Abstract
In our previous report, the experimental trauma hitting the mandible of 4-day-old rats with a force of 3 N could effectively produced the enamel hypoplasia accompanying inhibited crystal growth. We hyhothesized that the serum albumin from experimentally induced localized trauma could saturate into the enamel matrix and thus inhibit the crystal growth. The purpose of the present study was undertaken to localize serum albumin using the immunohistochemical method and autoradiography of albumin labeled with 125IT. rauma was given by hitting the mandibular incisor region of 4-day-old rats. Hitting was performed with by a force of 3 N. The rats were then sacrificed after 30-min,1 h,1 d and 1 W after being hit. The lower incisors were then removed together with the jaws and soft tissues. After fixing and demineralizing, paraffin sections were made 6μm thick. The ABC method was used for immunohistochemical staining. Goat anti-rat Albumin polyclonal antibody was used. The bound antibody was made visual by application of the DAB solution. Other sections were stained with hematoxylin and eosin. Albumin labeled with 125I was injected into rats. The incorporation pattern of the labeled albumin into the enamel organ was observed 60-min after the injection, using autoradiography. Hemorrhage was observed from the peripheral of the tooth germ to the distal ends of the ameloblasts within 1 h after the hitting. Vacuolation was observed between the distal ends of the ameloblasts and the enamel matrix. Albumin was identified and localized in the outer layer of the enamel matrix adjacent to the detatched secreting ameloblasts, in particular corresponding to Tome's process, within 60-min after the hitting. Also, albumin was still remained in the matrix even at the period of mineralizing enamel. These results suggested that albumin saturated into the enamel matrix through the secreting ameloblasts after trauma, and albumin was then left and undegrade within the enamel matrix, and that would inhibit the crystal growth and consequently lead the hypocalcification of the enamel.
