The traditional view that subchondral bone is richly vascularized, whereas hyaline cartilage is not, may no longer be true because histo-chemical studies have shown that the deep layer of hyaline cartilage is vascularized. The articular vasculature, therefore, derives its nutritional supply partly from the vascular bed of subchondral bone, as well as from the synovial fluid. Therefore, any loss of vascular tone in the subchondral bone could affect the cartilage. Early microvascular damages that affect the venous circulation in the bony tissue, therefore, may be considered a plausible cause of altered chondrocyte function . Whether these vascular changes are secondary to bony changes or their primary cause remains unexplored. However, OA and cardiovascular disease risk factors have been shown to be correlated [115,146,220], and abnormal vascularization of OA tissues may be a means to initiate cartilage tissue damage . The hypothesis that OA may be viewed as an atheromatous vascular disease has recently been proposed by Conaghan et al . Abnormal vascular function in OA may also be be linked to elevated leptin levels, because leptin acts on arterial wall thickness, decreases vessel distensibility, and elevates C-reactive protein levels .
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