Balanced Mineralization in the Arterial System

Abstract

Arterial calcification is the result of the same highly organized processes as seen in bone, which rely on a delicate balance between osteoblasts and osteoclasts. Although previously understood as passive precipitation, evidence has accumulated to suggest that arterial calcification is the result of organized, regulated processes bearing many similarities to osteogenesis in bone, including the presence of subpopulations of arterial wall cells that retain osteoblastic lineage potential. These cells have the potential to form mineralized nodules and express osteoblast markers, including bone morphogenetic protein-2, osteocalcin, osteopontin, and alkaline phosphatase. By contrast, osteoclastlike cells mediate the catabolic process of mineral resorption. Recent data shows that cells positive for tartrate-resistant acid phosphatase, a major marker for osteoclasts, have been histologically identified in atherosclerotic lesions and are referred to as osteoclast-like cells. Evidence has accumulated to suggest that initial arterial calcification through passive precipitation of calcium phosphate initiates balanced mineralization regulated by osteoclast-like and osteoblast-like cells. Subsequently, various pathogenic conditions may trigger an imbalance between osteoblastogenesis and osteoclastogenesis, leading to either calcification in stenotic/occlusive disease or destruction of the extracellular matrix in aneurysmal disease. Further elucidation of these newly emerging concepts could lead to a novel therapeutic approach to arterial stenotic/occlusive disease and/or abdominal aortic aneurysm. (Circ J 2012; 76: 2732 - 2737)

Osteopontin and Osteoprotegerin as Potential Biomarkers in Abdominal Aortic Aneurysm before and after Treatment

“…Osteopontin has been associated with changes in the extracellular matrix and depletion of vascular smooth muscle cells, leading to AAA development [ 2 , 4 , 22 ]. Our results concur with previous studies showing that OPN is associated with AAA formation and aortic dilatation as well [ 13 , 23 ]. Furthermore, there were previous researchers, such as Golledge et al, that correlated OPN serum levels with AAA growth and size [ 13 , 24 ].…”

Coconut Atrium in Long-Standing Rheumatic Valvular Heart Disease

“…Recent research on the mechanisms of ectopic calcification such as arterial calcification indicates that well-regulated processes, similar to those that drive osteogenesis, mediate vascular calcification. It is hypothesized that a subpopulation of vascular cells retains the potential to differentiate into osteoblasts and may play a pivotal role in vascular calcification by forming mineralized nodules and expression of osteoblast-specific proteins such as osteocalcin, bone morphogenetic protein-2, and alkaline phosphatase [ 4 ]. However, there currently are no published studies that define the mechanisms of calcification in the myocardium.…”

Role of Macrophages in the Progression and Regression of Vascular Calcification

“…Osteoblasts deposit bone matrix proteins that can subsequently become mineralized and coordinate with bone resorption by activated osteoclasts. Once the dynamic balance between osteogenesis and osteolysis is broken, vascular calcification or pathological bone remodeling (such as osteoporosis) can occur (Yamanouchi et al, 2012).…”