The results consistently and strongly indicate that higher OPG plasma levels are to be found in patients with asymptomatic carotid lesions. It is now established that bone formation and arterial calcification share many similarities. In bone, OPG is secreted by osteoblasts and acts as a decoy receptor for RANKL. Osteoprotegerin prevents RANKL fixation on its receptor RANK at the surface of osteoclasts, resulting in the inhibition of osteoclast proliferation and differentiation. This process finely tunes bone formation and resorption. In the arterial wall, osteoblast precursors and the OPG/RANKL/RANK axis have clearly been identified. During arterial calcification formation, cells with osteochondrogenic potential differentiate along the HhAntag691 osteoblastic lineage, yet the exact nature of these cells remains to be elucidated. Vascular smooth muscle cells represent the most common cell type studied. They have been shown to have important phenotypic plasticity and when exposed to hydroxyapatite cristals, high concentrations of phosphate or inflammatory cytokines, vascular smooth muscle cells differentiate into osteoblastic cells. However, other cells including pericytes have also been previously shown to be involved in the vascular calcification process and their potential as mesenchymal precursors has recently been highlighted. Our immunohistological results showed no difference in terms of smooth muscle cells and endothelial cells presence between symptomatic and asymptomatic plaques. In contrast, higher pericyte cell density was noted in asymptomatic lesions, suggesting that pericytes could be actively involved in plaque stability. The most studied potential sources of OPG in the artery wall are endothelial cells and smooth muscle cells. Upon inflammatory stimulation, these cells release OPG in the surrounding extracellular AZ 960 matrix as well as in the circulation, which is one of the possible sources of circulating OPG in atherosclerotic patients. Based on in vitro preliminary results, we observed that unstimulated pericytes had an intense secretion of OPG at baseline in comparison to smooth muscle cells and endothelial cells.