Again, by the older writers “gout in the liver” was most firmly believed in—as one authority puts it, “a subacute catarrh of the intrahepatic biliary system which may lead to a subacute parenchymatous hepatitis”! But more pertinent to my point is the insistence of older authors upon the frequent association of gout and _gall-stones_. Senac, of Vichy, claimed indeed that out of 166 cases of _biliary lithiasis_ 95 had gout or an hereditary predisposition thereto. Judging by modern experience, this is probably a gross over-estimate. In contrast, our own countryman Murchison dwelt upon the frequency of jaundice in gout independently of biliary colic. And, as we shall see later, Brinton held that many of the dramatic phenomena accredited to “retrocedent gout” were unrecognised examples of _biliary colic_. But, controversy aside, the point I would lay stress on is, that we should refrain from labelling offhand “dyspeptic” symptoms in a “gouty” subject as _gouty_, this when we are so constantly confronted with _local foci of infection_ in the _mouth_, or elsewhere, which afford us an explanation of the gastro-intestinal symptoms at once more obvious and more rational. This also the more especially in that—as far as subjective symptoms go—those deemed typical of so-called “gouty” dyspepsia are indistinguishable from those met with in _appendix-_ or _gall-bladder-dyspepsia_. Indeed, I might go further and point out that the _variations in free HCL_ in the gastric juice—as observed in _gout_—conform to those met with in the above disorders. Thus, in “gouty” dyspepsia, the free HCL may be normal, in excess, or wholly absent, as in gall-bladder or appendix-dyspepsia. I would therefore plead that in any “dyspepsia” arising in a genuinely _gouty_ subject we endeavour to elucidate the exact nature of the _underlying lesion_, but to this we shall return again when discussing diagnosis. Again, the fact that gall-bladder or appendix lesions may be the outcome of septic foci in the mouth enables us the more easily to explain the not infrequent co-existence of gout and _glycosuria_. For an infected gall-bladder may by extension determine a chronic _pancreatitis_. Lastly, what of the relationship of local foci of infection to _“gouty” synovitis_ and _arthritis_? Is one focal infection more than another particularly related to arthritides? Whatever be the true inference, if we take _arthritides_ as a whole, nothing seems so efficient a cause of their production as _oral sepsis_. Accordingly, some are inclined to think that organisms, _e.g._, _streptococcus viridans_, at the roots of the teeth or others in the tonsillar crypts, pass, _viâ_ the blood-stream, _direct_ to the _joints_. Others, again, hold that, given oral sepsis, infection of the stomach and lower levels of the alimentary tract and its accessory cavities ensues. And in sequence thereto infection of the joints may take place from local foci throughout gastro-intestinal tracts.