Роль ожирения в развитии и прогрессировании остеоартрита: влияние медикаментозных и хирургических методов лечения ожирения на течение воспалительных заболеваний суставов - Журнал Терапевтический архив №5 Вопросы ревматологии 2025

Роль ожирения в развитии и прогрессировании остеоартрита: влияние медикаментозных и хирургических методов лечения ожирения на течение воспалительных заболеваний суставов

Трошина Е.А., Паневин Т.С., Брискман Т.Д. Роль ожирения в развитии и прогрессировании остеоартрита: влияние медикаментозных и хирургических методов лечения ожирения на течение воспалительных заболеваний суставов. Терапевтический архив. 2025;97(5):449–454. DOI: 10.26442/00403660.2025.05.203230

© ООО «КОНСИЛИУМ МЕДИКУМ», 2025 г.

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Troshina EA, Panevin TS, Briskman TD. The role of obesity in the development and progression of osteoarthritis: the influence of medical and surgical therapies for obesity on the course of inflammatory arthritis: A review. Terapevticheskii Arkhiv (Ter. Arkh.). 2025;97(5):449–454. DOI: 10.26442/00403660.2025.05.203230

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Аннотация

Ожирение – наиболее важный фактор риска развития остеоартрита (ОА) – прогрессирующего воспалительного поражения суставов, которое считается одной из причин тяжелой инвалидности и длительной иммобилизации. Избыточно развитая жировая ткань не только увеличивает механическую нагрузку на суставы, но и участвует в поддержании хронического неспецифического воспаления посредством выработки адипокинов, цитокинов, хемокинов, факторов комплемента и гормонов. Адипокины, включая лептин, адипонектин, химерин и резистин, регулируют воспалительные иммунные реакции в хряще, оказывая влияние также на клетки синовиальной ткани и кости. В свою очередь, хондроциты, остеобласты и остеокласты производят некоторые адипокины локально, поддерживая воспалительную микросреду внутрисуставно. Снижение массы тела при ОА может улучшить качество жизни пациента, функциональные способности суставов, привести к клинически значимому уменьшению боли и замедлить или остановить прогрессирование структурных дегенеративных изменений. Цель нашего обзора – осветить основные патогенетические взаимосвязи между ожирением и воспалением, раскрыть механизмы патологического влияния адипокинов и провоспалительных медиаторов (интерлейкина-6, фактора некроза опухоли α и др.) на хрящевой и костный гомеостаз и, как следствие, оценить их участие в развитии ОА, так как понимание особенностей иммунной регуляции и разрешения воспалительного процесса при ожирении имеет решающее значение для разработки успешных подходов к лечению ОА у пациентов с избыточной массой тела. Также в статье рассмотрен анализ актуальных исследований влияния медикаментозной терапии (лираглутид, орлистат, сибутрамин) и хирургического лечения ожирения на течение воспалительных заболеваний суставов.

Ключевые слова: остеоартрит, ожирение, адипокины

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Obesity is considered the most important risk factor for the development of osteoarthritis (ОА) – progressive inflammatory disease of the joints, that is one of the causes of disability and long-term immobilization. Excessively developed adipose tissue not only increases the mechanical load on the joints, but also participates in the maintenance of chronic low-grade inflammation through the production of adipokines, cytokines, hemokines, complement factors and hormones. Adipokines influence cells of synovial tissue, cartilage and bone, which in turn produce some adipokines locally, maintaining an inflammatory microenvironment intraarticularly. Adipokines, including leptin, adiponectin, chemerin, and resistin, regulate inflammatory immune responses in cartilage, also affecting synovial tissue cells and bone. In turn, chondrocytes, osteoblasts and osteoclasts produce some adipokines locally, maintaining an inflammatory microenvironment intra-articularly. Weight loss in OA can improve the patient's quality of life, physical function, lead to reduce pain, and slow or halt the progression of structural degenerative changes. The purpose of this article is to clearly describe the pathogenetic ways between obesity and inflammation, to reveal the mechanisms of the pathological state of adipokines and proinflammatory mediators (IL-6, TNF-α, etc.) on cartilage and bone homeostasis and, as expected, to evaluate their participation in the development of OA. So understanding immune regulation and resolution of inflammation in obesity is critical to developing treatments approaches to OA for these patients. The article also analyzes current researches on the effect of drug therapy (liraglutide, orlistat, sibutramine) and bariatric surgery of obesity on the course of inflammatory joint diseases.

