EFFECTS ON THE TEETH 1 59 



could be accomplished in regard to the eradication of caries of the teeth than in 

 all other ways put together, and that rickets would be abolished from the earth." 



In experimental rickets in puppies, Voit ('80) noted that the teeth are small 

 and poorly developed. In spontaneous rickets in white rats, Weichselbaum and 

 Erdheim ('09) found imperfect calcification of the dentine, especially of the 

 youngest layer (adjacent to the odontoblasts), which was penetrated by vascular 

 loops. The rickety teeth are very transparent to the X-rays. They cited similar 

 observations by Fleischmann ('07) in human teeth during rickets. 



M. Mellanby ('18, '20, '21) has described a general hypoplasia of the teeth in 

 puppies with rickets caused by diets deficient especially in vitamin A. The 

 following defects are noted: (1) delayed shedding of the deciduous teeth; (2) 

 delayed eruption of the permanent teeth ; (3) irregular position and overlapping, 

 especially of the incisors; (4) enamel defective or partially absent; (5) general 

 softening of the teeth, due to low calcium content. The dental defects 

 appear independent of oral sepsis or other complications. 



In experimental rickets of young rats, Shipley, Park, McCollum and 

 Simmonds ('21) observed that the incisor teeth are frequently loose, fragile and 

 sometimes fractured. The conditions were studied more in detail by McCollum , 

 Simmonds, Kinney and Grieves ('22), who found the greatest percentage 

 of oral defects in the rats fed diets deficient in protein, calcium and vitamin 

 A. The next highest incidence occurred in rats on diets low in calcium; and a 

 still lower percentage occurred on diets low in both calcium and vitamin A. No 

 caries-like lesions, pulp exposure, osteodentine, or defects in the attaching tissue 

 or maxilla occurred in the stock rats on complete diet. They conclude that 

 severe oral disease may result from relatively defective diets, where the distur- 

 bance appears out of all proportion to the cause. The diet is thus of primary im- 

 portance in determining the quality of the teeth and their vitality in resisting 

 invasion by microorganisms. 



A further report by Grieves ('22) places the rats studied in 3 groups. In 

 group 1 (on low calcium diet causing a pseudorachitic condition with excess 

 osteoid), 22 per cent of the rats show caries-like defects and 3.65 per cent of their 

 molars are involved. In 41 per cent of these rats, attaching- tissue defects 

 occur, involving also the molars. Diets affecting the bones do not always affect 

 the tooth attachments, however. 



In group 2 (diets low in calcium and vitamin A), 31 per cent of the rats show 

 caries-like defects and 5.21 per cent of their molars are involved. Twenty per 

 cent of these rats show attaching-tissue defects. But many definitely rachitic 

 rats show little or no dental defects; rachitis and caries-like lesions are rarely 

 coexistent. 



In group 3 (diets high in calcium and butter fat), 17 per. cent of the rats 

 show caries-like defects and 1.71 per cent of their molars are involved. In 28 

 per cent of these rats, attaching-tissue defects occur, disturbing 33 per cent of 

 their molar attachments. 



The caries-like and attaching-tissue lesions are described by Grieves in detail. 

 The variability of the lesions in the test rats resembles that found in human 

 rickets, indicating differences in individual resistance. Endocrine and other 



