A relevant issue in the study of ectopic calcification affecting different vascular tissues is to elucidate whether and how much common pathogenetic mechanisms, calcific factors and degenerative events are shared mineralization hallmarks1. Previously, in calcifying subdermally implanted aortic valves, modified Cuprolinic Blue reactions revealed a distinct cell degenerative pattern culminating in clustering of acidic lipids at cell surfaces with subsequent blebbing of matrix-vesicle-like bodies, acting as major apatite nucleators2. Additional co-localization of calcium-binding sites, as ultrastructurally revealed by von Kossa reactions, and of immunogold labelled Annexin-V was also found. In the present work, the above procedures, in situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) method, and immunohistochemical reactions for calcium-binding proteins annexin-V, osteopontin, osteonectin and tenascin-C were used to study calcifying aortic wall and stenotic valve samples. Peculiar CB- and von-Kossa-reactive lipidic layers comparable with those in the experimental model actually resulted as degenerative forms also characterizing these two calcification types. In addition, the whole calcification patterns showed some similarities but also distinct dissimilarities to exist by comparing experimental model, vascular wall atherosclerosis and aortic valve disease. 1. Demer L 2001. Circulation 104, 1881-1883. 2. Ortolani F et al. 2003 Histol. Histopathol. 18, 1131-1140. 3. Ortolani F et al. 2007 Histol. Histopathol. 22, 261-272.
