Cardiovascular disease and decreased skeletal mineral density are interrelated processes. Osteopenia and osteoporosis progress in parallel with atherosclerotic lesions (including vascular calcification) and cardiovascular events with a definite age-related trend. The use of antilipidemic agents slows the progression of atherosclerosis and vascular calcification, and also reduces the risk of osteoporotic fractures. With regard to the relationship between fracture frequency and the degree of dyslipidemia correction, the available evidence is ambiguous, as is the question of whether the effect of bone remineralization is a unique property of agents of the class of hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins). Do statins HMGcoA Reductase Inhibitors decrease the risk of fractures?
Two body systems
Osteoporosis as the most common skeletal pathology is characterized by decreased bone mass, impaired bone microarchitecture and increased bone fragility. The precise etiology of osteoporosis is unknown, but pathogenetically it is an imbalance of bone formation and bone resorption by osteoblasts and osteoclasts, respectively. The goal of therapy in osteoporosis is to restore this balance.
In addition to slowing down demineralization and reducing the frequency of osteoporotic fractures, such agents do not cause a significant increase in bone formation. The use of agents stimulating skeletal remineralization would be a breakthrough in therapy for this pathology. Significant success in this area should be expected as a result of the emergence and clinical application of new agents of the statin group.
Bone and vascular tissue have a number of similar properties at the cellular and molecular level. Bone tissue and bone marrow contain endothelial cells, preosteoblast and osteoclast derived monocytes, all of which are also normal components of vascular wall cell populations.
The pathogenesis of atherosclerosis and osteoporosis involves monocytes with differentiation into macrophages with frothy cytoplasm within the vascular wall and into osteoclasts in bone tissue. Each osteon – a morphological unit of bone – contains a central vessel lined internally by endothelium localized on the subendothelial matrix. Cells – osteoblast precursors are localized directly on the periphery of the matrix. In the vascular wall there are cellular elements that differentiate into osteoblasts according to the stages of differentiation of bone osteoblasts, eventually producing the mineral component of bone.