Research progress on the interaction between osteoarthritis and cardiovascular diseases

doi:10.16352/j.issn.1001-6325.2025.02.0148

Abstract

Abstract: Osteoarthritis (OA) is closely related to cardiovascular disease (CVD). The incidence of CVD is significantly higher in the population of OA patients. This review first analyzes the epidemiology and common risk factors of OA and CVD, then discusses the pathogenesis of OA and CVD, and clarifies the roles of chronic low-grade inflammation, metabolic syndrome, endothelial dysfunction, as well as macrophages, T-cells, and inflammatory factors involved in the mechanisms of interaction between OA and CVD. The review further analyzes treatment strategies and preventive measures for OA and CVD, explores the impact of OA treatment drugs on cardiovascular safety, and elucidates the importance of cardiovascular risk assessment and management in OA patients for clinical diagnosis and treatment. Finally, this review orientes future research directions of OA and CVD, including in-depth exploration of the molecular and cellular mechanisms between OA and CVD, drug interactions, and the development of new treatment strategies, aiming to provide ideas for improving the clinical diagnosis, treatment and prognosis of OA and CVD.

Key words: osteoarthritis, cardiovascular disease, mechanism, treatment, prevention

CLC Number:

R682
R541

YANG Jianfeng, HAO Lin, WANG Yan, JI Quanbo. Research progress on the interaction between osteoarthritis and cardiovascular diseases[J]. Basic & Clinical Medicine, 2025, 45(2): 148-153.

