Effect of Experimentally Induced Trauma on Rat Incisor Enamel

The Crystallinity of The Enamel Hypoplastic Lesion

Abstract

In order to understand the mechanisms of permanent tooth enamel hypoplasia caused by injured primary teeth, rat incisors were given the experimental trauma and enamel hypoplasia, then was induced. The crystallinity and crystal form at the lesion of enamel hypoplasia were then examined. For this study 4-day-old and 3-week-old Wistar rats were used. Experimental trauma was carried out by needle pricking with 25- or 27-gauge sterile disposable needles, the pricking point being located at the skin 2 mm apart posteriorly of the lower lip. A needle was inserted 1.5 mm depth toward the alveolar bone. This point corresponds to the transitional region between the maturation and the secretory phase of the ameloblasts of the developing lower incisors of 4-day-old rats. The hitting point was also set on the same position for 4-day-old and 3-week-old rats, and the hitting was carried out by a force of 2-3 N and 3-5 N, respectively. The rat was then sacrificed one week after trauma, and the specimens obtained were used for contactmicroradiogram, microbeam X-ray diffraction and transmission electron microscopic (TEM) observation. In the needle pricking group, varying degrees of localized enamel hypoplasia were observed. The incidence was 73.7%. In the hitting group with 2 N, hypocalcified enamel was observed at the surface layer with the 3 N hypocalcified enamel extended to a deeper layer. As far as the crystallinity was concerned at the hypoplastic enamel lesion, it was lower both with the a- and c-axis. With the TEM observation, it was found that the crystal width and thickness at the hypoplastic lesion were reduced more than with normal enamel. In conclusion, both needle pricking and hitting caused in the enamel hypoplasia with lowered crystallinity and reduced crystal size, particularly hitting group with a force of 3 N consistent enamel hypoplasia was caused.