Keywords: osteoarthritis, obesity, adipokines

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4. Presle N, Pottie P, Dumond H, et al. Differential distribution of adipokines between serum and synovial fluid in patients with osteoarthritis. Contribution of joint tissues to their articular production. Osteoarthr Cartilage. 2006;14(7):6905. DOI:10.1016/j.joca.2006.01.009
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6. Longo M, Zatterale F, Naderi J, et al. Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications. Int J Mol Sci. 2019;20(9):2358. DOI:10.3390/ijms20092358
7. Pou KM, Massaro JM, Hoffmann U, et al. Visceral and subcutaneous adipose tissue volumes are cross-sectionally related to markers of inflammation and oxidative stress: the Framingham Heart Study. Circulation. 2007;16(11):1234-41. DOI:10.1161/CIRCULATIONAHA.107.710509
8. Li S, Schwartz AV, LaValley MP, et al. Association of Visceral Adiposity With Pain but Not Structural Osteoarthritis. Arthritis Rheumatol. 2020;72(7):1103-10. DOI:10.1002/art.41222
9. Jiang L, Tian W, Wang Y, et al. Body mass index and susceptibility to knee osteoarthritis: a systematic review and meta-analysi. Joint Bone Spine. 2012;79(3):291-7. DOI:10.1016/j.jbspin.2011.05.015
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13. Migacheva NB, Skvortsova OV, Kaganova TI, Ginzburg AS. Paradoxes of the Immune Response in Obesity. Effective Pharmacotherapy. 2023;19(28):30-6 (in Russian). DOI:10.33978/2307-3586-2023-19-28-30-36
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15. Massicotte F, Lajeunesse D, Benderdour M. Can altered production of interleukin-1β, interleukin-6, transforming growth factor-β and prostaglandin E2 by isolated human subchondral osteoblasts identity two subgroups of osteoarthritic patients. Osteoarthritis and Cartilage. 2002;10(6):491-500. DOI:10.1053/joca.2002.0528
16. Tchernot A, Despers JP. Pathophysiology of human visceral obesity: an update. Physiol Rev. 2013;93(1):359-404. DOI:10.1152/physrev.00033.2011
17. Mei J, Sun J, Wu J, Zheng X. Liraglutide suppresses TNF-α-induced degradation of extracellular matrix in human chondrocytes: a therapeutic implication in osteoarthritis. Am J Transl Res. 2019;11(8):4800-8.
18. Manferdini C, Paolella F, Gabusi E, et al. Adipose stromal cells mediated switching of the pro-inflammatory profile of M1-like macrophages is facilitated by PGE2: In vitro evaluation. Osteoarthr Cartil. 2017;25:1161-71. DOI:10.1016/j.joca.2017.01.011
19. Longo M, Zatterale F, Naderi J, et al. Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications. Int J Mol Sci. 2019;20(9):2358. DOI:10.3390/ijms20092358
20. La Cava A. Leptin in inflammation and autoimmunity. Cytokine. 2017;98:51-8. DOI:10.1016/j.cyto.2016.10.011
21. Gao M, Cui D, Xie J. The role of adiponectin for immune cell function in metabolic diseases. Diabetes Obes Metab. 2023;25(9):2427-38. DOI:10.1111/dom.15151
22. Carrion M, Frommer KW, Perez-Garcia S, et al. The Adipokine Network in Rheumatic Joint Diseases. Int J Mol Sci. 2019;20(17):4091. DOI:10.3390/ijms20174091
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Авторы

Е.А. Трошина¹, Т.С. Паневин^2,3, Т.Д. Брискман*¹

¹ФГБУ «Национальный медицинский исследовательский центр эндокринологии» Минздрава России, Москва, Россия;
²ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой», Москва, Россия;
³ФГБОУ ВО «Дальневосточный государственный медицинский университет» Минздрава России, Хабаровск, Россия
*bri_tanchik@mail.ru

________________________________________________

Ekaterina A. Troshina¹, Taras S. Panevin^2,3, Tatiana D. Briskman*¹

¹National Medical Research Center for Endocrinology, Moscow, Russia;
²Nasonova Research Institute of Rheumatology, Moscow, Russia;
³Far Eastern State Medical University, Khabarovsk, Russia
*bri_tanchik@mail.ru

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