SjS seemed to negatively affect the periodontal condition because gingival inflammation was more evident in the individuals with SjS, particularly those with SjS (S).
The anti-inflammatory treatment taken by RA patients might influence the periodontal inflammation status represented by IL-1beta and elastase in the GCF.
Background: The aim of this study was to monitor changes in periodontal inflammation in patients with juvenile idiopathic arthritis (JIA) for 2 years. We investigated the influence of rheumatic disease activity and antirheumatic medication on clinical and immunological parameters of periodontal inflammation in these individuals.Methods: Two years after a baseline examination, the periodontal and rheumatological conditions of 18 adolescents with JIA and 14 control subjects were described. The clinical periodontal inflammation was monitored by registration of visual plaque, marginal bleeding, probing depth, and clinical attachment loss (AL). Periodontal inflammation was also assessed by analysis of the cytokines interleukin (IL)-1b and IL-18 and the collagenase matrix metalloproteinase (MMP)-8 by enzyme-linked immunosorbent assay.Results: The erythrocyte sedimentation rate and clinical rheumatological parameters were significantly improved at the 2-year follow-up. The number of sites with plaque decreased, and the number of pockets ‡4 mm increased, whereas bleeding levels and the extension of AL remained unchanged. IL-1b in gingival crevicular fluid decreased significantly in the JIA group after 2 years. No differences were observed for IL-1b, MMP-8, or IL-18 levels between groups after 2 years.Conclusion: Two years after the baseline examination, no clinical or laboratory differences in periodontal inflammation could be found between JIA patients and control subjects.
The findings of increased serum IL-18 and IL-1beta in patients with JIA accompanied by a similar subgingival microbiota suggest that the increased frequency of incipient attachment loss observed in these patients might be due to their altered systemic inflammatory response, making them more susceptible to periodontal disease.
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