Porphyromonas gingivalis in the tongue biofilm is associated with the clinical outcome in rheumatoid arthritis patients

Fulvia Ceccarelli

Co-prime

;Germano Orrù

Co-prime

;Andrea Pilloni;Izabella Bartosiewicz;Carlo Perricone;Emilio Martino;Ramona Lucchetti;Sara Fais

Methodology

;Marta Vomero;Marta Olivieri;Manuela di Franco;Roberta Priori;Valeria Riccieri;Rossana Scrivo;Yehuda Shoenfeld;Cristiano Alessandri;Fabrizio Conti;Antonella Polimeni;Guido Valesini.

2018-01-01

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Abstract

Objective: Several evidences suggested a link between human microbiome and Rheumatoid Arthritis (RA) development. Porphyromonas gingivalis (P. gingivalis) seems involved in RA initiation and progression, as supported by the high occurrence of periodontitis. In this case- control study, we analyzed tongue P. gingivalis presence and quantification in a large healthy and RA cohort. Methods: We enrolled 143 RA patients (Male/Female 32/111, mean±SD age 57.5±19.8 years, mean±SD disease duration 155.9± 114.7 months); 36 periodontitis patients (M/F 11/25, mean±SD age56±9.9 years, mean±SD disease duration 25.5±20.9 months); 57 patients (M/F 12/45, mean ±SD age 61.4±10.9 years, mean ±SD disease duration 62.3±66.9 months) with knee osteoarthritis or fibromyalgia. All subjects underwent a standard cytologic swab to identify the rate of P. gingivalis/total bacteria by using quantitative real time PCR. Results: The prevalence of P. gingivalis resulted similar in RA and periodontitis patients (48.9% versus 52.7%, P=NS). Moreover, the prevalence of this pathogen was significantly higher in RA and PD patients in comparison with CS (P=0.01 and P=0.003, respectively). We found a significant correlation between P. gingivalis rate in total bacteria genomes and DAS28(ESR) (r=0.4, P=0.01). RA patients in remission showed a significantly lower prevalence of P. gingivalis in comparison with non-remission (P=0.02). Conclusions: We demonstrated a significant association between the percentage of P. gingivalis on the total tongue biofilm and RA disease activity (DAS28), suggesting that the oral cavity microbiological status could play a role in the pathogenic mechanisms of inflammation, leading to a more active disease.