AMEBJE AND PYORRHEA 143 



gums, eventually causing the teeth to fall out. As already stated, 

 over 50 per cent of all permanent teeth which are lost fall out as 

 the result of pyorrhea. 



Whether the formation of the pus pockets is initiated by the 

 amebse or by other organisms is not known, but certain it is that 

 Endamceba gingivalis is almost without exception found in the 

 lesions, and at the very bottom of them, often burrowing into the 

 inflamed tissues to a depth of several times its own diameter, 

 devouring cells and transporting bacteria. The belief in the role 

 of the amebse is based on these facts and on the fact that often, 

 though not always, the disease is greatly improved by treatment 

 with emetin, which has a specific action on amebse. Some in- 

 vestigators, notably Craig, consider it, to quote from Craig, 

 " more than doubtful that Endamceba gingivalis is the cause of 

 pyorrhea alveolaris, this conclusion being based upon the follow- 

 ing facts: the occurrence of the parasite in a large per cent of 

 healthy mouths and in the material that can be scraped from 

 healthy teeth and gums; the occurrence and persistence of the 

 parasite in patients treated with emetin, even when marked 

 improvement in the clinical symptoms have occurred; the ab- 

 sence of the parasite in some typical cases of pyorrhea; the lack 

 of improvement with emetin shown in numerous instances of the 

 disease, although the endamebse may disappear; and the fact 

 that emetin acts upon other organisms as well as upon endamebse 

 and the possibility that the improvement that often follows its 

 administration may be due to such action or to a favorable action 

 on the tissue cells." That these facts argue against the causa- 

 tion of pyorrhea by amebse alone is unquestionable. These 

 facts, however, are not only not opposed to the possibility of 

 amebse being partly or indirectly responsible for the disease, 

 but may be interpreted as being in support of such a view. It is 

 entirely in accord with the known facts about the disease to 

 suppose that the pus pockets may be initiated or enlarged by the 

 action of amebse, the damage being then continued by bacteria 

 which have been given a portal of entry. This would account for 

 the occasional absence of amebse in typical cases of pyorrhea and 

 for the occasional cases of the disease which are not improved by 

 emetin. It is further quite conceivable that the amebse may live 

 for a long time in crevices in the mouth without doing any 

 damage, and yet be capable of causing or aggravating pus pockets 



