OSTEOMALACIA 437 



hypothesis has attracted the most adherents. Through the favorable re- 

 sults of castration, Fehling was furnished the occasion for regarding the cause 

 of osteomalacia as a hyperfunction of the ovaries. Cristofoletti modified this 

 hypothesis by assuming that the internal secretory function of the ovary 

 lasts during pregnancy, and that this leads to a hypofunction of the chrom- 

 afnn tissue. 



For an especially functional disturbance of the interstitial glands speaks 

 the finding of Wallart that the interstitial substance in osteomalacia is 

 especially strongly developed. The assertion of Siegert and M. B. Schmidt 

 that infantilism and osteomalacia belong together is made scarcely plausible 

 by this fact alone. As, however, also in normal pregnancy the interstitial 

 glands are more strongly developed, it is questionable whether we may 

 estimate the value of the findings of Wallart as high, although I am unable 

 to bring anything else against them. 



I would not ascribe the hypofunction of the chromafrin tissue so great 

 a value as does Cristofoletti. As signs of it, Cristofoletti quotes: the hyper- 

 eosinophilia, the absence of the adrenalin glycosuria and the eventually 

 present pigmentations. But why, then, do we never find osteomalacic 

 manifestations in Addison's disease? The combination of hypofunction 

 of the chromafnn tissue with pregnancy can not be such an important factor, 

 for there are cases of osteomalacia without pregnancy. Moreover the 

 relations of the chromafrin tissue to the calcium metabolism are still rather 

 questionable. 



To my knowledge, there are no existing observations as to whether 

 there is in pregnancy a continuation of ovulation. After all, the assump- 

 tion of a hyperfunction of the ovaries is up to the present the only one that 

 can be supported by numerous and good observations. It is at all events 

 surprising that the osteomalacic process is as well influenced by both cas- 

 tration and by normal or artificially induced labor. We may, however, 

 suppose with Halban that the activity of the ovary and that of the chorionic 

 epithelium become summated, and that it is therefore sufficient to limit 

 only one of these factors. Also the hyperplasia of the parathyroids perhaps 

 is explained by this hypothesis. Already during normal pregnancy are 

 greater demands made on the parathyroid glands, still greater demands may 

 lead to hyperplasia (confer the chapter on the parathyroid glands) . 



The observations of Pal, that extracts of the anterior lobe of the hypo- 

 physis influence osteomalacia favorably, turn our attention to the hypophysis. 

 Perhaps in osteomalacia the normal hyperplasia of the anterior lobe during 

 pregnancy fails to take place. Up to the present, all these theories are hy- 

 potheses, as between the described and the supposed alterations in the func- 

 tion of the ductless glands and the profound disturbance in the osseous 

 system there is still a very wide gap. 



In a thorough monographic dissertation on osteomalacia and rachitis, 



