markedly less caries in the control group with normalosis and high-sucrose diet than in metabolic acidosis and respiratory alkalosis with the same diet. The group with respiratory alkalosis was slightly more affected by caries than the group with metabolic acidosis. These results were confirmed with Schiff staining. (The pilot studies supported the findings in the groups with metabolic acidosis and alkalosis.)

The occurrence and severity of dentinal caries were quite similar in the first and second molars, but different in the third ones. The first and second molars erupt almost at the same time, the first one 1-2 days before the second. Their eruption time is approximately the 16-18th day after birth (3-5 days before the beginning of the experiments) (Baker et al. 1980).

The caries lesions were most advanced and most numerous in the third molars in all the groups, even though the eruption of the 3rd molar occurs about 16 days later than that of the 1st and 2nd molars. The eruption time of the third molar is the 32-34th day after birth (11-13th day of the experiments) (Baker et al. 1980). The developmental stage of the third molars and, perhaps, the elevated amount of cariogenic micro-organisms in plaque at the time of eruption due to prolonged sucrose ingestion may make them more susceptible to caries.

Maturation of the enamel is incomplete at the time of eruption in all teeth, and this also increases the amount of caries in the molars in young rats, especially in the 3rd molar. Furthermore, the progression of dentinal caries has been found to be much slower in the teeth of adult rats than those of young ones (Kortelainen & Larmas 1994).

Metabolic alkalosis or acidosis were induced by using the alkalized or acidified drinking water. Thus, some of the effects of those waters on caries were probably mediated via the pH of the oral fluid locally. Bicarbonate-phosphate combinations (pH 7.4) added to sucrose has been demonstrated to reinforce oral natural buffers and lessen plaque fermentative pH fall in vitro (Luoma & Luoma 1967, 1968, Luoma et al. 1970) and in vivo (Luoma & Luoma 1968). With this method, caries prevention was observed in rats (Luoma et al. 1968). Although blood was not studied, the additive effect probably also reinforced the blood buffering.

In our study, respiratory alkalosis surprisingly had the strongest activating effect on caries, in spite of the fact that no local effect on mouth was present. Respiratory alkalosis is compensated in mammalian body by creating mild metabolic acidosis (and vice versa), although pH is never fully corrected (Brewer 1990). Metabolic compensation for respiratory alkalosis might be strong enough to enhance caries, but more likely there are also other, yet unknown effects, which accelerate caries progression in respiratory alkalosis. The changes in the dentinal growth and mineral contents were different between the groups with respiratory alkalosis and metabolic acidosis, which suggests that different mechanisms were involved in these states. These aspects need more experiments to be solved.

Previous research has demonstrated that chronic metabolic alkalosis increases the caries resistance of children"s teeth (Myllärniemi & Holmberg 1975), a finding which gains support from the present experiment with young rats" molar teeth. In spite of the small reduction in the dentine formation in the groups with metabolic alkalosis, the odontoblasts may build dentine of better quality, which, together with a possible rise in salivary pH, might increase the caries resistance.

Our results pointed to the harmful effect of the opposite state, chronic metabolic acidosis, on teeth. The results give reason to believe that, (in addition to the probable effects on saliva, which were not studied here), metabolic acidosis has a systemic impairing effect on the ability of pulp/dentine complex to resist caries attack, probably via the retarded growth, the altered structure and/or some other changes in the growth and development of dentine.

These factors are worth remembering in the treatment and prophylaxis of the teeth of chronically ill patients, especially of such children. Also, if no other reason is found for an exceptionally bad caries status, it seems to be worth while to check the acid-base status of the patient. This may sometimes help in finding an undiagnosed general disease, as has happened in our clinic (Bäckman et al. 1990). Furthermore, an interesting question arises: what are the effects of acidosis inducing high-protein diet and cola-drinks, in connection with candies and other sweet food, on the development and caries status of the yougsters" teeth?