**1. Introduction**

Atherosclerosis (AS) and osteoporosis (OP) are currently considered chronic noninfectious epidemics of the 21st century. These diseases are age-related but they are associated with both increase in life expectancy and etiopathogenetic relationships. AS and OP have a number of common features and, above all, asymptomatic course at the onset and a high risk of delayed complications; for AS, these are heart attack and stroke, for OP, low-trauma fractures with a rate of 30–40% [1].

Modern medicine finds it extremely important to identify certain relationships and common pathogenetic mechanisms between various diseases in order to develop an integrated and individualized approach to the treatment and prevention of diseases. The results of experimental and clinical studies conducted over the last decade confirm that AS and OP with asymptomatic onset had common pathogenetic links resulting in manifested complications. A relationship was shown between the development of AS and decrease in bone mineral density (BMD), regardless of the age of patients and increased risk of morbidity and mortality due to AS complications in patients with OP [2].

Various factors affecting bone metabolism are involved in the mechanisms of vascular diseases. In order to assess the relationship between OP and cardiovascular diseases (CVD) caused by AS, surrogate markers of these diseases are commonly used, such as parameters of vascular wall stiffness or vascular calcification and BMD. The vascular and bone tissues appeared to have a number of common properties and vascular calcification consists of the same elements as the bone tissue: calcium salts, type I collagen, phosphates, bone morphogenetic protein, etc. It has been suggested that low BMD may be a direct risk factor for AS of the coronary arteries [3].

The relationship between AS and OP is most evident in postmenopausal women. In estrogen deficiency, the ability of endothelial cells to produce nitric oxide, which supports the elasticity of the arteries and has stimulating effects on the osteoblasts, decreases, which results in endothelial dysfunction and bone metabolism disorders [2, 3].

Together with the deficit of sex steroids, negative calcium balance caused by vitamin D deficiency and reduced absorption of calcium in the intestine is of great importance, which ultimately results in secondary hyperparathyroidism and increased bone resorption [4, 5]. Disorders leading to both OP and CVD include increased activity of the sympathetic autonomic nervous system, which, together with endothelial dysfunction, causes disorders of the microcirculation system. The most important mechanism for reducing BMD is deterioration of bone tissue perfusion associated with disorders of the microcirculation system. Microcirculation that determines the value of peripheral vascular resistance, due to the "steal" syndrome, significantly affects the state of perfusion of internal organs, including bone tissue [6].

The role of angiotensin II in the development of CVD is well known. In addition to the vasoconstrictor effects, it has significant pro-inflammatory activity in the vascular wall (stimulating the production of reactive oxidized particles, inflammatory cytokines, and adhesion molecules) and contributes to the formation and progression of AS. Angiotensin II receptors have been identified in the culture of bone tissue cells (osteoblasts and osteoclasts). Angiotensin II promotes the production of the receptor activator of nuclear factor kappa-B ligand (RANKL) by osteoblasts, which leads to additional activation of the osteoclasts and increased bone resorption, as well as inhibition of bone mineralization [7, 8].

The results of clinical studies of the relationships between BMD and arterial hypertension (AH) and blood pressure (BP) levels have been controversial. Some *Characteristics of Pathogenetic Links in Vascular Remodeling and Bone Tissue Destruction… DOI: http://dx.doi.org/10.5772/intechopen.107444*

of them showed a negative relationship between BP and bone density, while others showed no relationship between BP and BMD [9, 10]. There are also published data showing that arterial stiffness is higher in women with moderate cardiovascular risk and postmenopausal OP and is closely associated with BMD and bone turnover markers. It was shown that decrease in BMD of the femoral neck is an independent factor for increase in arterial stiffness. The data obtained allowed us to assume that bone mineral metabolism disorders may be an additional risk factor for vascular wall damage, which must be taken into account when determining patients' total cardiovascular risk [11–14].

With steady aging of the population in the 21st century, data on the association of the processes of cardiovascular remodeling and bone tissue resorption in postmenopausal period remain of interest. More and more attention has been recently paid to the role of nonspecific immune inflammatory vascular response as a link in the common pathogenetic mechanisms of atherosclerotic lesions of the vascular bed with changes in the elastic properties of the arteries and the phenomena of degenerative bone changes, which is of great importance at subclinical level, to provide comprehensive measures for the prevention of complications of these comorbid conditions in general.

The purpose of our work was to study the role of nonspecific immune-inflammatory markers, parathyroid hormone, and female sex hormones as predictors of cardiovascular and degenerative bone changes in postmenopausal women with AH and OP.
