Further notes about the morphostasis concept – split files

(15) Atherosclerosis

There is much literature, now, on the involvement of inflammation and inflammasomes in the pathogenesis of atheromatous disease (often called atherosclerosis now; my pathology teachers were keen to retain arterioslerosis for hypertension associated vessel changes and insisted on atheroma rather than atherosclerosis). The one thing that I have not come across in the few articles I have read is the possible importance of the shift in the egress of inflammatory cells from a predominantly venous to a markedly arteriolar/arterial pattern as occurs with increasingly ramped up inflammatory processes. Examples include Behçet's syndrome (see the neuro–BS article in the unpublished section), graft rejection, hyper–acute EAE, tuberculosis and syphilis. Ideally, in the luckiest of animals, the inflammatory intensities will probably stay dominantly with a predominantly venular egress of inflammatory cells and avoid long term and cumulative damage to arterioles and large arteries. Atheromatous disease may follow a prolonged shift in emphasis from perivenous to periarteriolar inflammatory egress.