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Global epidemiology of rheumatoid arthritis

Abstract

Rheumatoid arthritis (RA) is a systemic autoimmune disease that predominantly affects the joints. The prevalence of RA varies globally, with generally a higher prevalence in industrialized countries, which may be explained by exposures to environmental risk factors, but also by genetic factors, differing demographics and under-reporting in other parts of the world. Over the past three decades, strong trends of the declining severity of RA probably reflect changes in treatment paradigms and overall better management of the disease. Other trends include increasing RA prevalence. Common risk factors for RA include both modifiable lifestyle-associated variables and non-modifiable features, such as genetics and sex. A better understanding of the natural history of RA, and of the factors that contribute to the development of RA in specific populations, might lead to the introduction of specific prevention strategies for this debilitating disease.

Key points

  • The estimated prevalence and disease burden of rheumatoid arthritis (RA) vary considerably between geographic regions, with generally higher estimates in industrialized countries and urban settings.

  • Aspects involved in the disparity in RA prevalence between populations include genetic factors, environmental exposures, demographics, socioeconomics and reporting of the disease.

  • Despite rising RA prevalence, the severity, mortality and disease-associated comorbidities seem to be decreasing.

  • The aetiopathogenesis of RA involves interaction between predisposing genetic factors and environmental triggers, mostly at mucosal sites (oral cavity, respiratory system and intestinal tract), resulting in the ‘mucosal origin’ hypothesis.

  • Many RA risk factors are modifiable, including dietary habits and inhalation of pollutants such as tobacco smoke; modifications are being incorporated in prevention strategies.

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Fig. 1: Global prevalence of rheumatoid arthritis.
Fig. 2: Known risk factors for rheumatoid arthritis.

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Acknowledgements

The authors thank L. Koller-Smith, L. March, E. Park, Y.-C. Kwon, K. Kim and S.-K. Cho for helpful discussions in the preparation of this manuscript. A.F. is supported in part by the Swiss National Science Foundation (grants 310030E_205559/1 and 320030_192471/1). S.-C.B. is supported in part by the Basic Science Research Program through the National Research Foundation of Korea, funded by the Ministry of Education (grant NRF-2021R1A6A1A03038899). R.T. is supported by Arthritis Queensland and the National Health and Medical Research Council of Australia (grant 2008287).

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A.F. received funding from Abbvie, Bristol Myers Squibb, Galapagos, and Pfizer to the Geneva University Hospital, and consultancy or honoraria from Abbvie, Bristol Myers Squibb, Eli-Lilly, MSD and Pfizer. R.T. received funding from Janssen Biotech to Uniquest (the commercialization company of the University of Queensland), consultancy or honoraria from Bristol Myers Squibb, Abbvie, Janssen, Merck, CSL, Viela Bio and Sandoz, and is a named inventor on patent 9,017,697 B2, relating to compositions and methods for modulating immune responses. K.D.D. received funding for consultancy from Inova Diagnostics, Bristol Myers Squibb and Janssen. D.A.R. is a scientific adviser for GlaxoSmithKline Mexico, unrelated to the topic of this manuscript. K.L. received consultancy or honoraria from Celltrion, Pfizer, Viatris and Galapagos. The other authors declare no competing interests.

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Finckh, A., Gilbert, B., Hodkinson, B. et al. Global epidemiology of rheumatoid arthritis. Nat Rev Rheumatol 18, 591–602 (2022). https://doi.org/10.1038/s41584-022-00827-y

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