226 STUDIES ON PATHOLOGIC OVA. 



nomenal case of a woman with endometritis, who had aborted a hydatiform mole 

 18 times in 9 years. Falgowski, on the contrary, concluded that the ova themselves 

 were diseased and argued that hydatiform degeneration should be much more com- 

 mon if it were due to endometritis. Taussig (1911) also stated that leucocytic 

 infiltration of the decidua is frequently present in hydatiform moles, but insisted 

 that "leucocytic infiltration in the placenta then should not be interpreted as 

 infection. . . . Inflammation and infection should be kept apart." I pre- 

 sume Taussig really meant infiltration and infection should be kept apart, and the 

 question then turns upon the structure of the normal decidua and the significance 

 of infiltration for the development of the ovum. 



It may be recalled that Marchand (1904) reported the presence of isolated 

 groups of small cells in the normal decidua which looked like mononuclears under 

 low magnification, and which he believed have often been confused with them. 

 But even granting this, and the further facts that the exact histologic changes in 

 the decidua are not fully known, and that it is rather difficult to ascertain just what 

 decidual changes are regarded as evidence of the existence of an endometritis, any 

 one examining a large series of cases of hydatiform degeneration aborted with the 

 decidua can not doubt the presence of marked decidual changes in a very large 

 percentage of them. These changes are not limited to infiltration with scattered 

 round cells or erythrocytes, or to focal accumulation of the same, but often extend 

 to almost complete fibrosis, as shown in figure 135, plate 13 (see Chap. IX), so 

 that experienced investigators have mistaken the thin, fibrous decidua for a part 

 of the chorionic vesicle. 



It is true that the existence of these changes in the decidua does not neces- 

 sarily imply that they were antecedent to the implanation of the ovum, but for- 

 tunately the clinical histories and material from curettage often supply crucial 

 evidence. From such cases and from the cumulative weight of evidence from the 

 large series of cases here reported, the great majority of which showed decidual 

 infiltration or other changes suggestive of endometritis, the frequent association 

 of abnormal deciduse with hydatiform degeneration is evident. The fact that the 

 incidence of hydatiform degeneration in the tubal was considerably higher than 

 that in the uterine series might be regarded as contradicting this relationship, 

 but such is not the case. The mucosa of the tubes at best is an unfavorable nidus 

 for implantation because of the absence of decidual formation alone. Hence, even 

 if salpingitis were somewhat less frequent than endometritis, difficult nidification 

 in the tube could easily more than account for the existing differences. Hence the 

 higher incidence of hydatiform degeneration in the tubal series in fact becomes 

 confirmatory of the conclusion that abnormal nidification really may be responsible 

 for the advent of hydatiform degeneration. 



The only fact which might be interpreted as indicating that germinal defects 

 primarily are responsible for the development of hydatiform degeneration is the 

 relatively higher incidence of the condition in older women. Against this, however, 

 stands the other fact that such women also show the cumulative effects of endo- 

 metritis and pregnancy upon the endometrium. Furthermore, since hydatiform 



