_Arteriosclerosis_, contrary to what has been stated by Huchard and others, is not constant in a considerable degree in old people, and therefore cannot, as Demange and others considered, be regarded as the cause of the atrophic changes seen in old age. Arteriosclerosis is due to several factors, namely, infection and intoxication of various kinds and to damage caused by long-continued high arterial blood pressure. The primary changes are degeneration and weakness, however brought about, in the middle coat. Ophülz[161] has recently discussed the question whether the degeneration is entirely or largely a senile change; if it were so, the curve of the incidence of arterial sclerosis would begin gradually about the age of 40 years, so as to include premature cases, and rise slowly until the age of 55 years, when there would be a sudden increase to 80 or 90 per cent, and at the age of 70 it would be improbable that any one would be free from well-marked arteriosclerosis. He found that the curve of incidence was very different from this; beginning much earlier its rise is gradual all the way without any sudden increase, and indeed seems, if anything, to be retarded by old age. Old persons may have practically healthy arteries, so, although arteriosclerosis may undoubtedly produce atrophy and senile changes in the tissues and organs by diminishing the blood supply, for example in the case of the red granular kidney, it cannot be regarded as the causal factor in healthy old age. The primary calcification of the middle coat, sometimes called Mönckeberg’s sclerosis, which leads to the formation of regular rings in the degenerated muscular media and the “pipe-stem” arteries associated with senile gangrene, may be independent of, or combined with, endarterial sclerosis. It follows fatty degeneration of the media, which is the commonest form of medial degeneration in the aged, and specially picks out the elastic fibres.[162] The femoral, tibial, radial arteries and the aorta are most often affected. It is difficult to estimate its incidence, but that it is not very common, at any rate in a high degree, seems probable from the comparative infrequency of its detection in _x_-ray examinations of the lower limbs in old people. It would be natural to associate its occurrence with the rarefaction of bone that goes on in advanced life, and so to consider it as in some respects different from the secondary calcification in endarteritic sclerosis; in answer to an enquiry Professor W. T. Councilman of Harvard kindly wrote to me that he did not regard calcification as characteristic of any particular type of arterial disease, lime salts being in certain cases more easily deposited in any pre-existing lesions. Klotz describes fatty and calcareous change in the middle third of the media of the aorta as quite characteristic of senescence.