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Regulation of bone formation using osteogenic supplements in an osteoporotic model
Krčmářová, Eliška ; Filová, Eva (advisor) ; Zadražil, Zdeněk (referee)
Osteoporosis is a disease of the bone metabolism which is characterised with a decrease of bone substance. The cause of this disease is the imbalance between the creation of a new bone substance by osteoblasts and the resorption of a bone tissue by osteoclasts, in favour of the bone resorption. The risk group of the development of this disease are women after menopause, who naturally register a decline of the estrogen hormone. Estrogen operates as an inhibitor of proosteoclastic factors such as receptor activator of NFκB ligand (RANKL), interleukin (IL)-1, IL-6 or TNF-α. The imbalance of the bone metabolism can also be caused by a disbalance in the production of Prostaglandin E2 (PGE2) and 1α,25-dihydroxyvitamin D3. They are strong mediators which can both stimulate and inhibit an osteoclastogenesis in vitro in concordance with the conditions of the culture/co-culture. This thesis focuses on the examination of an influence of those mediators (PGE2 in the concentration of 10-6 M and 10-8 M; 1α,25-dihydroxyvitamin D3 in the concentration of 10-8 M and 10-9 M) on the osteoclastogenesis from the rat PBMC at the presence of osteoblasts, with or without the combination of proosteoclastic factors macrophage colony-stimulating factor (M-CSF) and RANKL. Osteoclastogenesis was stimulated if PGE2 and...

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