Introduction. Unsatisfactory consequences of bone regeneration disorders in diabetes mellitus (DM) patients, their high prevalence, complication number, and difficulties in treatment require further study and deeper understanding of reparative osteogenesis mechanisms under chronic hyperglycemia and finding new effective and affordable approaches to their treatment. Therefore, the aim of our work was to study the histological, ultramicroscopic, and histomorphometric features of reparative osteogenesis in rats with chronic hyperglycemia (CH), as well as to investigate the possibility of platelet-rich plasma (PRP) use in a fracture area in order to correct the negative effects of CH on reparative osteogenesis processes. Study Object and Methods. The studies were performed on 70 white laboratory rats, mature males, which were divided into the following groups: control group, animals with posttraumatic tibial defect under conditions of CH exposure, rats with experimental CH that were administered with PRP into the bone defect, and animals for the assessment of glucose homeostasis and confirmation of simulated CH. Light microscopy was performed using an Olympus BH-2 microscope (Japan). Ultramicroscopic examination was performed using REM-102 scanning electron microscope. The statistical analysis was performed using SPSS-17 software package. Results. The formation of new bone tissue in animals with CH did not occur after two weeks. Only on the 30th day of reparative osteogenesis the newly formed woven bone tissue was 61.54% of the total regenerated area. It was less than the reference value by 22.89% (). On the 14th day of reparative osteogenesis, the regenerated area in a group of animals with CH and PRP injection consisted of connective tissue by 68.94% (4.94% less than in animals with CH ()) and woven bone tissue by 31.06%, (13.51% less than in the control group ()). On the 30th day, the area of woven bone tissue in a regenerate of this group was less than that of the control group by 12.41% (). Conclusion. Thus, chronic hyperglycemia contributes to inflammation delay within the bone defect site, which makes the process of reparative osteogenesis more prolonged. The results of chronic hyperglycemia effect on bone regeneration are also impairment of osteogenic cell proliferation and shift of their differentiation towards the fibrocartilage regenerate formation. The PRP corrects the negative impact of chronic hyperglycemia on reparative osteogenesis, promoting more rapid inflammatory infiltrate removal from the bone defect site and osteogenic beam formation and remodeling of woven bone into lamellar membranous bone tissue.

中文翻译：

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慢性高血糖影响下长管骨再生的形态学特征及矫正。

简介。糖尿病（DM）患者骨再生障碍的不良后果、高患病率、并发症数量和治疗困难需要进一步研究和深入了解慢性高血糖下的修复性成骨机制，并寻找新的有效且负担得起的治疗方法。因此，我们工作的目的是研究慢性高血糖 (CH) 大鼠修复性成骨的组织学、超显微和组织形态学特征，以及研究在骨折区域使用富血小板血浆 (PRP) 的可能性为了纠正 CH 对修复性成骨过程的负面影响。研究对象和方法. 对 70 只成年雄性白色实验室大鼠进行了研究，将其分为以下组：对照组、在 CH 暴露条件下患有创伤后胫骨缺损的动物、在骨缺损处注射 PRP 的实验性 CH 大鼠，以及动物用于评估葡萄糖稳态和确认模拟 CH。使用Olympus BH-2显微镜（日本）进行光学显微镜检查。使用REM-102扫描电子显微镜进行超显微检查。使用SPSS-17软件包进行统计分析。结果. 两周后，患有 CH 的动物没有形成新的骨组织。仅在修复性成骨第30天，新形成的编织骨组织占总再生面积的61.54%。比参考值低22.89%（）。在修复性成骨的第 14 天，注射 CH 和 PRP 的一组动物的再生区域由 68.94% 的结缔组织组成（比 CH 的动物少 4.94%（)）和编织骨组织减少 31.06%，（比对照组减少 13.51%（））。第30天，本组1次再生的编织骨组织面积比对照组减少12.41%（）。 结论。因此，慢性高血糖有助于骨缺损部位的炎症延迟，这使得修复性成骨过程更加延长。慢性高血糖对骨再生的影响的结果也是成骨细胞增殖的损害和它们的分化向纤维软骨再生形成的转变。PRP 纠正了慢性高血糖对修复性成骨的负面影响，促进从骨缺损部位更快地清除炎症浸润和成骨束形成以及将编织骨重塑为板层膜状骨组织。