Патогенетическое единство механизмов прогрессирования хронического пародонтита и ревматоидного артрита подтверждается общими звеньями иммуновоспалительных реакций. Повреждение тканей пародонта опосредовано цитотоксическими эффектами вырабатываемых бактериями Porphyromonas gingivalis ферментов и их метаболитов. Нейтрофилы способствуют развитию пародонтита и участвуют в его прогрессировании, рекрутируя Т-хелперы 17 (Th17) и способствуя накоплению плазматических клеток в поражённых тканях. Активация иммунокомпетентных клеток способствует генерации активных форм кислорода, инициирующих свободнорадикальное окисление липидов, что в сочетании с невозможностью их нейтрализации вследствие сниженного антиоксидантного потенциала приводит к развитию оксидативного стресса. Связь между ревматоидным артритом и хроническим пародонтитом была в центре внимания многочисленных исследований, что обусловлено их общими патогенетическими механизмами. Хроническое воспаление, связанное как с ревматоидным артритом, так и с хроническим пародонтитом, сходно по преобладающему адаптивному иммунному фенотипу, дисбалансу между про -и противовоспалительными цитокинами. Значимым является вовлечение микроорганизма Porphyromonas gingivalis в генерацию антител к цитруллинированным пептидам у пациентов с ревматоидным артритом. Общность эпитопа (SE)-кодирующего аллель HLA-DRB1, связывающего цитруллинированные пептиды, может служить основанием для утверждения генетической предрасположенности и взаимопотенцирования данных заболеваний. Таким образом, имеющаяся взаимосвязь хронического пародонтита и ревматоидного артрита обосновывает необходимость проведения исследований, направленных на разработку новых методов в диагностике, лечении и профилактике рассматриваемых заболеваний с целью разобщения общих патогенетических механизмов воспалительных реакций и процессов остеорезорбции, приводящих к стойким функциональным и органическим расстройствам.
Abstract. The molecular level of physiological processes in the context of studying the pathogenesis of diseases is the basis for their diagnosis and treatment. Thus, the features of the pathogenesis of periodontitis are the direct participation of pro-inflammatory cytokines in the development of alterative inflammation. The study of the cytokine profile is relevant for both diagnostic and therapeutic purposes, since the dynamics of indicators of inflammatory mediators reflects the degree of activity and specificity of pathological reactions present in periodontitis. The purpose of the study Study of cytokine profile indicators in experimental periodontitis. Materials and methods. In an experiment on 50 white non-linear rats weighing 190-280 g, the model of experimental periodontitis proposed by Shkolnaya K.D., Atrushkevich V.G. was reproduced. (Patent RU No. 2625295 dated 07/12/2017). Assessment of the dynamics of the cytokine status of blood serum was carried out by the level of pro-inflammatory (IL-1β, TNF, IL-6, IL-17), anti-inflammatory (IL-4, IL-10) and regulatory (IL-2) cytokines using enzyme-linked immunosorbent assay using reagent kit "Bender MedSystems". Results. The study revealed the presence of an imbalance in the cytokine system, characterized by a violation of the physiological balance between pro-inflammatory and anti-inflammatory cytokines with a predominance of the former. Hyperproduction of cytokines persisted throughout the experiment with an increase in the above uncoupling by day 25, which indicates the formation of an immunoinflammatory process in the periodontium. Conclusion. The data obtained during the study confirm the presence of an imbalance of the cytokine network, which indicates the formation and progression of the inflammatory process of the periodontal complex, and also necessitates the introduction of drugs that inhibit the synthesis of pro-inflammatory mediators into complex therapy.
The pathogenetic mechanisms of progression of chronic periodontitis and psoriatic arthritis have common components in immune and inflammatory responses.The pathogenesis of chronic periodontitis involves interaction of microbial and immunological components. As a chronic immune-mediated inflammatory disease and a consequence of an infectious trigger that originally affects gingival soft tissue, periodontitis is typically characterized by periodontal destruction and damage to adjacent connective tissues. Neutrophils contribute to the development of periodontitis and participate in its progression by recruiting T helper 17 cells and stimulating synthesis of the receptor activator of the nuclear factor kappa-β ligand (RANKL), contributing to bone resorption.Macrophages as producers of proinflammatory cytokines (interleukin (IL)-1β, IL-6, IL-22, IL-23, tumor necrosis factor (TNF)), free radicals, and matrix metalloproteinases contribute to the chronic course of the disease. Tissue destruction results in generation of reactive oxygen species by neutrophils, which, against the background of a decrease in the antioxidant potential, leads to development of oxidative stress. These processes together lead to tooth mobility, formation of periodontal pockets, and bone resorption.The key factors in the formation of psoriatic arthritis against the background of periodontitis are overproduction of proinflammatory cytokines in target tissues (skin, joints, gingival microflora) and development of an excessive systemic immune response to the microbiota inhabiting the epithelial and periodontal tissues. A statistically confirmed correlation of the progression of periodontal destruction with the presence of psoriatic arthritis proves the significance of the effects of inflammation as a background for the progression of a comorbidity. Increased IL-17 synthesis plays a crucial role in the development of immune responses of pathological bone remodeling and bone resorption in periodontitis and psoriatic arthritis.
Lipid peroxidation analysis and identification of the main damage predictors lead to introduction of new diagnostic and treatment technologies into medical practice. The aim of the study was to evaluate the activity of free radical damage processes and identify their association with collagen metabolism disorders in the disease dynamics in experimental periodontitis. Materials and Methods. An experimental study was carried out on 60 white non-linear rats. A rat model of periodontitis was reproduced according to K.D. Shkolnaya and V.G. Atrushkevich method (Patent RU No. 2625295, December 07, 2017). The overall activity of free radical oxidation and antioxidant potential was assessed according to biochemiluminescence parameters. Lipid peroxidation activity was assessed according to the parameters of primary and secondary peroxidation products. Collagen metabolism was assessed by P.N. Sharaev method. Results. The rat model of periodontitis demonstrated a high level of free radical oxidation parameters. At the same time decrease in the antioxidant potential was observed throughout the experiment. It proved a significant inhibition of the antioxidant system ability to neutralize bioradical oxidation reactions. The resulting free radicals caused the collagen destruction, which formed the frame of the periodontal connective tissue structures. It was confirmed by hydroxyproline increase due to its free and peptide-bound fractions throughout the experiment. Finally, an increase in protein-bound hydroxyproline was determined against the background of high levels of free hydroxyproline, which was explained by the formation of pathological granulations and fibrillar collagen with an inferior short-chain structure. Conclusion. Chronic periodontitis is characterized by disturbances in the bioradical balance followed by the oxidative stress development, which induces the dystrophy of periodontal collagen structures. The data obtained substantiate the use of collagen peroxidation and metabolism markers as diagnostic criteria to predict the course of periodontitis, and also prove the importance of antioxidants.
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