Experimental arthritis exacerbates Aggregatibacter actinomycetemcomitans‐induced periodontitis in mice

Abstract Aim This study aimed to investigate whether chronic antigen‐induced arthritis ( AIA ) influences infection‐induced periodontitis ( PD ) in mice and whether PD modifies the clinical course of AIA . The contribution of anti‐ TNF ‐α therapy was also evaluated. Materials and methods The PD was induced in C57 BL /6 mice by oral infection with Aggregatibacter actinomycetemcomitans . AIA was induced after infection. Anti‐ TNF ‐α and chlorhexidine therapies were used to investigate the role of TNF ‐α and oral infection on PD and AIA interaction. Maxillae, knee joints, lymph nodes and serum samples were used for histomorphometric, immunoenzymatic and/or real time‐ PCR analyses. Results Antigen‐induced arthritis exacerbated alveolar bone loss triggered by PD infection. In contrast, PD did not influence AIA in the evaluated time‐points. PD exacerbation was associated with enhanced production of IFN‐γ in maxillae and expression of the Th1 transcription factor tBET in submandibular lymph nodes. Increased serum levels of IL‐6 and C‐reactive protein were also detected. Anti‐TNF‐α and antiseptic therapies prevented the development and exacerbation of infectious‐PD. Anti‐TNF‐α therapy also resulted in reduced expression of IFN‐γ, TNF‐α and IL‐17 in maxillae. Conclusions Altogether, the current results indicate that the exacerbation of infection‐induced PD by arthritis is associated with an alteration in lymphocyte polarization pattern and increased systemic immunoreactivity. This process was ameliorated by anti‐ TNF ‐α and antiseptic therapies.