According to Adami the effects of syphilis upon the aorta are the following: (1) the primary disturbance is a granulomatous, inflammatory degeneration of the media; (2) this leads to a local giving way of the aorta; (3) if this be moderate it results in a strain hypertrophy of the intima and of the adventitia, with the development of a nodose intimal sclerosis; (4) if it be extreme, there results, on the contrary, an overstrain atrophy of the intima and aneurysm formation; (5) the intimal nodosities are here not of an inflammatory type and are nonvascular, although, with the progressive laying down of layer upon layer of connective tissue on the more intimal aspect of the intima, the earlier and deeper-placed layers of new tissue gain less and less nourishment, and so are liable to exhibit fatty degeneration and necrosis; (6) these products of necrosis exert a chemotactic influence upon the nearby vessels of the medial granulation tissue, with, as a result, (a) a secondary and late entrance of new vessels into the early and deeply-placed atheromatous area, (b) absorption of the necrotic products, (c) replacement by granulation tissue, (d) contraction of the granulation tissue, and (e) depression and scarring of the sclerotic nodules so characteristic of syphilitic sclerosis. In the smaller arteries and arterioles the arteriosclerotic process appears on superficial examination to be a different process from that in the aorta and large arteries, but the difference is only apparent. It will be recalled that there is relatively much more muscle tissue in the arterioles than in the large arteries. The size, of course, is much less. Large nodular plaques are not possible. The atheromatous degeneration is not marked. In the smaller muscular arteries is seen the intimal proliferation, the stretching of the Moenckeberg type, and the calcification of the media rather than the intima. The media is thinned beneath the marked intimal proliferation so that the artery exhibits translucent areas when held to the light. Again, there is seen degeneration of the muscle and replacement by connective tissue with or without hypertrophy of the intima. In the arterioles three kinds of changes occur: a muscular hypertrophy; a fibrosis of all the coats; or a marked proliferation of the intimal endothelium. The last two are probably the same process, the connective tissue having its origin in the proliferated endothelial cells. Such a deposition of layer upon layer of cells in an arteriole and the resulting fibrosis leads to the condition of disappearance of the lumen of the vessel, endarteritis obliterans. This obliterating endarteritis is not, of course, due alone to syphilis. Syphilis is only a type of poison which produces such changes as have been described above. It is in the organs such as the kidney, liver, spleen, and intestines that one sees the most perfect examples of this obliterating endarteritis. Endarteritis deformans is a