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Sixty female Wistar rats were injected with tritiated thymidine and killed at intervals between 1 hr and 72 hr after injection. Autoradiographs of paraffin and Vestopal W embedded sagittal sections of the maxillary incisors were prepared. The distribution of labeled cells after 1 hr revealed the basal pulp cells and the preodontoblasts as proliferative cells. The growth rate of the incisor and the migration of the basal pulp cells were established from the position of labeled cells at 72 hr observation time. The number and localization of labeled and unlabeled mitoses were registered in order to determine the duration of the generation cycle of the proliferative cells. The identical cell generation time of preodontoblasts and basal pulp cells and the migration pattern of the latter indicate that the preodontoblasts are renewed by preodontoblast multiplication and not by migration of basal pulp cells.

Rats were injected with Calcein and killed 1 h, and 1, 2 and 3 days after injection. Incisors were stained with glyoxal-bis-(2-hydroxyanil) (GBHA) and the enamel surface examined in a fluorescence microscope with incident-light excitation. In maturing enamel Calcein produced five fluorescent double bands across the long axis of the tooth. GBHA produced a series of single red stripes, each of which was imposed on a double Calcein band 1 h after injection. At longer intervals after injection GBHA stripes were seen to be gradually displaced in the apical direction from the Calcein double bands. Since GBHA is known to stain enamel adjacent to smooth-ended ameloblasts this supports the view of a cyclic modulation of ameloblast morphology and function.

The effects of a large dose of vinblastine sulfate (2 mg/kg body weight) on proliferating odontoblast precursors and secretory odontoblasts in the continuously growing rat incisor were studied. The rats were killed 6 h, 24 h, 3 d and 7 d after vinblastine injection. Most cells in the proliferating zone contained arrested mitoses, or had perished after 24 h. After 3 and 7 d, the odontoblasts derived from this zone were reduced in number, and showed altered cell shapes. The odontoblasts had produced irregular dentin. The secretory odontoblasts had displaced nuclei and altered cell shapes after 24 h. Those most affected were opposite early mineralized dentin. In some incisors the cells had perished. In the protracted experiments almost all the odontoblasts were changed and had produced abnormal dentin. In the early mineralized dentin area, accumulations of cells were present after 3 d, and osteodentin-like material after 7 d.

To study cytological changes in the migrating cell layer of the ameloblasts in the rat incisor with semithin Epon sections the ideal section plane would consequently be along the midsagittal plane of the incisor. However, the small dimensions and the complex three-dimensional structure of the apical part of the odontogenic organ covered by alveolar bone make it difficult to orientate and position sections in the midsagittal plane. Serial sectioning of the apical half of the maxillary incisor in the horizontal and sagittal planes clarified the relation of the midsagittal plane of the odontogenic organ to the alveolar bone, and the changes of the sectional profile of the odontogenic organ as a function of its position on the transverse axis of the incisor. From this information a method was designed whereby the two axes of the midsagittal plane were marked directly on the block surface before sectioning, and the position of sections in the midsagittal zone of the ameloblasts standardized.

Bleomycin was administered to four groups of rats in a single intravenous injection of 25 mg/kg, 50 mg/kg, 75 mg/kg and 100 mg/kg, respectively. The animals were killed by perfusion or by decapitation followed by immersion fixation at 24 h and 5 days after injection. Sections were made of maxillary incisors and evaluated by light microscopy. Bleomycin produced a transitory arrest of dividing cells resulting in an apparent synchronization of the cell population. Necrotic cells were found within the basal pulp and the preodontoblasts at 1 day observation time. After 5 days a dentinal lesion was observed at the two highest dose levels and the necrotic areas were filled in by proliferating adjacent cells. A better quality of fixation, especially of cells surrounded by dentin, was observed in perfusion fixed animals but the fixation procedure did not influence the alterations found in experimental animals.

-0.7 mg/kg VCR was given to nine rats in three experimental groups. Twenty-three hours after VCR injection the animals were injected with 3H-thymidine. The animals were sacrificed 24, 48 and 72 h after the VCR injection, and by comparison with nine control animals similarly injected with sodium chloride solution and nucleotide, it was shown that VCR causes a delayed migration of pulp cells from the proliferative pool and a small but distinct inhibition of the incisal growth of the incisors. The growth inhibition corresponded to the normal growth over a 24-h period in non-VCR-injected animals.