There is not much that can be done currently in regards to prevention and treatment of arterial calcification. Some people have suggested supplementing with vitamin K, although solid studies appear to be lacking. I was browsing through a book entitled "Biological Calcification: Normal and Pathological Processes in the Early Stages" and came across an interesting study conducted on rats. It appears that an osteoclast inhibitor named SB 242784 has the potential to inhibit aterial calcification (specifically in vitamin-D intoxicated rats).
"Studies by Dhore et al. (2001) showed the constitutive immunoreactivity of MGP, OC and BSP, and the absence of OPN, BMP-2, BMP-4 and ON, in normal human aortas; the calcification or ossification of atherosclerotic plaques were associated with up-regulation of the latter (OPN, BMP-2, BMP-4 and ON,) and sustained immunoreactivity of the former (MGP,OC and BSP). Moreover, the same authors found that osteoprotegerin (OPG), an osteoclastogenesis inhibitory factor, and its ligand (RANKL), were detectable in normal aortas and early atherosclerotic lesions, and that, in advanced calcified plaques, OPG was present in bone structures and RANKL was only detectable around calcified deposits. In this connection, it has been
14.3 Ectopic Calcifications 401 reported by Bucay et al. (1998) that OPG−/− mice exhibited osteoporosis, as expected, but unexpectedly developed widespread calcification of the aortas and renal arteries, suggesting that OPG inhibits artery calcification, as demonstrated later (Price et al. 2001). These findings, which suggest a link between the local factors that regulate osteoclasticbone resorption, the immune system and calcification of the arterial wall (Schoppet et al. 2002; Collin-Osdoby 2004), have found support in the observation that the inhibition of osteoclast activity by SB 242784 – a selective inhibitor of the osteoclast V-H+-ATPase – prevents arterial calcification in vitamin D-intoxicated rats (Price et al. 2002)."Edited by Aphrodite, 05 November 2009 - 03:41 PM.