Abstract
Previous studies have reported that infants from diabetic mothers (IDM)manifest widened neonatal lines and enamel hypoplasia of the postnatal enamel in the primary dentition. It has been suggested that neonatal hypocalcemia may contribute to this process. However, this hypothesis has not yet been proven.
The purpose of the present study was, therefore, to investigate the effect of experimentally induced diabetes in rats on the tooth enamel structure of their offsprings and further, to study the correlation between neonatal hypoplasia and the function of the ameloblast at different developmental stages.
Six-year-old female Wistar strain rats were injected i. v. with streptozotocine to induced diabetes continuouslly. After the female rats were matured they were mated with normal male rats. Thus 1∼4 day old offspring of diabetic rat dams were used as the diabetic group and normal rat dams as the control group. Serum Ca and P analysis were performed with a spectrophotometer. From each lower incisor mid-sagittal and cross sections were prepared. Contact microradiographic analysis and electron-probe Micro-analysis were employed.45CaCl2,3H-proline, or 3H-thymidine was injected i. p. and the distribution of silver grain on autoradiogram were then measured on the sections stained with hematoxylin and eosin.
The results were as follows:
1) in 1-day-old rats in the diabetic group significant decrease of serum Ca concentration was noticed, and it recover within 2-days, this suggesting neonatal hypocalcemia in the diabetic group.
2) Microradiographic findings showed diffused hypocalcified enamel and enamel hypoplasia of lower incisors during the maturation stage of the ameloblasts in the 8-day-old diabetic group. Eelectron-probe microanalysis revealed decreased intensities of Ca k αand P kα at the region of the enamel hypoplasia.
3) The cellpopulation renewal of the lower incisors was studied on 2-day-old rats injected with 3H-thymidine. The ameloblasts migration rate was estimated approximately 527 μm/day. Correation was assumed between the site of the enamel hypoplasia and that ol the amelo-blasts allected by hypocalcemia.
4) An inhibition of 3H-proline and 45Ca incorporation into the ameloblasts and enamel affected by hypocalcemia was recognized in the diabetic group.
These results suggest that enamel hypoplasia found in IDM is presumably caused by the ameloblasts disfunction, namely by disturbances of the enamel protein synthesis and serection and by alteration in Ca transportation.
