Background/Purpose: Oral pathogens that cause periodontitis have been implicated as triggers for rheumatoid arthritis (RA), via antibodies to citrullinated proteins. Gingivitis is common in children and is a chronic inflammatory precursor to periodontitis. Patients with juvenile idiopathic arthritis (JIA) rarely produce anti-citrullinated peptide antibodies (ACPA). The children with polyarticular JIA who carry ACPA tend to have more aggressive arthritis, similar to adult RA patients. We hypothesized that gingival inflammation is associated with JIA, and that ACPA may represent a link between JIA and oral health. Our objectives were to: (a) Test for increased frequency of gingivitis in children with JIA compared to controls and (b) Test for correlations between ACPA and dental clinical outcomes.

Methods: This was a cross-sectional study of 85 patients with JIA and 62 dental clinic patients at a children’s hospital. A second control group was derived from 11 healthy child volunteers. Serum from an additional historic cohort of 30 healthy children was used to study ACPA. Dental indices were compared between groups using linear regression adjusting for demographic characteristics. ACPA were detected with a commercial CCP3 assay and also to 29 citrullinated full-length peptides using a custom multiplex autoantibody assay. Elevated levels for antibodies to each peptide were defined as values larger than the maximum value for the historical controls. Positive ACPA was defined as elevated levels of antibodies specific for more than 4 of the citrullinated proteins. The prevalence of positive ACPA was compared across groups using the Fisher’s exact test.

Results: Although JIA patients overall had better oral health than dental controls they had significantly more bleeding on probing of the gingiva, the most specific sign of active inflammation (p = 0.007). There was no correlation between JIA disease activity or immunosuppression with dental indices. TMJ arthritis was associated with a higher gingival index. Patient smoking (only present in dental group) and household smoking exposure in JIA group correlated with a worse ‘decay, missing, filling teeth’ index (DMFT) score. By commercial CCP3 assay ACPA were detected in only four JIA patients (all poly-JIA), but elevated levels were detected by the custom array in 15/41 (37%) of poly JIA, 14/36 (39%) of oligo JIA, and 19/58 (33%) of dental controls. Antibodies to more than 4 citrullinated peptides were most common in poly JIA 9/41 (22%) compared with 1/36 (3%) for oligo JIA, and 2/58 (3.4%) for dental controls, (p=0.002). We found no associations between ACPA status and any dental index.

Conclusion: Gingival inflammation was associated with JIA, suggesting that a systemic immune response could be triggered by oral bacteria involved in both oral and synovial inflammation, and cannot be attributed to poor dental hygiene secondary to JIA disability. Microbial analysis of plaque will help understand this relationship further. No association was found between ACPA and gingival inflammation; however more sensitive and specific tests for ACPA may lead to improved prognosis and understanding of the triggers for arthritis in children.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/oral-health-and-anti-citrullinated-peptide-antibodies-in-juvenile-idiopathic-arthritis/