ABSTRACT
In the development of tooth, the first sign is the localized thickening of oral ectoderm to form the tooth bud, and then through the dialogue between the bud and underlying mesenchyme, proliferation and differentiation of bud cells and surrounding mesenchymal cells continue, and cap and bell stages follow. In each step of development, various teratogens may act directly and indirectly, and may result a certain congenital anomalies. To reveal the action mechanism of ionizing radiation on odontogenesis morphologically, 4 Gy X-ray irradiated on the rat (Sprague-Dawley strain) fetus on GD 12.7, and observed the histological changes of the upper incisor tooth from GD 13.5 to GD 20.5, daily. In the normal development of upper incisor tooth of rat, the bud stage was from GD 12.5 ~GD 15.5, the cap stage was from GD 16.5 to GD 17.5, and the bell stage was GD 18.5 to GD 20.5. After X-irradiation on GD 12.7, the development of incisor tooth was delayed markedly, the bud stage was prolonged from GD 13.5 to GD 17.5, and the cap stage was GD 18.5 and the bell stage was from GD 19.5 to GD 20.5. After X-irradiation, from GD 13.5 to GD 16.5, apoptosis is observed in the dental organ and surrounding mesenchyme, hemorrhagic necrosis began from GD 16.5 at the center of dental pulp, followed ischemic necrosis of dental organ and surrounding mesenchyme. After GD 19.5, the development of tooth was ceased. These suggest that at least 2 mechanisms involved during X-ray teratogenesis on developing tooth. After X-irradiation on GD 12.7, initially, X-ray induced apoptosis of the cells of dental lamina and dental bud, which resulted the delayed proliferation and differentiation of dental bud and shortage of the number of cells having signal molecules which induce aggregation of the underlying mesenchymal cells. Lately, disorganization of the endothelial cells differentiated from the damaged mesenchymal cells, which resulted in rupture of capillaries and the hemorrhagic necrosis.