Pathological Calcification: Crystallization, Infection, or Cell Transdifferentiation

Abstract

It is becoming increasingly clear that the pathophysiology of calcification within diseased human tissues is complex. Inflammation appears to be associated with many calcific processes, including advanced atherosclerosis, nephrolithiasis, and calciphylaxis of end-stage renal disease. In all three instances characteristic cellular responses could potentially either mediate or ameliorate the calcific response. Increasingly, microorganisms are being identified as an unexpected cause of disease, with a recent well-known example being the association of H. pylori and peptic ulcer. The possibility that microorganisms contribute to pathologic calcification and the associated inflammation is, however, controversial. This symposium will examine evidence for three possible but not mutually exclusive mechanisms of pathologic calcification: (1) processes that drive and influence inorganic crystallization; (2) the mechanisms by which cells mediate crystallization, including cell transdifferentiation; and (3) evidence for the presence of calcifying microorganisms within diseased human kidneys and arteries. The program will conclude with a panel discussion led by a moderator who will comment on divergent points from the perspective of a pathologist.