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Journal of Zhejiang University SCIENCE B

ISSN 1673-1581(Print), 1862-1783(Online), Monthly

Epidemiology and pathogenesis of the link between rheumatoid arthritis and periodontitis

Abstract: Rheumatoid arthritis (RA), an autoimmune disease characterized by chronic inflammation of synovial tissue, is divided into two subtypes—anti-citrullinated protein antibody (ACPA)-positive and ACPA-negative RA. While the pathogenic mechanisms of ACPA-positive RA are well-understood, the etiology of ACPA-negative RA remains largely unknown. The association between RA and periodontitis (PD) has been observed since the early 1900s, with the two diseases sharing common genetic and environmental risk factors that lead to the progressive destruction of bone and connective tissue. However, the associations between PD and the two subtypes of RA differ. This comprehensive review aims to provide an updated understanding of the epidemiological association between RA and PD, explore potential pathogenic mechanisms linking the two diseases, and highlight the key distinctions between the subtypes of RA and their respective associations with PD. We also discuss the possibility of early intervention or the treatment of the two diseases. Ultimately, this review aims to provide valuable insights for future research in this field.

Key words: Rheumatoid arthritis; Periodontitis; Pathogenesis; Citrullination; Anti-citrullinated protein antibody (ACPA)

Chinese Summary  <16> 类风湿关节炎与牙周炎在流行病学及发病机制上的关联

方惠雅1,林进1,邱一吾2,程子健3,陈伟钱1
1浙江大学医学院附属第一医院风湿免疫科,中国杭州市,310003
2浙江中医药大学基础医学院,中国杭州市,310053
3浙江大学医学院附属口腔医院,浙江省口腔疾病临床研究中心,浙江省口腔生物医学研究重点实验室,浙江大学癌症研究院,中国杭州市 310000
摘要:类风湿关节炎(rheumatoid arthritis,RA)是一种以慢性滑膜炎为特征的自身免疫性疾病,分为抗瓜氨酸蛋白抗体(ACPA)阳性/阴性两种亚型。目前对ACPA阳性RA致病机制已有充分了解,但对ACPA阴性RA病因学的研究仍较为有限。RA和牙周炎(periodontitis,PD)间的关联自20世纪初被发现,他们具有共同的遗传和环境风险因素,可导致骨骼和结缔组织的进行性破坏。然而,RA两种亚型与PD间可能存在不同的联系。本文旨在通过对RA与PD间在流行病学关联上最新的研究结果进行综述,并探讨两种疾病间潜在的致病机制,同时强调RA两种亚型间的关键区别及其与PD的相关性。此外,本文提出早期干预或治疗这两种疾病的可能性,以期为该领域未来研究和临床工作提供有效见解。

关键词组:类风湿关节炎;牙周炎;发病机制;瓜氨酸化;抗瓜氨酸蛋白抗体


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DOI:

10.1631/jzus.B2300519

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On-line Access:

2025-05-28

Received:

2023-07-18

Revision Accepted:

2023-12-13

Crosschecked:

2025-05-29

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