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A6.4 Periodontopathogens in Rheumatoid Arthritis and Periodontal Disease
  1. O Laugisch1,
  2. B Moeller2,
  3. T Kantyka3,
  4. PJ Vernables4,
  5. PM Villiger2,
  6. A Sculean1,
  7. J Potempa3,5,
  8. S Eick1
  1. 1Department of Periodontology, School of Dental Medicine, Freiburgstrasse 7, 3010 Bern, Switzerland
  2. 2Department of Rheumatology, Immunology and Allergology, University of Bern, Inselspital, 3010 Bern, Switzerland
  3. 3Institute of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University of Krakow, Gronostajowa 7, 30–387 Krakow, Poland
  4. 4Kennedy Institute of Rheumatology, Imperial College London, London, UK
  5. 5Department of Oral Health and Rehabilitation, University of Louisville, 501 South Preston, Louisville KY 40202-1701, USA

Abstract

Background and Objectives A relationship between rheumatoid arthritis (RA) and periodontitis is suggested. Pathogenesis of periodontitis as one of the most common chronic infectious diseases is thought to be host response on subgingival plaque. Among species known to be associated with severe periodontitis, Porphyromonas gingivalis plays an important role. Its virulence is most related to cysteine proteases. Moreover, a peptidylarginine deiminase was described to be able to citrullinate microbial and host proteins. The aim of this study was to characterise a group of RA patients for several variables associated with RA and/or periodontitis in comparison with periodontally healthy and periodontitis subjects without RA. In a first part, clinical data of periodontitis and the load of selected periodontopathic species were analysed.

Methods 51 patients with RA, 27 patients with periodontitis and without RA as well as 16 subjects without periodontitis and RA were recruited. Periodontal disease status was determined by using Periodontal Screening index (PSI). Subgingival plaque was analysed semi-quantitatively by PCR followed by a reverse hybridisation (microIdent, Hain Lifescience) for Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia and Treponema denticola. In addition, real-time PCR was used to detect very low loads of P. gingivalis (detection level 10 bacteria). For statistical analysis Kruskal-Wallis and Mann-Whitney tests were used.

Results Among the 51 RA patients, 45 were characterised positively for periodontitis. 18 (35%) had a severe periodontitis (PSI 4). Analysing the four subgroups (incl. RA with/without periodontitis) showed differences in A. actinomycetemcomitans (p = 0.043) and T. denticola (p = 0.028). P. gingivalis was detected in 63% of the RA patients and in 49% of the subjects without RA. In all RA patients and in special without periodontitis, A. actinomycetemcomitans was found more often (p = 0.018 for all, p = 0.007 for subjects without periodontitis). In both RA and non-RA subjects, patients with periodontitis had more T. denticola in their plaque (p = 0.026; p = 0.042).

Conclusions P. gingivalis induces immune responses which may be of relevance in RA pathogenesis, but other microbes may also play a role in RA associated periodontitis.

This study was supported by a DGP-GABA research grant.

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