Rheumatoid arthritis as a modifier of periodontitis

Abstract

Periodontitis is a chronic tissue-destructive condition in which the tooth-supporting collagen fibers of ligament and bone are broken down mainly by the host s overreactive immune inflammatory response. The relation between periodontitis and other chronic inflammatory destructive diseases, such as rheumatoid arthritis (RA), has been dealt with in some studies because, in spite of their different etiologies, similar mechanisms of tissue destruction have been described in these conditions. The findings concerning the periodontal conditions of adults with RA are disputed. Some studies have shown no association between the two conditions while others have supported a worse periodontal status in these patients. Little is known about the oral conditions of individuals with the forms of arthritis that affect children and adolescents, i.e. juvenile idiopathic arthritis (JIA), except for a higher caries prevalence. Information regarding periodontitis in JIA subjects is lacking and thus is needed.

The aims of this thesis were to assess the periodontal conditions of adolescents with JIA relating this to their rheumatological status, to investigate the possible effect of their aberrant inflammatory response on serum and gingival crevicular fluid (GCF) markers of inflammation and subgingival microbiota, to monitor changes in periodontal inflammation in these individuals for 2 years after continuous rheumatological treatment and finally to evaluate the effect of anti-rheumatic medication on markers of periodontal inflammation in GCF from a group of individuals with RA. Study I showed that adolescents with JIA present more frequently incipient periodontal attachment loss than healthy controls, in spite of similar plaque and marginal bleeding levels. Individuals with JIA with attachment loss (AL) tended to have higher levels of C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and joints with swelling, pain and limitation on movement. Study II demonstrated that serum levels of interleuin-1β (IL- 1β) and interleukin-18 (IL-18) were significantly elevated in the JIA group, especially in those presenting AL, suggesting that the early periodontal destruction observed in these patients might be related to their altered systemic inflammatory response. In Study III, the clinical and laboratory rheumatological parameters were significantly improved after 2 years of follow-up. Accompanying this, the total amounts of IL-1β decreased in GCF and no differences were observed in periodontitis parameters. In Study IV, total amounts of IL-1β and total elastase were significantly lower in an adult RA group compared to matched controls. These markers were significantly correlated in the RA group. The heavy antiinflammatory treatment taken by RA patients might influence the periodontal inflammatory status in GCF represented by IL-1β and elastase.

In conclusion, this thesis shows that adolescents with JIA, especially those more systemically affected, have a worse periodontal condition than controls. However, longitudinally, the effects of disease remission and anti-rheumatic treatment are potentially able to modulate the inflammatory process in the periodontium.