MORPHOLOGICAL FEATURES OF OSTEOGENIC CELLS IN YOUNG RATS UNDER CONDITIONS OF CHRONIC HYPERGLYCEMIA
About the author:
Ponyrko A. A., Boomeister V. I., Dmitruk S. N., Teslyk T. P
Heading:
MORPHOLOGY
Type of article:
Scentific article
Annotation:
Abstract. The article presents the data of structural and functional analysis of changes in bone tissue in conditions of chronic hyperglycemia. The study was conducted on 72 white laboratory rats. To simulate chronic hyperglycemia, a solution of alloxan dihydrate was used, which was administered after a 10-hour fasting of the animals. The study of long bones was carried out using scanning electron microscopy and the expression of osteopontin and RANKL in the cytoplasm of cells was assessed. It has been proven that significant changes in the microarchitecture of the bones of the skeleton cause disturbances in the functioning of osteoblasts and destructive changes in osteocytes. With an increase in the duration of hyperglycemia, pathological changes only progress and become more pronounced. In our study, we found a pronounced reaction of osteoblasts in young rats on the 30th day of observation in the form of significant hypertrophy of the hEPS, destruction of organelles in the cytoplasm, and swelling of mitochondria. At the same time, a compensatory reaction in the form of hEPS hypertrophy was observed in young rats – starting from the 120th day of observation. A special feature is that for all periods of observation up to 180 days in young rats, osteoblast dysfunction manifested itself in the form of hePS hypertrophy. During the experiment, the increasing death of osteocytes in rats was established during the entire observation period, starting from the 30th day of the experiment. In addition, a change in the shape of the lacunae was found starting from the 60th day of observation. Thus, under conditions of chronic hyperglycemia, starting from the 30th day of observation, there is a violation of the functioning of osteoblasts and destructive changes in osteocytes in the bones of experimental young rats. The results of immunohistochemical studies indicate a decrease in the secretory activity of osteoblasts and dysfunction of osteitis. Disruption of the synthesis of osteopontin and RANKL negatively affects the osteogenesis of inert tissue. As a result of prolonged exposure to hyperglycemia on the bones of the skeleton, inhibition of the work of both osteoblasts and osteocytes is observed.
Tags:
hyperglycemia, long tubular bones, osteoblasts, osteocytes, osteopontin
Bibliography:
- Yamagishi S. Role of advanced glycation end products (AGEs) in osteoporosis in diabetes. Curr Drug Targets. 2011;12(14):2096-102.
- Pacios S, Andriankaja O, Kang J, Alnammary M, Bae J, de Brito Bezerra B, et al. Bacterial infection increases periodontal bone loss in diabetic rats through enhanced apoptosis. Am J Pathol. 2013;183(6):1928-35
- Cunha JS, Ferreira VM, Maquigussa E, Naves MA, Boim, MA. Effects of high glucose and high insulin concentrations on osteoblast function in vitro. Cell and tissue research.2014;358(1):249-256. doi: 10.1007/s00441-014-1913-x.
- Gennari L, Merlotti D, Valenti R, Ceccarelli E, Ruvio M, Pietrini MG, et al. Circulating sclerostin levels and bone turnover in type 1 and type 2 diabetes. The Journal of clinical endocrinology and metabolism. 2012;97(5):1737-1744. doi: 10.1210/jc.2011-2958.
- Kanazawa I, Sugimoto T. Diabetes Mellitus-induced Bone Fragility. Internal medicine. 2018;57(19):2773-2785. doi: 10.2169/ internalmedicine.0905-18.
- Ogawa N, Yamaguchi T, Yano S, Yamauchi M, YamamotoM, Sugimoto T. The combination of high glucose and advanced glycation endproducts (AGEs) inhibits the mineralization of osteoblastic MC3T3-E1 cells through glucose-induced increase in the receptor for AGEs. Hormone and metabolic research. 2007;39(12):871-875. doi: 10.1055/s-2007-991157.
- Pacicca DM, Brown T, Watkins D, Kover K, Yan Y, Prideaux M, et al. Elevated glucose acts directly on osteocytes to increase sclerostin expression in diabetes. Scientific reports. 2019;9(1):17353. doi: 10.1038/s41598-019-52224-3.
- Wongdee K, Krishnamra N, Charoenphandhu N. Derangement of calcium metabolism in diabetes mellitus: negative outcome from the synergy between impaired bone turnover and intestinal calcium absorption. The Journal of Physiological Sciences. 2017;67(1):71-81.
- Ryabenko TV. Suchasni aspekty reparatyvnoyi reheneratsiyi kistkovoyi tkanyny ta analiz pokaznykiv kistkovoho metabolizmu. Ukrayinsʹkyy zhurnal medytsyny, biolohiyi ta sportu. 2020;5.3(25):89-97. [in Ukrainian].
- Portal-Núñez S, Lozano D, de Castro LF, de Gortázar AR, Nogués X, Esbrit P. Alterations of the Wnt/beta-catenin pathway and its target genes for the N- and C-terminal domains of parathyroid hormone-related protein in bone from diabetic mice. FEBS letters. 2010;584(14):3095-3100. doi: 10.1016/j. febslet.2010.05.047
- Villarino ME, Sánchez LM, Bozal CB, Ubios AM. Influence of short-term diabetes on osteocytic lacunae of alveolar bone. A histomorphometric study. Acta odontologica latinoamericana: AOL. 2006;19(1):23-28.
- Bouillon R, Bex M, Van Herck E, Laureys J, Dooms L, Lesaffre E, et al. Influence of age, sex, and insulin on osteoblast function: osteoblast dysfunction in diabetes mellitus. J Clin Endocrinol Metab. 1995;80(4):1194-202. doi: 10.1210/jcem.80.4.7714089.
- Jiao H, Xiao E, Graves DT. Diabetes and Its Effect on Bone and Fracture Healing. Curr Osteoporos Rep. 2015;13(5):327-35. doi: 10.1007/ s11914-015-0286-8.
- Hamann C, Goettsch C, Mettelsiefen J, Henkenjohann V, Rauner M, Hempel U, et al. Delayed bone regeneration and low bone mass in a rat model of insulin-resistant type 2 diabetes mellitus is due to impaired osteoblast function. Am J Physiol Endocrinol Metab. 2011;301(6):1220-8. doi: 10.1152/ajpendo.00378.2011.
- Uikly B. Elektronnaya mikroskopiya dlya nachinayushchikh. Moskva: Mir; 1975. 328 s. [in Russian]. 16.Reynolds ES. The use of lead citrate at high pH as an electron-opaque stain in electron microscopy. J Cell Biol. 1963;17:208-212.
Publication of the article:
«Bulletin of problems biology and medicine» Issue 2 (160), 2021 year, 231-235 pages, index UDK 616.379-008.64:616.71-091-092.9