114 VITAMINS A AND CAROTENES 



As the epithelial changes in vitamin A deficiency and in recovery form a 

 cycle that could not happen in animals in natui'al habitat, it is of interest 

 to note that the recovery phenomena cannot be those of a pattern estab- 

 lished phylogenetically, but they do follow a familiar mammalian physi- 

 ological pattern. 



h. Teeth 



Mtamin A deficiency produces severe defects in the incisor teeth of rats 

 and guinea pigs because, as in all rodents, these teeth are continuously 

 growing at a rapid rate, and throughout life the odontogenic epithelium 

 persists and remains acti^'e both as tooth organizer and producer of enamel. 

 On the labial side the odontogenic epithelium extends for the entire length 

 of the incisor tooth as the enamel-forming organ; on the lingual side it 

 extends only for a short distance, acts only as an organizer, and forms no 

 enamel. The primary consequence of vitamin A deficiency is upon the 

 odontogenic epithelium. At the basal formative end of the tooth, growth 

 continues but differentiation is incomplete and there is loss of organizing 

 influence which results in inadequate and defective dentine formation asso- 

 ciated with atrophic odontoblasts. The continuation of the growth of the 

 odontogenic epithelium, because of the excessively thin dentine, may cause 

 columns of epithelial cells to press into the pulp. Another consequence of 

 the defective formation of dentine is plication and buckling of the wall of 

 dentine near the formative end. More distally, the rate of dentine formation 

 on the lingual side and lateral sides of the tooth is greatly retarded, and the 

 odontoblasts are without orderly arrangement and resemble osteoblasts. 

 On the labial side, where there has been enamel deposited, the odontoblasts 

 remain columnar in shape and ample dentine continues to be deposited 

 until atrophy of the enamel organ is complete. The vitamin A-deficient 

 rodent incisor tooth has, therefore, a distinctive structure characterized by 

 relatively great thickness of dentine on the labial side and excessively thin 

 dentine elsewhere (Fig. 29). Complete organ atrophy results in loss of 

 odontoblast morphology on the labial side also. Wolbach and Howe^^ 

 called attention to the continuous organizing influence of the enamel- 

 forming epithelium through the growth of the incisor tooth, and they 

 characterized the odontoblast as a polarized osteoblast which lost its po- 

 larity following atrophy of the odontogenic epithelium. Depolarization of 

 the odontoblasts and distortions of the tooth as a whole at its l)ase or 

 formative end are other consequences, all of which are specific results of 

 suppression of the odontogenic epithelium functions of tooth organizer and 

 enamel producer. These generalizations are also those of Pohto-** and Schour 



19 S. B. Wollnich and P. R. Howe, .1///. ./. Pathol. 9, 275 (1933). 



20 M. Pohlo, Di!S.sort:iti()ii Mod. Chem. I.;il.. uiid Odoni . Inst., Univorsity of Helsinki, 

 1938. 



