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A5.16 Characterisation of an arthritis rat model with a periodontal disease induced by Porphyromonas Gingivalis
  1. M Rinaudo-Gaujous1,
  2. G Courbon2,
  3. V Blasco-Baque3,
  4. S Paul1,
  5. H Marotte2,4
  1. 1Immunology and Immunomonitoring Laboratory, CIC CIE3, University Hospital, Saint-Etienne, France
  2. 2INSERM U1059/LBTO, Jean Monnet University, Lyon University, Saint-Etienne, France
  3. 3Institute of Cardiovascular and Metabolic Diseases, CHU Rangueil, France
  4. 4Department of Rheumatology, Hospital University of Saint-Etienne, Saint-Etienne, France

Abstract

Background and objectives Epidemiological studies have demonstrated the association between rheumatoid arthritis (RA) and periodontal disease (PD) susceptibility and severity. The missing link between RA and PD association could be Porphyromonas gingivalis ( PG) involved in PD pathogenesis. Role of PG is growing fast since it is the only bacteria able to citrullinate peptides and could induce autoimmune response through development of anti-citrullinated protein antibodies (ACPA). We have already demonstrated that anti- PG antibodies were correlated with ACPA in RA patients. The aim of this study is to develop a physiopathological rat model of PD induced by PG infection to follow the occurrence of early signs of RA and to score bone loss.

Materials and methods Female rats Lewis were randomly divided into two groups: oral infection with PG or negative control. The oral infection was performed by oral gavage with PG during 1 month. Clinical parameters including articular index were monitored during the experiment. Blood samples were collected at different time point for determination of ACPA, RF, MMP-3 (biomarker for RA and PD destruction) and anti- PG antibodies by ELISA assay. Count of activated T lymphocytes that secrete IL-17 was performed by ELISPOT. Bone microarchitecture, bone mineral density (BMD) profiles were obtained by µ-computed tomography (µ-CT) and dual energy x-rays absorptiometry (DXA) x-rays, respectively.

Results ELISA assay for ACPA determination in rats is set up and correlation between arthritis and ACPA has been established (p < 0.01). Moreover, ACPA is found in early phase of arthritis compared to controls (p < 0.01). Development of RF, MMP-3 assay, ELISPOT and radiological evaluation are still ongoing.

Conclusions The development of a reliable animal model of arthritis induced by periodontal disease with PG is essential for the test of new therapeutics in the future.

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