VII. VITAMIN A DKFKIKXrV I\ ANIMALS 



129 



as (Ictcrniiiu'd l)y l he local ion and >lio\\ n, i-('s|)cct i\('ly, at t lie proximal cud 

 ot" the tibia and tlu> niidshatt of the lemur (Fifis. 37 and 3<S). 



riu' donrcc or latc ot acceleration ot these i>;ro\vth seciuenccs \aries with 

 the amount ol' \itamin A administered and with the <>;ro\\ t h ])attern of 

 eacli hone. In the hhula in rat, jiuinea piji;, and dog, i)ecause jj;ro\\tli recjuires 

 increasing!; separation from tlie tilna and a swinji; j)ostei"ioi'ly, I'emodeling is 

 noi'mally lapid and clearly shown hy cement lines. In liypei-\itainino.sis A 



Fig. 40. Hypervitaininosis A in the rat. Lonjiiludinal section ot" a fonuir with a 

 fracture near the distal epiphysis from a rat whic-li had received 1250 l.U. of crystal- 

 line vitamin A per gram daily for 7 days following weaning at 21 days of age. The 

 resorption of tlie e.xterior of the shaft and new formation of hone on the interior are 

 apparent. There is considerahle diminution of tlie width of the epiphyseal cartilage. 



only traces of mature bone may remain at certain levels, while at the ends 

 of the fibula where the normal rate of mo\'ement is slower, considerable 

 mature bone remains (Fig. 39). The explanation of the fractures of long 

 bones in rats, freciuently erroneously ascribed either to "'brittle l)ones" or 

 to decalcihcation, is that, although new bone formation keeps pace with 

 bone resoi'ption, mat mat ion of the newly foiined bone matrix and its calci- 

 fication exhibit the same lag as in normal bone growth, aiul hence the bone 

 at sites of remodeling is structurally weak (Fig. 40). Fractures occurring 

 during the deficiency are accompanied by xoluminous callus formation. 

 This applies to guinea pigs as well as to rats. Ascorbic acid up to 250 mg. 



