Microbial communities in the mouth have been associated with the chronic inflammation of periodontitis and rheumatoid arthritis (RA), and there is higher prevalence of periodontitis in RA. Although periodontitis is rare in children, severe gingivitis, a chronic inflammatory precursor to periodontitis, is quite prevalent. We have found that children with juvenile idiopathic arthritis (JIA) have increased bleeding on probing, a marker of gingival inflammation, compared to controls. For this study, we hypothesize that kids with JIA have an altered microbiota presenting a link between gingivitis and JIA.

Methods:

Plaque samples were collected by dentists from 22 patients with JIA between the ages of 11 to 18 years who satisfied the International League of Association for Rheumatology (ILAR) classification criteria and 10 healthy adolescent controls. The JIA cohort included children with polyarticular JIA (8), oligoarticular JIA (10), and extended oligoarticular JIA (4). Samples were obtained by inserting a sterile endodontic paper point into the pockets or sulci of 6 teeth in each subject. Total genomic DNA was extracted from paper points containing oral plaque and amplicon libraries of the 16S rRNA gene were generated. Sequencing was performed on the Illumina MiSeq according to the manufacture’s guidelines. Qiime (Quantitative Insights Into Microbial Ecology) software was used for microbial analysis of the raw sequencing data. For core diversity analysis, only samples with ≥2700 bp sequences were used. Diversity analysis was performed based on operational taxonomic units (open references using 20 sequences to OTU and clustering using 97% similarity in OTUs). A principle coordinate analysis plot was created using weighted unifrac distance between samples.

Results:

Higher microbial diversity (using rarefraction measure of observed OTUs) was observed in the JIA popuation compared to the healthy controls. Principle coordinate analysis showed the JIA cohorts clustering apart from the healthy controls, indicating that there is a potential difference in the oral microbial profile between the two groups. On further analysis, distinct operational taxonomic units classified as periopathogens were found to be enriched in the JIA cohort.

Conclusion:

This small study suggests that the dental plaque microbiota is distinct in JIA patients compared to healthy controls. Periodontal bacteria such as Prevotella and Porphyromonas have been suggested to play a pathogenic role in RA. In our study we found periopathogens to be higher in the JIA cohort, further supporting our prior finding of increased gingival inflammation in JIA and suggesting a possible mechanistic link between JIA and gingivitis.