446 CALCIFICAriOX, COyCKETIOXH, AXD IXCRL STATIONS 



INIore modern analyses** show a relative increase in water and 

 magnesium, with a persistence of the normal ratio of calcium phos- 

 phate and carbonate.**'' Cattaneo *"^ finds the increase in magnesium 

 to var}- in different parts of the skeleton, being greatest in the ribs. 

 The blood of children with rickets shows greater variations from the 

 usual CaO content (8-10 mg. per 100 c.c.) than are found in normal 

 children ( Asehenheim) .*'"' 



As an essential difference from osteomalacia is the fact that in 

 rickets there is a failure on the part of the osteoid tissues to calcify, 

 Avhereas in osteomalacia absorption of calcified tissue takes place 

 with subsequent substitution by osteoid tissue. Furthermore, in 

 rickets the deficiency in calcium is said to be present only in the 

 bones/'^ whereas in osteomalacia the soft tissues are also poor in lime 

 salts. According to Schmorl *'^ the first structural abnonnality in 

 rickets is a failure to lay on calcium by small islands of cartilage in 

 the zone of preparatory calcification. 



None of the various hypotheses as yet advanced to explain this 

 defective ossification has satisfactorily explained all the observed 

 facts. That a deficiency of calcium in the food is the cause of 

 rickets is a most natural assumption, but it has not been proved 

 that this is the case. Young animals fed on calcium-poor foods show, 

 naturally enough, defective development of the bone,*'^ but this differs 

 essentially from rickets in that the bone formed is defective chiefly 

 in amount rather than in quality (Stoltzner). Furthermore, such 

 "pseudo-rachitic bone" jDOSsesses' a marked affinity for calcium salts^ 

 and takes them up as soon as they are supplied (Pfaundler). In 

 view of the fact that rickets is not solely a disease of bone tissue, but 

 that all the various important viscera, as well as the muscles and 

 tendons, show pathological changes, it seems most reasonable that 

 rickets should be looked upon as a constitutional disease, in which 

 the bone changes are prominent chiefly because the disease occurs at a 

 time when the bone tissue is most actively forming and when the 

 other organs are relatively quite completely developed. Stoltzner,*^ 

 finding evidence that rickets does not depend upon either lack of 

 calcium in the food or deficient absorption of calcium, and that the 

 blood in rickets is of normal alkalinity, looks upon the failure of 

 calcification as depending upon an abnormality in the calcified bone 

 tissue itself. He finds evidence of a preliminary alteration in normal 



44 Gassniann. Zoit. pliysiol. Clicm., iniO (70), 101. 



•»4<i The hones and muscles in Barlow's disease show quite the same deficiency 

 in calcium as in rickets (Balirdt and Kdelstein. Zcit. Kindcrheilk., 1913 (9), 415). 



«La Pediatria, VIT, 497. 



^fia.Tahrb. Kinderheilk.. 1914 (79), 446. Howland and Marriott found normal 

 fipures (Trans. Amer. Ped. Soc, vol. 28, p. 202). 



■<<^ There is a d<'crease in the calcium of tlie muscles according to Aschenlieim 

 and Kaunihfimer ( Monatschr. f. Fvinderheil.. 1911 (10), 4.'i5). 



47Vcrliandl. Dcut.. Path, desell., 190.") (9). 248. 



47a See Weiser. iJiochem. Zeit., 1914 (fifi), 95. 



48Jahrb. f. Kinderheilk., 1899 (50), 208. 



