New insights into inflammatory osteoclast precursors as therapeutic targets for rheumatoid arthritis and periodontitis.

IF 14.3 1区 医学 Q1 CELL & TISSUE ENGINEERING Bone Research Pub Date : 2023-05-22 DOI:10.1038/s41413-023-00257-w
Emilie Hascoët, Frédéric Blanchard, Claudine Blin-Wakkach, Jérôme Guicheux, Philippe Lesclous, Alexandra Cloitre
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引用次数: 3

Abstract

Rheumatoid arthritis (RA) and periodontitis are chronic inflammatory diseases leading to increased bone resorption. Preventing this inflammatory bone resorption is a major health challenge. Both diseases share immunopathogenic similarities and a common inflammatory environment. The autoimmune response or periodontal infection stimulates certain immune actors, leading in both cases to chronic inflammation that perpetuates bone resorption. Moreover, RA and periodontitis have a strong epidemiological association that could be explained by periodontal microbial dysbiosis. This dysbiosis is believed to be involved in the initiation of RA via three mechanisms. (i) The dissemination of periodontal pathogens triggers systemic inflammation. (ii) Periodontal pathogens can induce the generation of citrullinated neoepitopes, leading to the generation of anti-citrullinated peptide autoantibodies. (iii) Intracellular danger-associated molecular patterns accelerate local and systemic inflammation. Therefore, periodontal dysbiosis could promote or sustain bone resorption in distant inflamed joints. Interestingly, in inflammatory conditions, the existence of osteoclasts distinct from "classical osteoclasts" has recently been reported. They have proinflammatory origins and functions. Several populations of osteoclast precursors have been described in RA, such as classical monocytes, a dendritic cell subtype, and arthritis-associated osteoclastogenic macrophages. The aim of this review is to synthesize knowledge on osteoclasts and their precursors in inflammatory conditions, especially in RA and periodontitis. Special attention will be given to recent data related to RA that could be of potential value in periodontitis due to the immunopathogenic similarities between the two diseases. Improving our understanding of these pathogenic mechanisms should lead to the identification of new therapeutic targets involved in the pathological inflammatory bone resorption associated with these diseases.

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炎性破骨细胞前体作为类风湿关节炎和牙周炎治疗靶点的新见解。
类风湿性关节炎(RA)和牙周炎是导致骨吸收增加的慢性炎症性疾病。预防这种炎症性骨吸收是一项重大的健康挑战。这两种疾病具有相似的免疫致病性和共同的炎症环境。自身免疫反应或牙周感染刺激某些免疫因子,导致慢性炎症,使骨吸收永久化。此外,类风湿关节炎和牙周炎有很强的流行病学相关性,这可以通过牙周微生物失调来解释。这种生态失调被认为通过三种机制参与RA的起始。牙周病原体的传播引起全身炎症。(ii)牙周病原体可诱导瓜氨酸化新表位的产生,导致抗瓜氨酸化肽自身抗体的产生。(iii)细胞内危险相关的分子模式加速局部和全身炎症。因此,牙周生态失调可以促进或维持远端炎症关节的骨吸收。有趣的是,在炎症条件下,破骨细胞的存在不同于“经典破骨细胞”,最近有报道。它们有促炎的起源和功能。在类风湿性关节炎中已经发现了几种破骨细胞前体,如经典单核细胞、树突状细胞亚型和关节炎相关的破骨细胞巨噬细胞。这篇综述的目的是综合了解破骨细胞及其前体在炎症条件下,特别是在类风湿性关节炎和牙周炎。由于两种疾病的免疫致病性相似,将特别关注与RA相关的近期数据,这些数据可能对牙周炎具有潜在价值。提高我们对这些致病机制的理解,将有助于发现与这些疾病相关的病理性炎症性骨吸收相关的新治疗靶点。
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来源期刊
Bone Research
Bone Research CELL & TISSUE ENGINEERING-
CiteScore
20.00
自引率
4.70%
发文量
289
审稿时长
20 weeks
期刊介绍: Established in 2013, Bone Research is a newly-founded English-language periodical that centers on the basic and clinical facets of bone biology, pathophysiology, and regeneration. It is dedicated to championing key findings emerging from both basic investigations and clinical research concerning bone-related topics. The journal's objective is to globally disseminate research in bone-related physiology, pathology, diseases, and treatment, contributing to the advancement of knowledge in this field.
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