Abstract
BackgroundAn infection-immune association of periodontal disease with rheumatoid arthritis has been suggested. This study aimed to investigate the effect of pre-existing periodontitis on the development and the immune/inflammatory response of pristane-induced arthritis.MethodsWe investigated the effect of periodontitis induced by ligature placement and Porphyromonas gingivalis (P. gingivalis) infection, in combination with Fusobacterium nucleatum to promote its colonization, on the development of pristane-induced arthritis (PIA) in rats (Dark Agouti). Disease progression and severity of periodontitis and arthritis was monitored using clinical assessment, micro-computed tomography (micro-CT)/intraoral radiographs, antibody response, the inflammatory markers such as α-1-acid glycoprotein (α-1-AGP) and c-reactive protein (CRP) as well as cytokine multiplex profiling at different time intervals after induction.ResultsExperimentally induced periodontitis manifested clinically (P < 0.05) prior to pristane injection and progressed steadily until the end of experiments (15 weeks), as compared to the non-ligated arthritis group. Injection of pristane 8 weeks after periodontitis-induction led to severe arthritis in all rats demonstrating that the severity of arthritis was not affected by the pre-existence of periodontitis. Endpoint analysis showed that 89% of the periodontitis-affected animals were positive for antibodies against arginine gingipain B and furthermore, the plasma antibody levels to a citrullinated P. gingivalis peptidylarginine deiminase (PPAD) peptide (denoted CPP3) were significantly (P < 0.05) higher in periodontitis rats with PIA. Additionally, there was a trend towards increased pro-inflammatory and anti-inflammatory cytokine levels, and increased α-1-AGP levels in plasma from periodontitis-challenged PIA rats.ConclusionsPre-existence of periodontitis induced antibodies against citrullinated peptide derived from PPAD in rats with PIA. However, there were no differences in the development or severity of PIA between periodontitis challenged and periodontitis free rats.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-1067-6) contains supplementary material, which is available to authorized users.
Highlights
An infection-immune association of periodontal disease with rheumatoid arthritis has been suggested
The processes linked to the generation of anti-citrullinated protein antibody (ACPA) are an area of interest in studies investigating the pathogenesis of this disease
In support of this hypothesis, it has been shown that citrullinated proteins are present in the inflamed periodontium and ACPAs have been detected in sera from patient with periodontitis [27, 28]
Summary
An infection-immune association of periodontal disease with rheumatoid arthritis has been suggested. The signs of an on-going inflammation are visible locally in the periodontal pockets and systemically [12] as elevated levels of inflammatory mediators are present in the blood of patients with periodontitis [13] This may have a direct bearing on the development of atherosclerotic plaque and aggravation of other chronic inflammatory diseases [14], including RA, reported to be increased in population affected by periodontitis [15, 16]. P. gingivalis could represent a link between periodontitis and RA In support of this hypothesis, it has been shown that citrullinated proteins are present in the inflamed periodontium and ACPAs have been detected in sera from patient with periodontitis [27, 28]. The aim of this study was to explore the effect of preexisting experimental periodontitis, induced by ligatures and periodontal pathogens P. gingivalis in combination with F. nucleatum on the development of arthritis, induced by pristane, a well-established model for RA [34]
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