VII. VITAMIN' A DEFICIENCY IN ANIMALS 



117 



ceases. Colls of llic cpipliNscal cartilajic slop (li\i(liii<i;, and cells which ha\'e 

 ahiiost reached lull size uiuleri>;o no further growth and may atropliy. Cells 

 which lia\e proo;ressed to the vesicular stage complete their cycle and dis- 

 appear, jiermitting penetration of blood vessels and osteoblasts from the 

 medulla. Cartilage jireN'iously calcified is removed by osteoclasis. The 

 matrix of the atrophic epiphyseal cai'tilage b(>comes calcified for a depth of 



Fic. 30. Til)ia-fihula conii)lex of three rats of the same age. On the left, that of a 

 rihoflavin-dcficient rat; on the right, that of a normal rat; in the center, that from 

 a vitamin .\-deficient rat. Xote tlie convexity and thickness of the uppe' end of the 

 tibia, the result of failure of remodeling sequences. Compare also the fil)ulae. 



a few cells on the diaphyseal border, and in long-continued experiiiKMits a 

 thin i)late of bone is formed across the face of the e))iphyseal disc. The I'csult 

 is similar, if not identical, to that caused by inanition fi'om undei-feeding 

 and by dehciencies of other \-itamins not specifically affecting bone growth, 

 .such as riboflavin and pyridoxine, extensi^•ely studied in the lal)orat()ry of 

 the wiitei-. Two facts distinguish the el'fects of \-itamin .\ deficiency, one 

 mentioned in a previous paragraph (the continued growth of soft tissues, 

 including the nervotis .system), the othei' the cessation of remodeling 

 sequences, while appositional bone formation coniinues. In the .second 

 category are included gi-eall_\' diminislie(| resoijition of trabecular bone, 



