RICKETS 451 



rickets in that the bone formed is defective chicfl}' in amount rather 

 than in quality (Stoltzner), Furthermore, such "pscudo-rachitic 

 bone" possesses a marked affinity for calcium salts, and takes them up 

 as soon as the}' are supplied (Pfaundler). As the blood in rickets 

 contains nearly normal amounts of calcium^^ it seems quite certain 

 that calcium starvacion is not the fundamental trouble. 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. Stdltzner,^'' 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 nor- 

 mal 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 osteoid tissue which prepares it 

 to take the salts out of the blood, and Pfaundler-^^ supports this 

 view, suggesting that this preparatory change in the osteoid tissue 

 may depend upon autolysis, which is perhaps deficient in rickets. ^^ 



On the other hand, after extensive experimental work, Dibbelt^^ 

 comes to the conclusion that rickets results from excessive elimination 

 of calcium into the intestine, presumably because of the presence of 

 precipitating substances in the intestinal contents, such as P-Oo from 

 casein. Agreeing with Dibbelt that the excessive elimination of cal- 

 cium is chiefly through the feces, Schabad^" aftei' equally extensive 

 investigations, believes .that calcium starvation in children, from defec- 

 tive absorption, may cause at least a pseudo-rickets, indistinguishable 

 clinically or chemically from true rickets. But the fact that children 

 with rickets show nearly normal figures for blood calcium does not 

 agree with these calcium starvation hypotheses. 



As with osteomalacia, attempts have been made to associate with 

 the etiology of rickets defects in the ductless glands, especially the 

 adrenals,'" thymus, ^^ and parathyroids,'- but as yet without convinc- 

 ing evidence. ^^ There has also been an attempt to include rickets 



"Howland and Marriott, ' Trans. Assoc. Amer. Phys., 1917 (32), 307. 



«« Jahrb. f. Kinderheilk., 1899 (50), 268. 



^'' How metallic i)hosphorus causes growing bones to laj' on increased calcium 

 is an unsolved problem, but a striking fact. (See Phemister, Jour. Amer. Med. 

 Assoc, 1918 (70), 1737.) 



«8 See also Nathan, Med. News, 1904 (84), 391. 



*^ Articles in the Arbeiten a. d. Path. Inst. Tubingen, Vols. 6 and 7; also ^'erh. 

 Deut. Path. GeselL, 1910 (-14), 294; Miinch. nied. Woch., 1910 (57), 2121. 



'0 Arch. f. Kinderheilk., 1909 (52), 47; 1910 (53), 381; 1911 (54), 83; Fortschr. 

 Med., 1910 (28), 1057. 



'"■ Stoeltzner, Verh. Deut. Path. Ges., 1909 (13), 20. 



^2 Erdheim et al, Frankfurter Zeit. Path., 1911 (7), 178. 



'^ Concerning the chemical changes of osteogenesis imperfecta (congenital fra- 

 gility of bones), see Schabad, Zeit. Kinderheilk., 1914 (11), 230. 



