Multidisciplinary Department of Medical-Surgical and Dental Specialties, University of Campania 'Luigi Vanvitelli', Naples, Italy.
Curr Opin Rheumatol. 2019 Sep;31(5):542-545. doi: 10.1097/BOR.0000000000000611.
The purpose of this review is to evaluate the mechanisms that underlie the association between periodontal pathogens and rheumatoid arthritis (RA).
This review focuses on the cross-reactivity hypothesis as a mechanism that might contribute to explain the pathologic evolution of periodontal infections from periodontitis to RA. The scientific rationale is that immune reactions following infection by periodontal bacteria might cross-react with RA autoantigens, in this way eventually leading to autoimmunity.
Using the rheumatoid antigen associated with RA-A47 arthritis as an antigen model and analyzing five periodontal bacteria (eg, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Treponema denticola, Tannerella forsythia and Prevotella intermedia), an extremely varied pattern of peptide sharing was found. In the context of the cross-reactivity hypothesis, the data allow us to glimpse the possibility of distinguishing the periodontal bacteria capable of attacking the periodontal tissue from those that are additionally equipped with a rheumatologic potential by virtue of the sharing of peptide sequences with RA antigens.
本综述旨在评估牙周病病原体与类风湿关节炎（RA）之间关联的潜在机制。
本综述重点关注交叉反应假说作为一种可能有助于解释牙周感染从牙周炎向 RA 发展的病理演变的机制。科学依据是，牙周细菌感染后引发的免疫反应可能与 RA 自身抗原发生交叉反应，从而最终导致自身免疫。
使用与 RA-A47 关节炎相关的类风湿抗原作为抗原模型，并分析五种牙周细菌（如牙龈卟啉单胞菌、伴放线放线杆菌、牙髓卟啉单胞菌、福赛坦纳菌和中间普氏菌），发现了极其多样化的肽共享模式。在交叉反应假说的背景下，这些数据使我们有可能区分能够攻击牙周组织的牙周细菌和那些由于与 RA 抗原共享肽序列而具有风湿学潜力的细菌。
