Among dentists, dental caries is thought to merely imply the dissolution of the tooth minerals by bacterial functions. In fact, this is principally the case in the enamel, and undeniably also in dentine, although perhaps less exclusively.
In the dentine, the vital processes are principally regulated by the cells of the pulp/dentine complex in a way that makes dentinal caries a process notably resembling the bone resorption. Thus, the function of the cariogenic bacteria in the dentine may be comparable to the function of the osteoclasts in the bone.
The rate of the destruction in dentinal caries seems to be associated with the rate of the dentinogenesis. Caries proceed faster in the teeth of the young animals with rapid growth of the dentine than in the teeth of the older animals (Hietala & Larmas 1992, Kortelainen & Larmas 1994). On the other hand, a high-sucrose diet and metabolic acidosis slow down the rate of the dentinogenesis and induce caries (Kortelainen & Larmas 1990, Tjäderhane et al. 1994, Bäckman et al. 1996).
The aim of this work was to find out whether the high-sucrose diet and the acid-base imbalance of the body have the same kind of systemic effects on caries (on cariogenic bacteria) and on the odontoblasts in the dentine as they have on the osteoclasts, osteoblasts and osteocytes in the bone and whether these processes are connected. The slower rate of formation, as such, of the dentine is thought to be analogous to bone resorption, as no resorption by tissue cells occurs in the normal dentine.
The tested central hypotheses were:
Sucrose affects odontoblasts causing reduction in dentine formation and acceleration in caries progression at least partly via metabolic acidosis.
Metabolic alkalosis eliminates most of the effects of sucrose, if the hypothesis number one is correct.