Abstract The effects of dietary sucrose and systemic glucocorticoid treatment on the response of the pulpodentinal complex to dental caries were examined in an experimental rat model. The possible role of dentinal caries on dentin formation was also examined. After 5-6 weeks of a dietary and/or medication period, the areas of dentin formation and dentinal caries were quantified in the molars of growing animals. Also the number and severity of caries lesions were estimated. The 43% sucrose diet significantly reduced dentin formation and increased dentinal caries progression. Although glucocorticoid medication alone reduced dentin formation, without dietary sucrose it did not have an effect on caries. In combination of these two, glucocorticoids further increased the progression of dentinal caries, however without significant increase in the number of caries lesions. The cariogenic bacterial inoculation of rats fed a sucrose or control diet increased the progression of dentinal caries. The relationship between cariogenic bacteria and caries was not strong, but there was a stronger relationship between the total amount of dietary sucrose and dentinal caries. In addition to the overall reduction of dentin formation there was no difference in the amount of dentin formed between intact and carious fissures in the sucrose diet group. On the contrary, rats receiving the control diet positively responded to the dentinal caries by increasing dentin formation to prevent pulpal exposure. Whereas the high sucrose diet impaired both the deposition and mineralization of the dentin matrix, glucocorticoids affected matrix formation only. These results indicate that the functional alterations in the pulpo-dentinal complex might contribute to dentinal caries progression in a cariogenic environment, irrespective of the causative mechanism.

[Truncated abstract] There is a large body of evidence describing the benefits and risks, to the human fetus, of antenatal glucocorticoid treatment, but no published research on the effects on lactation. The withdrawal of progesterone, in the presence of high levels of endogenous glucocorticoids and prolactin, triggers the onset of copious milk secretion (lactogenesis II) at the end of pregnancy. The alteration of lactogenesis II by exogenous glucocorticoids could potentially have adverse impacts on postnatal nutrition in both term and preterm infants. I aimed to determine the effects of maternal antenatal glucocorticoid treatment on lactogenesis II in both ewes and women. I found profound adverse effects on lactation in ewes, and similar but more subtle effects on lactation in women . . . This thesis represents the first investigation of the effects of antenatal glucocorticoid treatment on lactogenesis II in both ewes and women. I found that, in ewes, antenatal glucocorticoid treatment stimulated premature lactogenesis II, and this was caused by disruptions to hormonal regulation during pregnancy. This event was followed by profound delays in lactogenesis II after term parturition. More subtle effects in women suggest that antenatal glucocorticoid treatment did not have a major, prolonged impact on postnatal lactogenesis II. Very preterm gestational age strongly predicted delays in lactogenesis II stressing the importance of assistance for these mothers when they are establishing lactation.