ssmuБюллетень сибирской медициныBulletin of Siberian Medicine1682-03631819-3684Siberian State Medical University, the Ministry of Healthcare of the Russian Federation10.20538/1682-0363-2022-4-183-192ssmu-5038Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEW AND LECTURESПатогенетические аспекты взаимосвязи хронического генерализованного пародонтита и псориатического артритаPathogenetic aspects of the development of psoriatic arthritis in people with generalized chronic periodontitishttps://orcid.org/0000-0003-2010-3296ПорядинГ. В.PoryadinG. V.

Порядин Геннадий Васильевич – член-корреспондент РАН, доктор медицинских наук, профессор кафедры патофизиологии и клинической патофизиологии

117997, г. Москва, ул. Островитянова, 1

1, Ostrovityanova Str., Moscow, 117997

poryadin_gv@rsmu.ruhttps://orcid.org/0000-0003-1433-0337ЗахватовА. Н.ZakhvatovA. N.

Захватов Алексей Николаевич – доктор медицинских наук, профессор кафедры общей хирургии им. профессора Н.И. Атясова

Республика Мордовия, 430005, г. Саранск, ул. Большевистская, 68

68, Bolshevistskaya Str., Saransk, 430005, Republic of Mordovia

zachvatan78@mail.ruhttps://orcid.org/0000-0003-0415-1132ПаршинаА. Ю.ParshinaA. Yu.

Паршина Алина Юрьевна – студентка

Республика Мордовия, 430005, г. Саранск, ул. Большевистская, 68

68, Bolshevistskaya Str., Saransk, 430005, Republic of Mordovia

alinaparshina2000@gmail.comРоссийский национальный исследовательский медицинский университет (РНИМУ) им. Н.И. ПироговаРоссияPirogov Russian National Research Medical UniversityRussian FederationМедицинский институт, Национальный исследовательский Мордовский государственный университет (МГУ) им. Н.П. ОгарёваРоссияMedical institute, National Research Ogarev Mordovia State UniversityRussian Federation202222012023214183192Copyright © Порядин Г.В., Захватов А.Н., Паршина А.Ю., 20232023Порядин Г.В., Захватов А.Н., Паршина А.Ю.Poryadin G.V., Zakhvatov A.N., Parshina A.Y.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://bulletin.ssmu.ru/jour/article/view/5038

Патогенетическое единство механизмов прогрессирования хронического пародонтита и псориатического артрита подтверждается общими звеньями иммуновоспалительных реакций.

Патогенез хронического пародонтита заключается во взаимодействии микробного и иммунологического компонентов. Как хроническое иммуновоспалительное заболевание и следствие инфекционного триггера, который первоначально поражает мягкие ткани десен, пародонтит классически характеризуется разрушением периодонта и окружающих соединительных тканей. Нейтрофилы способствуют развитию пародонтита и участвуют в его прогрессировании, рекрутируя Т-хелперы 17 и стимулируя синтез активатора мембраносвязанного рецептора ядерного фактора каппа-β (RANKL), способствуя остеорезорбции.

Макрофаги как продуценты провоспалительных цитокинов (интерлейкин (IL)-1β, IL-6, IL-22, IL-23, фактор некроза опухоли), свободных радикалов, матриксных металлопротеиназ способствуют хронизации процесса. Деструкция тканей влечет за собой генерацию нейтрофилами активных форм кислорода, что на фоне снижения антиоксидантного потенциала ведет к развитию оксидативного стресса. Данные процессы в совокупности ведут к формированию патологической подвижности зубов, пародонтальных карманов, процессам остеорезорбции.

Ключевым фактором в формировании псориатического артрита на фоне пародонтита является гиперпродукция провоспалительных цитокинов в тканях-мишенях (кожа, суставы, микросреда десен) и развитие чрезмерного системного иммунного ответа на микробиоту, населяющую поверхность эпителия и ткани пародонта. Статистически подтвержденная корреляция развития деструкции пародонта с наличием псориатического артрита доказывает значимость эффектов воспалительного процесса как фона для развития коморбидной патологии. Повышенный синтез IL-17 выполняет ключевую роль в развитии иммунных реакций патологического костного ремоделирования и остеорезорбции при пародонтите и псориатическом артрите.

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.

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The authors declare that there are no conflicts of interest present.