Abstract
The fact is disturbance of the processes of bone tissue remodeling leads to a change in the balance between synthesis and resorption of bone and the development of osteoporosis. The most common cause of secondary osteoporosis is the use of glucocorticoid therapy. The aim of this study is to investigate the cellular-molecular mechanisms of disturbance of the processes of bone remodeling regulation, reflected by hormones and intercellular mediators (for example parathyroid hormone, calcitonin, RANKL, osteoprotegerin, P-selectin, interleukin-17, transforming growth factor-β1, adiponectin and visfatin) on the background experimental glucocorticoid osteoporosis. The experimental study carried out in two groups of white female rats. Disturbance of bone tissue remodeling was verified by histological examination of the femoral head, vertebrae of the thoracic and lumbar spine of rats and the measurement of bone density. The study of the levels of hormones and intercellular mediators in the blood serum of animals was carried out by the method of enzyme immunoassay. The bone mineral density of the experimental group was reduced compared to the bone mineral density of the control group. The study of the histostructure of the femoral head and vertebrae in rats of the experimental group in comparison with the animals of the control group revealed changes in the structural organization of bone tissue, confirmed by histomorphometry, indicating inhibition of the processes of osteosynthesis. The article analyzes the nature of the involvement of hormones and cytokines in pathogenetic mechanisms of development of bone tissue disorders. The levels of cytokines RANKL, osteoprotegerin, interleukin-17 and calcitonin in the blood serum of animals of the group with the violation of bone tissue remodeling by glucocorticoids were higher than in intact animals. Serum levels of P-selectin, parathyroid hormone, transforming growth factor-β1, adiponectin and visfatin were lower than similar levels in animals from the control group. The use of glucocorticoids increases the expression of RANKL and inhibits the synthesis of osteoprotegerin, resulting in stimulation of bone resorption. The effect of glucocorticoids in the experimental model is realized by changing the production of the studied hormones, cytokines and adhesion molecules. These changes stimulate the apoptosis of osteoblasts and inhibit their proliferation and differentiation, which is another mechanism of bone loss. Correlations found during the study reflect the relationship in the system of regulation of bone tissue remodeling under the influence of glucocorticoids. A complex system for regulating bone remodeling, which includes many regulatory pathways and their interactions, requires further study.
Highlights
When bone remodeling processes are disturbed, the balance between formation and resorption of bone tissue changes, controlled and coordinated by different types of bone cells
The aim of the study was to investigate the cellular-molecular mechanisms of disturbance of bone tissue remodeling regulation processes, as reflected by intercellular mediators in experimental glucocorticoid osteoporosis
The measured bone mineral density of the animal group with the violation of bone tissue remodeling with glucocorticoids was significantly decreased in comparison with the bone mineral density of the animals in the control group (1.37 ± 0.041 and 1.62 ± 0.059 g/cm3 respectively, P < 0.05)
Summary
When bone remodeling processes are disturbed, the balance between formation and resorption of bone tissue changes, controlled and coordinated by different types of bone cells. This often leads to the development and progression of osteoporosis, which, according to World Health Organization data, is the second most important health problem after cardiovascular disease (Klimova et al, 2014). With prolonged glucocorticoid therapy, the number of osteoclasts is usually maintained in the normal range, while the number of osteoblasts is significantly reduced, in contrast to postmenopausal osteoporosis, in which there is increased bone resorption (Weinstein, 2011). Apoptosis of osteoblasts, induced by the constant use of glucocorticoids, is identified as the main cause of osteoporosis, bone loss and fractures
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