References 40

[1]	GBD 2015 Disease And Injury Incidence And Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990—2015: a systematic analysis for the global burden of disease study 2015[J]. Lancet, 2016, 388: 1545-1602. doi:10.1016/S0140-6736(16)31678-6.
[2]	Peng X, Lu Y, Chen PY, et al. The mediating effect of depression on the relationship between osteoarthritis and cardiovascular disease mortality: a cohort study[J]. J Affect Disord, 2023, 341: 329-334. doi:10.1016/j.jad.2023.08.108.
[3]	Katz JN, Arant KR, Loeser RF. Diagnosis and treatment of hip and knee osteoarthritis: a review[J]. JAMA, 2021, 325: 568-578. doi:10.1001/jama.2020.22171.
[4]	GBD 2021 Osteoarthritis Collaborators. Global, regional, and national burden of osteoarthritis, 1990—2020 and projections to 2050: a systematic analysis for the global burden of disease study 2021[J]. Lancet Rheumatol, 2023, 5: e508. doi:10.1016/S2665-9913(23)00163-7.
[5]	Boutet MA, Nerviani A, Fossati-Jimack L, et al. Comparative analysis of late-stage rheumatoid arthritis and osteoarthritis reveals shared histopathological features[J]. Osteoarthritis Cartilage, 2024, 32: 166-176. doi:10.1016/j.joca.2023.10.009.
[6]	Motta F, Barone E, Sica A, et al. Inflammaging and osteoarthritis[J]. Clin Rev Allergy Immunol, 2023, 64: 222-238. doi:10.1007/s12016-022-08941-1.
[7]	WHO CVD Risk Chart Working Group. World health organization cardiovascular disease risk charts: revised models to estimate risk in 21 global regions[J]. Lancet Glob Health, 2019, 7: e1332-e1345. doi:10.1016/S2214-109X(19)30318-3.
[8]	刘明波,何新叶,杨晓红,等.《中国心血管健康与疾病报告2023》要点解读[J]. 中国心血管杂志,2024,29:305-324. doi:10.3969/j.issn.1007-5410.2024.04.002
[9]	Kishore SP, Blank E, Heller DJ, et al. Modernizing the world health organization list of essential medicines for preventing and controlling cardiovascular diseases[J]. J Am Coll Cardiol, 2018, 71: 564-574. doi:10.1016/j.jacc.2017.11.056.
[10]	Mathieu S, Couderc M, Tournadre A, et al. Cardiovascular profile in osteoarthritis: a meta-analysis of cardiovascular events and risk factors[J]. Joint Bone Spine, 2019, 86: 679-684. doi:10.1016/j.jbspin.2019.06.013.
[11]	Wang Z, Kang C, Xu P, et al. Osteoarthritis and cardiovascular disease: a mendelian randomization study[J]. Front Cardiovasc Med, 2022, 9: 1025063. doi:10.3389/fcvm.2022.1025063.
[12]	Larsson S, Burgess S. Appraising the causal role of smok-ing in multiple diseases: a systematic review and Meta-analysis of mendelian randomization studies[J]. eBioMedicine, 2022, 82: 104154. doi:10.1016/j.ebiom.2022.104154.
[13]	Churg A, Dai J, Tai H, et al. Tumor necrosis factor-alpha is central to acute cigarette smoke-induced inflammation and connective tissue breakdown[J]. Am J Respir Crit Care Med, 2002, 166(6): 849-854. doi:10.1164/rccm.200202-097OC.
[14]	Gill D, Karhunen V, Malik R, et al. Cardiometabolic traits mediating the effect of education on osteoarthritis risk: a mendelian randomization study[J]. Osteoarthritis Cartilage, 2021, 29: 365-371. doi:10.1016/j.joca.2020.12.015.
[15]	Tahrani AA, Morton J. Benefits of weight loss of 10% or more in patients with overweight or obesity: a review[J]. Obesity, 2022, 30: 802-840. doi:10.1002/oby.23371.
[16]	Bendele AM, Neelagiri M, Neelagiri V, et al. Develop-ment of a selective matrix metalloproteinase 13 (mmp-13) inhibitor for the treatment of osteoarthritis[J]. Eur J Med Chem, 2021, 224: 113666. doi:10.1016/j.ejmech.2021.113666.
[17]	Little CB. Cholesterol, systemic inflammation, interleukin-1β, and osteoarthritis risk-aligning animal models with specific patient endotypes provides novel insights[J]. Osteoarthritis Cartilage, 2023, 31: 298-299. doi:10.1016/j.joca.2022.11.009.
[18]	Bloom S, Islam M, Lesniewski L, et al. Mechanisms and consequences of endothelial cell senescence[J]. Nat Rev Cardiol, 2023, 20: 38-51. doi:10.1038/s41569-022-00739-0.
[19]	Nguyen B, Alexander M, Harrison D. Immune mech-anisms in the pathophysiology of hypertension[J]. Nat Rev Nephrol, 2024, 20: 530-540. doi:10.1038/s41581-024-00838-w.
[20]	Ghigo A, Laffargue M, Li M, et al. PI3K and calcium signaling in cardiovascular disease[J]. Circ Res, 2017, 121: 282-292. doi:10.1161/CIRCRESAHA.117.310183.
