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Elin Kindstedt

WCMM-associated researcher

The association between periodontitis and rheumatoid arthritis

Periodontitis and rheumatoid arthritis (RA) are both diseases that are characterized by chronic inflammation in soft tissue sites that eventually causes degradation of adjacent bone. The epidemiological association between periodontitis and RA is evident and increasing evidence suggest that periodontitis might be causative of RA development.
 
The inflammatory process in PD is caused by bacterial dysbiosis, which in disease-susceptible individuals progresses to destruction of jawbone. However, the inflammatory immune response in PD has not been descriptively mapped but it has been demonstrated that B cells and plasma cells constitute the majority of infiltrating cells. Although jawbone destruction occurs in a local manner, sometimes limited to individual teeth and and/or tooth surfaces, PD is reflected by a systemic increase in inflammatory mediators. The etiology of RA is to some extent unknown but is currently regarded as an autoimmune multifactorial disease that arises as result of interactions between genetic and environmental factors.
The presence of antibodies against citrullinated peptides (ACPA) is evident in a majority of RA individuals and are associated with a more severe disease course. ACPA are detectable in blood years prior to disease onset, but it is unknown what triggers production of ACPA. It has been shown that Porphyromonas gingivalis, a gram-negative anaerobe which is strongly associated with PD development, expresses an enzyme that is able to citrullinate proteins and consequently generate ACPA. Therefore, it has been hypothesized that PD could be causative of RA development through production of ACPA, which a later stage reacts against citrullinated epitopes in the joint and thus drives the inflammatory process in RA.
 
In this project, we want to characterize inflammatory infiltrate in PD, particularly focusing on the B-cell population. Furthermore, we want to investigate local occurrence of ACPA in periodontitis and explore which epitopes they bind and pathogenic capacity.
 
Hopefully, our research will contribute to an increased understanding of the association between periodontitis and RA. The long-term goal is to find treatment strategies for PD and possibly RA.

Elin Kindstedt