Raphaèle Seror1, Sandrine Le Gall-David2, Martine Bonnaure-Mallet2, Thierry Schaeverbeke3, Alain Cantagrel4, Jacques Minet2, Jacques-Eric Gottenberg5, Philippe Chanson6, Philippe Ravaud7, Xavier Mariette1. 1. Hôpitaux Universitaires Paris-Sud, Hôpital Bicêtre, AP-HP, Université Paris-Sud, and INSERM U1012, Le Kremlin Bicêtre, France. 2. EA 1254, Université de Rennes 1, and Université Européenne de Bretagne, Rennes, France. 3. Université de Bordeaux, Bordeaux, France. 4. Université de Toulouse, Toulouse, France. 5. Centre National de Référence des Maladies Auto-Immunes Rares, INSERM UMRS 1109, Fédération de Médecine Translationnelle de Strasbourg, Hôpitaux Universitaires de Strasbourg, and Université de Strasbourg, Strasbourg, France. 6. Hôpitaux Universitaires Paris-Sud, AP-HP, and Université Paris-Sud, Le Kremlin Bicêtre, France. 7. Université Paris-Descartes, Paris, France.
Abstract
OBJECTIVE: To investigate the possible link between Porphyromonas gingivalis infection and rheumatoid arthritis (RA), according to antibody profile, genetic and environmental factors, and RA severity. METHODS: For assessing P gingivalis infection, serum levels of antibodies directed against P gingivalis lipopolysaccharide were measured in 694 patients with early RA who were not exposed to steroids or disease-modifying antirheumatic drugs. Anti-P gingivalis antibody titers were compared between patients with early RA and various control groups, and according to various patient characteristics. RESULTS: Anti-P gingivalis antibody titers did not significantly differ between patients with RA and controls and did not significantly differ with anti-citrullinated protein antibody (ACPA), rheumatoid factor (RF), or HLA shared epitope status. Anti-P gingivalis antibody titers were significantly higher among patients who had never smoked compared to patients who had ever smoked (P = 0.0049). Among nonsmokers, high anti-P gingivalis antibody levels were associated with a higher prevalence of erosive change (47.5% versus 33.3% with modified Sharp/van der Heijde score erosion subscale ≥1; P = 0.0135). CONCLUSION: In this large early RA cohort, we did not detect any association of anti-P gingivalis antibodies with RA or with ACPA status. These results suggest that the association of periodontitis and RA could be linked to bacterial species other than P gingivalis or to a mechanism other than citrullination. Nevertheless, we found higher anti-P gingivalis antibody titers in nonsmokers. In addition, in this population of nonsmokers, high anti-P gingivalis antibody titers were associated with more severe disease. We hypothesize that the role of tobacco in RA pathogenesis is so high that the effect of P gingivalis could be revealed only in a population not exposed to tobacco.
OBJECTIVE: To investigate the possible link between Porphyromonas gingivalis infection and rheumatoid arthritis (RA), according to antibody profile, genetic and environmental factors, and RA severity. METHODS: For assessing P gingivalis infection, serum levels of antibodies directed against P gingivalis lipopolysaccharide were measured in 694 patients with early RA who were not exposed to steroids or disease-modifying antirheumatic drugs. Anti-P gingivalis antibody titers were compared between patients with early RA and various control groups, and according to various patient characteristics. RESULTS: Anti-P gingivalis antibody titers did not significantly differ between patients with RA and controls and did not significantly differ with anti-citrullinated protein antibody (ACPA), rheumatoid factor (RF), or HLA shared epitope status. Anti-P gingivalis antibody titers were significantly higher among patients who had never smoked compared to patients who had ever smoked (P = 0.0049). Among nonsmokers, high anti-P gingivalis antibody levels were associated with a higher prevalence of erosive change (47.5% versus 33.3% with modified Sharp/van der Heijde score erosion subscale ≥1; P = 0.0135). CONCLUSION: In this large early RA cohort, we did not detect any association of anti-P gingivalis antibodies with RA or with ACPA status. These results suggest that the association of periodontitis and RA could be linked to bacterial species other than P gingivalis or to a mechanism other than citrullination. Nevertheless, we found higher anti-P gingivalis antibody titers in nonsmokers. In addition, in this population of nonsmokers, high anti-P gingivalis antibody titers were associated with more severe disease. We hypothesize that the role of tobacco in RA pathogenesis is so high that the effect of P gingivalis could be revealed only in a population not exposed to tobacco.
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