2.6. High-sucrose diet and dentine

Reduction in the growth of dentine in the molar teeth of young rats caused by a high-sucrose diet has been observed in numerous studies (Larmas et al. 1992, Tjäderhane et al. 1995, Huumonen et al. 1997, etc.). This effect is independent on the other dietary constituents as well as on the severity of caries (Tjäderhane et al. 1994).

The results also indicate that the reduction of dentine apposition is not caused by the caries, but by the systemic effects of a high-sucrose diet, because dentinogenesis was slowed down even under the intact fissures (Huumonen et al. 1997). And vice versa: slower dentinogenesis has not been found to increase (or decrease) the caries initiation or progression. This result has been obtained by reducing the dentine formation by means other than sucrose during the primary dentinogenesis (Huumonen et al. 1996).

Concerning molar fissures, it is difficult to confirm if microbial effects on dentine are totally avoided or not. The bacteria seem to be able to invade the enamel through surface microdefects. A cross-section reveals only one plane of enamel and the defects may remain unobserved (Seppä 1984, Seppä et al. 1989). Also, dentine may be infected through an incipient enamel lesion, even when no cavitation has occurred on the enamel surface. This has been reported both in rats (Luoma A-R. et al. 1984, Luoma H. et al. 1987, Seppä et al. 1989) and in humans (Brännström et al.1980, Seppä 1984, Seppä et al. 1985).

During secondary dentinogenesis, the rate of the dentine formation and the caries progression both are less than 1/10 of that during the the primary dentinogenesis. This suggests that there is a connection between the rate of caries progression and the deposition of the dentine. (Hietala & Larmas 1992, Kortelainen & Larmas 1994)

The concentration of sucrose in the diet must be high to reduce the dentine formation in the rats. When young rats were fed on a diet containing 15%, 30% or 43% of sucrose, significant reduction in the dentinogenesis was only seen in the animals with 43% of sucrose in the diet. The rats were not inoculated with cariogenic bacteria. The critical amount of sucrose seemed to be between 30 and 40 g/ 100 g. (Huumonen et al. 1997)

All kinds of high-sucrose diets seem to have the same effect on dentine formation in the young rats. Autio et al. (1997) reported only a slightly stronger reduction in rats fed on the modified Stephan-Harris diet (43% of sucrose, Table 1) than in those fed on the R36 diet (special diet for growing rats and mice, Brood Stock Feed for Rats and Mice R36, Finnewos Aqua Oy, Turku, Finland), in which most of the barley and wheat flour were replaced by sucrose (41%) and casein was added to compensate the loss of protein.

Both of the sucrose diets mentioned above slightly increased the width of predentin compared with the control diet (R36) (Autio et al. 1997). In this respect, the effects of both sucrose diets were equal. The same effect, but more pronounced, has also been reported in the study of Hietala et al. (1997), in which the modified Stephan-Harris diet was used. The increased width of predentin indicates disturbed mineralization in the rats fed on the high-sucrose diets (Butler 1995).

Also quantitative changes in the amounts of mineral elements of dentine of the young rats" molars has been observed in connection with the high-sucrose diet (the modified Stephan-Harris diet) compared to the standard diet (Ewos R3, Table 1) and to the modified Stephan-Harris diet in which sucrose has been replaced with potato flour (starch) (Tjäderhane 1996). Calcium, phosphorus, fluoride, sodium, magnesium, zinc and the total content of minerals in dentine were determined with SEM equipped with an electron probe microanalyzer (EPMA). Reduction in all the elements measured, except F and Zn, was found in the sucrose group.

In the study referred to above (Tjäderhane 1996), the dentinal Ca/P ratios did not differ before or during the experiment or between the groups. A Stephan-Harris diet in which sucrose had been replaced with complex carbohydrate (starch) gave identical results to the Ewos R3 standard diet, which suggests that nutritional deficiences were not the cause of the changes in the mineral contents in the dentine of the rats fed on the sucrose diet.

The high-sucrose diet has also been reported to suppress the rate of fluid movement in the molar dentine of young rats (Steinman & Leonora 1971). The rate of the fluid movement was inversely related to the incidence of dental caries. The authors assume that the products of metabolism (lactic acid) accumulate and the nutrient uptake decreases in the dentine as a consequence of the suppressed fluid movement. Unlike the bone, the dentine is avascular and thus more dependent on the fluid transport system.

The dentinal fluid movement has been found to be regulated by parotid hormone (”parotin”) in rat (Leonora et al. 1992) and in pig (Tieche et al. 1994). Parotidectomized rats had a suppressed fluid movement in the dentine regardless of the quality of the diet. A high sucrose-diet reduces the secretion of the parotid hormone and thereby suppresses the rate of the dentinal fluid movement in both the rats and the pigs (Leonora et al. 1992, Tieche et al. 1994).