Abstract

Objective . The aim was to study the functional activity of platelets in periodontitis. Materials and methods. Experiments were performed on 20 white nonlinear male rats weighing 320.0 ±30.0 g. Experimental periodontitis was modeled by the method of L. V. Peshkova. Blood for the study of platelet aggregation was taken by a syringe from the heart. Induced platelet aggregation was examined using a Computerized Platelet Aggregation Analyzer SOLAR 2110. Adenosine diphosphate (ADP) was used as an inducer at 2.5 μmol/L and 10.0 μmol/L concentration. The resulting aggregation was recorded at 37 °C for 10 min. Samples of periodontal tissues were fixed in a 10 % neutral-buffered formalin solution, dehydrated in an ascending concentration series of alcohol, followed by chloroform, chloroform-paraffin and embedded into paraffin. Sections 4–6 microns thick were cut on a sliding microtome and stained with hematoxylin-eosin and van Gieson’s stain. Results. Analysis of aggregograms revealed a decrease in the functional activity of platelets in rats with experimental periodontitis at aggregation inducer concentrations of 2.5 μmol/L and 10.0 μmol/L. Reduction in the degree of platelets aggregation and aggregation rate were observed at an inductor concentration of 2.5 μmol/L in a group of rats with experimental periodontitis in comparison with the control. Microscopic examination showed a violation of the connective periodontal tissue histoarchitectonic. Dilatation of small capillaries in the connective tissue layers and in some preparations microvascular congestion were observed which indicated a violation of blood microcirculation, failure of repair regulatory mechanisms and the pathological process’s reaching the systemic level. The interaction of connective tissue cells with platelets played a significant role in these processes. Conclusions. Decrease in thrombocytes aggregation activity is observed in rats with experimental periodontitis. Changes in the periodontal connective tissue manifested by the vascular pattern transformation, microcirculation violations, disruption of repair regulatory mechanisms and the pathological process’s reaching the systemic level.

Highlights

  • Analysis of aggregograms revealed a decrease in the functional activity of platelets in rats with experimental periodontitis at aggregation inducer concentrations of 2.5 μmol/L and 10.0 μmol/L

  • Reduction in the degree of platelets aggregation and aggregation rate were observed at an inductor concentration of 2.5 μmol/L in a group of rats with experimental periodontitis in comparison with the control

  • The interaction of connective tissue cells with platelets played a significant role in these processes

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Summary

Introduction

Изменения функциональной активности тромбоцитов у крыс при экспериментальном нарушении состояния соединительной ткани пародонта Анализ агрегатограмм показал уменьшение функциональной активности тромбоцитов у крыс с экспериментальным пародонтитом при концентрациях индуктора агрегации 2,5 мкмоль/л и 10,0 мкмоль/л. Снижение степени агрегации тромбоцитов и скорости агрегации по сравнению с контролем наблюдали при концентрации индуктора 2,5 мкмоль/л в группе крыс с экспериментальным пародонтитом. Changes in the functional activity of thrombocytes in rats with experimental disruption of the periodontal connective tissue

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