[21]	Batushansky A, Zhu S, Komaravolu RK, et al. Fundamentals of oa. an initiative of osteoarthritis and cartilage. obesity and metabolic factors in oa[J]. Osteoarthritis Cartilage, 2022, 30: 501-515. doi:10.1016/j.joca.2021.06.013.
[22]	Tuckermann J, Adams R. The endothelium-bone axis in development, homeostasis and bone and joint disease[J]. Nat Rev Rheumatol, 2021, 17: 608-620. doi:10.1038/s41584-021-00682-3.
[23]	Sanchez-Lopez E, Coras R, Torres A, et al. Synovial inflammation in osteoarthritis progression[J]. Nat Rev Rheumatol, 2022, 18: 258-275. doi:10.1038/s41584-022-00749-9.
[24]	Zhou K, Yang C, Shi K, et al. Activated macrophage membrane-coated nanoparticles relieve osteoarthritis-induced synovitis and joint damage[J]. Biomaterials, 2023, 295: 122036. doi:10.1016/j.biomaterials.2023.122036.
[25]	Chen W, Schilperoort M, Cao Y, et al. Macrophage-targeted nanomedicine for the diagnosis and treatment of atherosclerosis[J]. Nat Rev Cardiol, 2022, 19: 228-249. doi:10.1038/s41569-021-00629-x.
[26]	Sohn H, Choi J, Jhun J, et al. Tolerogenic nanoparticles induce type Ⅱ collagen-specific regulatory t cells and ameliorate osteoarthritis[J]. Sci Adv, 2022, 8: eabo5284. doi:10.1126/sciadv.abo5284.
[27]	Saigusa R, Winkels H, Ley K. T cell subsets and functions in atherosclerosis[J]. Nat Rev Cardiol, 2020, 17: 387-401. doi:10.1038/s41569-020-0352-5.
[28]	Nedunchezhiyan U, Varughese I, Sun A, et al. Obesity, inflammation, and immune system in osteoarthritis[J]. Front Immunol, 2022, 13: 907750. doi:10.3389/fimmu.2022.907750.
[29]	Horváth E, Sólyom Á, Székely J, et al. Inflammatory and metabolic signaling interfaces of the hypertrophic and senescent chondrocyte phenotypes associated with osteoarthritis[J]. Int J Mol Sci, 2023, 24: 16468. doi:10.3390/ijms242216468.
[30]	Bally M, Dendukuri N, Rich B, et al. Risk of acute myocardial infarction with nsaids in real world use: bayesian meta-analysis of individual patient data[J]. BMJ, 2017, 357: j1909. doi:10.1136/bmj.j1909.
[31]	Graham W, Flanigan D. Venous thromboembolism following arthroscopic knee surgery: a current concepts review of incidence, prophylaxis, and preoperative risk assessment[J]. Sports Med, 2014, 44: 331-343. doi:10.1007/s40279-013-0121-2.
[32]	Simon SJ, Patell R, Zwicker JI, et al. Venous thromboembolism in total hip and total knee arthroplasty[J]. JAMA Netw Open, 2023, 6: e2345883. doi:10.1001/jamanetworkopen.2023.45883.
[33]	Guo Z, Di J, Zhang Z, et al. Antihypertensive drug-associated adverse events in osteoarthritis: a study of a large real-world sample based on the faers database[J]. Front Pharmacol, 2024, 15: 1404427. doi:10.3389/fphar.2024.1404427.
[34]	Schoofs MW, van der Klift M, Hofman A, et al. Thiazide diuretics and the risk for hip fracture[J]. Ann Intern Med, 2003, 139:476-482. doi: 10.7326/0003-4819-139-6-200309160-00010.
[35]	Akagi T, Mukai T, Mito T, et al. Effect of angiotensin Ⅱ on bone erosion and systemic bone loss in mice with tumor necrosis factor-mediated arthritis[J]. Int J Mol Sci, 2020, 21: 4145. doi:10.3390/ijms21114145.
[36]	Apostu D, Lucaciu O, Mester A, et al. Systemic drugs with impact on osteoarthritis[J]. Drug Metab Rev, 2019, 51: 498-523. doi:10.1080/03602532.2019.1687511.
[37]	Szeto C, Sugano K, Wang J, et al. Non-steroidal anti-inflammatory drug (nsaid) therapy in patients with hypertension, cardiovascular, renal or gastrointestinal comorbidities: joint apage/aplar/apsde/apsh/apsn/poa recommendations[J]. Gut, 2020, 69: 617-629. doi:10.1136/gutjnl-2019-319300.
[38]	Ching K, Houard X, Berenbaum F, et al. Hypertension meets osteoarthritis-revisiting the vascular aetiology hypothesis[J]. Nat Rev Rheumatol, 2021, 17: 533-549. doi:10.1038/s41584-021-00650-x.
[39]	Arden NK, Perry TA, Bannuru RR, et al. Non-surgical management of knee osteoarthritis: comparison of esceo and oarsi 2019 guidelines[J]. Nat Rev Rheumatol, 2021, 17: 59-66. doi:10.1038/s41584-020-00523-9.
[40]	Saueressig T, Owen PJ, Zebisch J, et al. Evaluation of exercise interventions and outcomes after hip arthroplasty: a systematic review and meta-analysis[J]. JAMA Netw Open, 2021, 4: e210254. doi:10.1001/jamanetworkopen.2021.0254.