Lastly, says Garrod, “cases illustrative of the effects of the suppression of an habitual hæmorrhoidal discharge are by no means uncommon, and ... numerous instances arising from _boils and carbuncles_ have come under my notice.” By Garrod and his contemporaries all these various determinants of gouty paroxysms, _i.e._, loss of blood, etc., were believed to exert their influence _viâ_ the _nervous_ system, with consequent disturbed equilibrium of nutritive processes throughout the body. But while it may be admitted that depression of the _vis resistantiæ_ plays a part, it does so, I believe, by favouring the occurrence of _infection_. Let us turn now to modern findings, and we shall see that they do but confirm those of the older clinicians. Lambert in 125 cases of gout found the teeth unsound in 82 per cent. of males and 1 per cent. of females, while in 9 per cent. of the former and 17 per cent. of the latter there was associated _chronic dyspepsia_. Two years after (1909) Wynn, Wirgman and Turner noted the invariable correlation of gout with local foci of infection. In the majority, _pyorrhœa alveolaris_ was present. _Tonsillar sepsis_, too, was not uncommon, and much more rarely _nasal_ disorders. Again, out of fifty-two examples of so-called “gouty” throat Edward McCracken found _pyorrhœa alveolaris_ to be present in thirty-nine, and Fenner also tells us that this affection is common in the subjects of gout. In truth, the victims of _gouty_ arthritis are no more immune from _dental_ lesions than those of other types of joint disease. Thus, Mr. Macdonald, dental surgeon to the Royal Mineral Water Hospital, Bath, informs me that this form of _oral sepsis_ is extremely common in _gouty_ individuals, and in my experience it is but rarely that evidences of its presence are not forthcoming in these subjects. The desirability of early recognition of such foci—in light of their highly probable _etiological_ significance—can scarcely be overestimated. For their consequences, both local and remote, are of paramount importance. Thus, G. I. Stewart’s recent observations have conclusively demonstrated that “bad teeth” are causally related to _tonsillar_ affections. How illumining this, in view of McCracken’s experiences in “gouty throats.” As we saw, _pyorrhœa alveolaris_ was present in more than half the examples. But, more pertinently to the point at issue, he comments on the frequency with which the victims of gout develop _acute tonsillitis_, of lacunar or parenchymatous type, also that such attacks frequently precede outbreaks of _arthritic_ gout. Duckworth again noted the same liability of the gouty to unsound teeth and tonsillitis, and that the latter was often followed by articular outbreaks. Luff also observed that “gouty” tonsillitis was occasionally a precursor of articular gout, always subsiding on the appearance of the latter complication.