VIII. EFFECTS OF DEFICIENCY IN ANIMALS 281 



results ill serious limitations to their usefulness. Regardless of the difficulties 

 and dangers involved in the use of these methods, however, we can doubt- 

 less look forward to substantial progress in this rapidly developing field of 

 investigation. 



In summary, it may be stated that present knowledge indicates definitely 

 that ascorbic acid is essential for the production of fibers and for the matur- 

 ation of reticulin to collagen. It also appears to have a role in the organiza- 

 tion of the interfibrillar substance, possibly for the production of its protein 

 components and/or their conjugation with the carbohydrate complex. 



b. Bones and Cartilage 



Just as in connective tissue, the effect of ascorbic acid on the bones and 

 cartilage is chiefly in relation to collagen synthesis. Rogers et al.^'' found that 

 collagen or collagen-like proteins comprised about 90 to 96 % of the organic 

 matrix in the bones examined of rabbits, oxen, and humans. Lightfoot and 

 Coolidge^' found that the decrease from the normal values of collagen ni- 

 trogen of the bones in scurvy was marked in guinea pigs 10 days old, ap- 

 preciable in those 36 days old, and much less in the older animals. Sadhu^® 

 reported that the chondroitin sulfate content of bones was considerably 

 decreased in scurvy. 



Lack of ascorbic acid produces a pathological condition at the growing 

 ends of the bones characterized by a disorderly organization of the cells 

 and a resulting weakness. The changes are to be found at the costochondral 

 junctions and at the junction of the diaphysis and epiphysis. Aschoff and 

 Koch'" have studied the changes in bone structure in human scurvy, and 

 Hojer,^ Wolbach and Howe,^ Meyer, ^^ Ham and Elliott ^^ and MacLean et 

 al.^^ have investigated them in the guinea pig. Follis^"" describes and illus- 

 trates the changes in bone, and the reader is referred to his account for a 

 more detailed picture than can be presented here. 



In scurvy there is a failure of the osteoblasts to form osteoid tissue. 

 Wolbach^^i describes their behavior as follows: "Formation of cartilage and 

 bone matrices ceases, and the osteoblasts become elongated, assume the 

 shapes of fibroblasts and migrate toward the diaphysis. Here these cells be- 

 come surrounded by liquid, presumably a deficient product of continued 

 activity toward matrix formation, and give rise to an apparent region of 

 edematous connective tissue at the ends of the diaphysis, the Geriistmark 



" H. T. Rogers, S. M. Weidmann, and A. Parkinson, Biochem. J. 50, 537 (1952). 



98 A. W. Ham and H. C. Elliott, Am. J. Pathol. 14, .32.3 (1938). 



" D. L. MacLean, M. Sheppard, and E. W. McHenrv, Brit. J. Exptl. Pathol. 20, 451 



(1939). 

 i«» R. H. Follis, Jr., The Pathology of Nutrition Disease. Charles C Thomas, Spring- 

 field, 111. (1948) 

 ">' S. B. Wolbach, J. Arn. Med. Assoc. 108, 7 (1937). 



