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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional
A P Trombone1, M Claudino, P Colavite
1Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto--FMRP/USP, Sao Paulo, Brazil.
Genes and Immunity
|April 30, 2010
Summary
Periodontitis and rheumatoid arthritis share inflammatory pathways. Genetic predisposition influences disease severity and interaction, highlighting shared immune responses in bone resorption.
Area of Science:
- Immunology
- Oral Biology
- Rheumatology
Background:
- Periodontitis (PD) and rheumatoid arthritis (RA) are chronic inflammatory diseases associated with bone resorption.
- The underlying mechanisms linking PD and RA remain largely unknown.
- This study investigates the interaction between experimental PD and arthritis in mice.
Purpose of the Study:
- To elucidate the mechanisms underlying the association between periodontitis and rheumatoid arthritis.
- To examine the interaction between Actinobacillus actinomycetemcomitans- and Porphyromonas gingivalis-induced PD and pristane-induced arthritis (PIA) in mice.
- To assess the role of genetic predisposition in the co-induction of PD and PIA.
Main Methods:
- Induction of PD and PIA in genetically distinct mouse strains (AIRmax and AIRmin).
- Assessment of inflammatory markers (TNF-alpha, IL-1beta, IL-17, IFN-gamma), bone resorption markers (MMP-13, RANKL), and T-cell subset transcription factors (T-bet, RORgamma, GATA-3).
- Evaluation of alveolar bone loss and PIA severity parameters.
Main Results:
- Higher PD severity in AIRmax mice correlated with increased inflammatory markers and bone resorption mediators.
- Co-induction of PD and PIA in AIRmax mice led to significantly elevated levels of IL-1beta, IFN-gamma, IL-17, RANKL, and MMP-13.
- PD/PIA co-induction did not affect disease course in AIRmin mice, but altered T-cell subset transcription factors in AIRmax mice.
- PIA induction caused alveolar bone loss, dependent on oral commensal bacteria, with no change in PIA severity upon PD co-induction.
Conclusions:
- The interaction between experimental PD and arthritis in mice is influenced by a shared hyper-inflammatory genotype.
- Functional interferences in innate and adaptive immune responses contribute to the observed disease association.
- Genetic factors play a critical role in modulating the interplay between periodontitis and rheumatoid arthritis.
