Periodontitis increases rheumatic factor serum levels and citrullinated proteins in gingival tissues and alter cytokine balance in arthritic rats.

Mônica G Corrêa,Suzana Peres Pimentel,Fernanda Vieira Ribeiro,Fabiano Ribeiro Cirano,Marcio Z Casati,Silvana B Sacchetti,Renato Corrêa Viana Casarin,Salomon Amar

doi:10.1371/journal.pone.0174442

Mônica G Corrêa, Suzana Peres Pimentel + Show 6 more

Open Access

https://doi.org/10.1371/journal.pone.0174442

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Journal: PloS one	Publication Date: Mar 30, 2017
Citations: 23	License type: CC BY 4.0

Affiliation: Universidade Paulista

Abstract

This study investigated some immunological features by experimental periodontitis (EP) and rheumatoid arthritis (RA) disease interact in destructive processes in arthritic rats. Rats were assigned to the following groups: EP +RA; RA; EP; and Negative Control. RA was induced by immunizations with type-II collagen and a local immunization with Complete Freund’s adjuvant in the paw. Periodontitis was induced by ligating the right first molars. The serum level of rheumatoid factor (RF) and anti-citrullinated protein antibody (ACCPA) were measured before the induction of EP (T1) and at 28 days after (T2) by ELISA assay. ACCPA levels were also measured in the gingival tissue at T2. The specimens were processed for morphometric analysis of bone loss, and the gingival tissue surrounding the first molar was collected for the quantification of interleukin IL-1β, IL-4, IL-6, IL-17 and TNF-α using a Luminex/MAGpix assay. Paw edema was analyzed using a plethysmometer. Periodontitis increased the RF and ACCPA levels in the serum and in the gingival tissue, respectively. Besides, the level of paw swelling was increased by EP and remained in progress until the end of the experiment, when EP was associated with RA. Greater values of IL-17 were observed only when RA was present, in spite of PE. It can be concluded that periodontitis increases rheumatic factor serum levels and citrullinated proteins level in gingival tissues and alter cytokine balance in arthritic rats; at the same time, arthritis increases periodontal destruction, confirming the bidirectional interaction between diseases.

Highlights

Both rheumatoid arthritis (RA) and periodontitis are chronic inflammatory diseases that lead to tissue destruction
Considering the above evidence, this study evaluates the impact of experimental rheumatoid arthritis and experimental periodontitis in rats in regards of seric and local mediators that could contribute to the better understanding of RA-PD link
There is some evidence about the bidirectional pathway to the development of rheumatoid arthritis and periodontitis, there is no clear pathway by which it occurs

Summary

Introduction

Both rheumatoid arthritis (RA) and periodontitis are chronic inflammatory diseases that lead to tissue destruction. Periodontitis, per se, is a bacterial chronic inflammatory condition that leads to the occurrence of supporting tissue destruction and is host-mediated by the local production of immune-inflammatory mediators in response to periodontopathogens [3]. Mercado et al [8, 9] showed that RA patients had a greater level of tooth loss and higher percentage of pockets than the control group (healthy patients), with no differences in plaque index and bleeding on probing. These authors showed that the number of deep pockets Considering the above evidence, this study evaluates the impact of experimental rheumatoid arthritis and experimental periodontitis in rats in regards of seric and local mediators that could contribute to the better understanding of RA-PD link

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