[Hierarchically organized model of interconnected cellular and tissue mechanisms of calcium exchange between bone and blood].

The objective of this study was to propose, on the basis of the results of authors' own research and literature data, the hierarchically organized model of the interrelation of morphological mechanisms with the participation of biochemical bases of Ca2+ exchange between bone and blood. It is shown that osteocytes control the activity of main known mechanism of skeleton architecture remodeling (osteoclast-osteoblast remodeling, modeling, osteocyte remodeling etc.), that is the destruction and formation of mineral matrix component, thus influencing calcium turnover between bone and blood. The hierarchical organization of the mechanisms of this exchange is established. The first level of Ca2+ metabolism corresponds to the borderline between bone and takes place without bone matrix disintegration by paracellular energy-free Ca2+ diffusion from blood to bone and transcellular energy-dependent Ca2+ transfer from bone to blood. At the second level, calcium exchanger takes place at the borderline between between bone matrix and extracellular fluid by osteocyte remodeling during resorption or formation of the matrix of lacunar-canalicular system walls. The third level includes the mechanisms of osteoclast-osteoblast remodeling acting at the borderline between bone and blood. The mass of rapidly exchanging calcium pool was calculated to reach 58,5 g, thus being 11 times higher than previously suggected.

[Osteocytes and the pathways of mechanical homeostasis optimization from the point of view of functional osteology].

The aim of this work was to determine, on the basis of the results of authors' own research and literature data, the main pathways of osteocyte (OC) influence on the mechanical homeostasis of the skeleton. The following pathways of reorganization of the architecture of bone structures are postulated: at the ultrastructural level without direct cell participation, through the bone matrix synthesis by osteoblasts and OC, through bone matrix resorption by osteoclasts and OC, the latter being able to resorb the surrounding mineral and organic matrix both separately, and conjointly. This reorganization results in local changes of the mechanical characteristics of bones due to changes in: porosity of interstitial spaces, transport ability of the lacunar-canalicular system, porosity of the area of osteoblastic-osteoclastic remodeling, modeling of bone structures. From the point of view of adaptation theory it is highly significant that the subtle local control of bone structures is able to induce changes in the parameters of the mechanical environment, which, on the one hand, would correspond to OC metabolic requirements and, on the other hand, would support the parameters of body mineral homeostasis.

[Interconnection of morpho-functional changes at various levels of the cortical bone hierarchic organization in aging].

The authors define two groups of levels of cortical bone hierarchic organization. The first three levels (molecular, supra-molecular and tissue) are characterized by age-dependent changes in connections and geometry of collagen fibers, deviations in orientation and interaction between collagen and minerals, increase in crystallinity and size of the latter, resulting in matrix hypermineralization. It causes water and organic fraction displacement, as well as intermolecular space reduction, which provides for lesser amount of matrix deformations under the influence of mechanical forces. At the next three levels (structural-functional, organ-forming structures, organ) adaptation processes contribute to deformation increase due to a greater volume of cavities (Haversian canals and medullar cavity of the diaphysis of long tubular bones). These are due to the fact that osseous tissue cells possess superior and inferior thresholds of deformation perception, and through modeling/remodeling provide for extracellular matrix migration in the direction limited by these thresholds. Bone geometry changes leading to bone mass loss are also caused by age-dependent rise of the inferior threshold of sensitivity to mechanical impulses and decrease of muscle functional activity. Prevention of the described changes may be possible through elaboration of new, pathogenesis-based ways of drug therapy, including 1) osseous tissue mineralization reduction with the help of osteocyte pump regulators for predominant washing out of Ca2+, 2) lowering the threshold of electric impulses initiation arising in the osteocyte network under mechanical deformations.

[Precision error minimization algorithm for dual-energy X-ray absorptiometry to clinically insignificant values].

OBJECTIVE: To propose an algorithm for using dual-energy X-ray absorptiometry (DEXA) on the basis of the authors' findings and the data available in the literature on the estimation of the projectional bone mineral density (PBMD), which can minimize the precision error (PE) to clinically insignificant values while solving the problems of diagnosis, prognosis, and therapeutic effectiveness monitoring in a specific patient. MATERIAL AND METHODS: The results of the authors' ex vivo studies and literature data on PE during DEXA in a densitometry room were systematized. RESULTS: The performed analysis allowed the elaboration of a PE minimizing algorithm in the individual control in terms of clinical problems to be solved. The elements of a working place passport system, which allow the head of a radiological service to control the work of a densitometry room and a densitometer operator to make self-control, have been developed. CONCLUSION: The elaborated algorithm for using DEXA in a densitometry room to estimate PBMD permits one to minimize PE when solving the problems of diagnosis, prognosis, and therapeutic effectiveness monitoring in a specific patient in the clinically permissible limits.