150 INANITION AND MALNUTRITION 



either calcium or phosphorus. Thus there is apparently a low-calcium rickets 

 and a low-phosphorus rickets, each of which may produce the essential lesions, 

 including the osteoid substance. There are minor differences in the histological 

 details, which vary much according to the stage and severity of the disease, but 

 the low-phosphorus rickets appears morphologically to resemble more closely 

 the ordinary human rickets. As noted above, however, most investigators 

 have obtained osteoporosis, rather than rickets, on low calcium diets. 



Vitamin Deficiency. — The probability of a "fourth vitamin" factor in rickets 

 was mentioned above. Skeletal changes in other vitamin deficiencies will now 

 be considered. In young rats on a vitamin-free diet (polished rice with salt), 

 Ishido ('23) found in the bone marrow of the femur and tibia numerous fat cells, 

 which did not occur in rats exposed to ultraviolet light, or in full-fed controls. 



Vitamin A. — Herter ('97) noted mucoid degeneration of the bone marrow, 

 and also bloody synovial fluid in the knee-joints, in pigs during fat starvation, 

 involving deficiency in vitamin A. Tozer ('18, '20, '21) found that the changes 

 in the costochondral junctions of guinea pigs on a diet deficient in vitamin A, 

 but otherwise adequate, closely resemble those of mild experimental scurvy in 

 these animals. Mackay ('21) and Tozer ('21a) obtained similar results in 

 kittens on a diet deficient in vitamin A, but otherwise adequate. Hess, McCann 

 and Pappe'nheimer ('21) likewise obtained no rickets in young rats on diets 

 deficient merely in vitamin A, although histological examination showed 

 retarded osteogenesis. Emmett and Peacock ('22) noted enlarged knee-joints 

 and beading of the ribs in chicks on a diet deficient in vitamin A, but give no 

 histological data. Findlay and Mackenzie ('22) found that diets deficient in 

 vitamin A cause gelatinous degeneration of the marrow in the femur of the rat. 

 Shipley, Park, McCollum and Simmonds ('21) observed that diets deficient in 

 vitamin A, but otherwise complete, produce merely osteoporosis in the bones of 

 rats. 



Vitamin B. — But few changes have been observed in the skeleton during 

 beriberi or polyneuritis, due to deficiency in vitamin B. Shipley, McCollum 

 and Simmonds ('21) found that under these conditions rats show no gross 

 deformity of the skeleton, but histologically present lesions essentially identical 

 with those seen in guinea pigs with scurvy. These changes include osteoporosis; 

 thin epiphyseal cartilage with strongly calcified zone of provisional calcification; 

 no zone of osteoid; marrow congested and hemorrhagic, sometimes showing 

 reticulum only. Findlay and Mackenzie ('22) likewise found that diets deficient 

 in vitamin B produce hemorrhagic congestion in the bone marrow of the femur 

 in the rat. Findlay ('21) noted atrophy of the skeleton in avian beriberi. 



Vitamin C. Scorbutus. — Although scurvy has doubtless occurred in the 

 human race at various intervals since ancient times, it was not clearly recognized 

 and differentiated as a distinct deficiency disease until about the 17th century. 

 Fragility of the bones in scurvy was noted by Gideon Harvey (1675). The 

 classical treatise by Lind (1772) mentioned briefly the gross skeletal lesions, 

 including the occasional separation of the epiphyses in young patients. Since 

 that time, a voluminous literature on scurvy has accumulated, which has 

 recently been well summarized by Hess ('20) and Hojer ('24). 



