Structural and functional changes of osteoblasts under conditions of chronic hyperglycemia
DOI:
https://doi.org/10.29038/NCBio.21.1.85-92Keywords:
ultramicrostructure, long tubular bones, hyperglycemia, osteogenic cellsAbstract
The aim of our study was to examine the structural and functional changes of osteogenic cells of the long tubular bones of elderly rats and to determine the relationship between the ultramicroscopic structure of osteoblasts and the intensity of osteopontin and RANKL expression in chronic hyperglycemia. The experiment was simulated by intraperitoneal injection of a single injection of alloxan dihydrate at a dose of 150 mg / kg body weight in 0.9% sodium chloride solution. The following methods were used to study the structure of the femur and humerus: transmission electron microscopy and immunohistochemical. In the study of osteoblasts and osteocytes evaluated the following indicators: the integrity of cellular elements and membrane organelles, vacuolation of the cytoplasm.
As a result of the experiment, it was found that in senile rats under conditions of prolonged hyperglycemia, there is a significant hypertrophy of the EPS, increasing the destruction of organelles in the cytoplasm, respectively, increasing the duration of chronic hyperglycemia. From the 30th day of the experiment, osteoblast hyperfunction was detected in elderly rats as an adaptive response to elevated glucose levels and their pronounced response in the form of significant hypertrophy of EPS, destruction of organelles in the cytoplasm and swelling of mitochondria with subsequent active progression up to 180 days.There is the formation of residual cells, which is a sign of a compensatory reaction.
Suppression of osteopontin expression is a consequence of elevated glucose levels, which in turn disrupts the normal formation of bone tissue in chronic hyperglycemia. Immunohistochemical studies confirmed disturb-ances in the structure and function of osteoblasts and destructive changes in osteocytes, manifested by decreased expression of osteopontin (one of the markers of bone formation) and a gradual increase in RANKL (a marker directly involved in bone resorption).
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