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Abstract Number: 2017

Oral Microbiota in New-Onset Juvenile Idiopathic Arthritis

Albert Chow1,2,3, Sriharsha Grevich1,2,3, Peggy Lee4, Jeffrey McLean4, Sarah Ringold1,3,5, Roger Bumgarner6 and Anne Stevens1,2,3, 1Pediatrics, University of Washington, Seattle, WA, 2Center for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA, 3Pediatric Rheumatology, Seattle Children's Hospital, Seattle, WA, 4Dentistry, University of Washington, Seattle, WA, 5Center for Clinical and Translational Research, Seattle Children's Research Institute, Seattle, WA, 6Microbiology, University of Washington, Seattle, WA

Meeting: 2018 ACR/ARHP Annual Meeting

Keywords: juvenile idiopathic arthritis (JIA), microbiome, oral, pediatric rheumatology and pediatrics

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Session Information

Date: Tuesday, October 23, 2018

Title: Pediatric Rheumatology – Basic Science Poster

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: Oral microbial dysbiosis of specific organisms such as Porphyromonas, Aggregatibacter, Tannerella, and Treponema in dental plaque has been implicated in the pathogenesis of adult rheumatoid arthritis (RA) and periodontitis, while Neisseria may play a protective role. Whether oral dysbiosis is also associated with juvenile idiopathic arthritis (JIA) is less clear, as periodontal disease-related organisms are rare in children. Comparing the microbiomes from JIA patients with those of their mothers provide another avenue to explore the role of dysbiosis in arthritis, because healthy children derive much of their microbiome from their mothers. We previously demonstrated increased gingivitis in treated JIA patients compared to healthy children. For this current study, we hypothesized that oral microbial dysbiosis was associated with systemic inflammation, and children with JIA have an altered oral microbiome compared to their mothers. By examining only new-onset JIA patients, the confounding effects of previous treatment should be eliminated.

Methods: Saliva was collected from 14 new-onset, treatment-naïve JIA patients of all JIA subtypes, aged 3-15 years, and their mothers. Subjects who received antibiotics within the previous 3 months were excluded. V3/V4 16S rRNA sequencing was performed on the Illumina MiSeq platform. Sequences were paired and merged using BBMerge. Merged reads were trimmed to remove bases with a Q value <20, and filtered to retain only sequences greater than 400 bp and no more than 1N. Processed reads were classified by comparison to the Human Oral Microbiome 16S Database V15.1. Relative frequencies as percentages of bacterial genera and species were calculated in individual patients and compared to frequencies found in each patient’s mother. Paired T-tests and signed rank Wilcoxon tests were performed on all species between probands and mothers; significance level was set at p = 0.05.

Results: We assessed all species detected in either probands or mothers. There were no significant differences in the relative frequencies of Prevotella, Neisseria, Leptotrichia, Fusobacterium, or Porphyromonas species between probands and mothers. Tannerella forsythia and Treponema species were detected at low relative frequencies in all subjects. Aggregatibacter actinomycetecomitans was not detected in our cohort. With paired T-tests, three species were detected at low frequencies in mothers but not in any probands: Bacteroidetes HMT 511, Veillonellaceae HMT 155, and Selenomonas HMT 134. These species were identified by sequencing only; their functional nature have not been explored. Microbial diversity calculated using Shannon Diversity Index was similar in probands and mothers.

Conclusion: In an inception cohort of new-onset JIA patients, organisms implicated in the pathogenesis of adult RA were not detected at higher frequencies in probands or in their mothers. This is the first study to examine the oral microbiome of untreated JIA patients. Further work to compare the oral microbiota of JIA families against aged-matched healthy family members may elucidate patterns that predispose children to JIA.


Disclosure: A. Chow, None; S. Grevich, None; P. Lee, None; J. McLean, None; S. Ringold, None; R. Bumgarner, None; A. Stevens, None.

To cite this abstract in AMA style:

Chow A, Grevich S, Lee P, McLean J, Ringold S, Bumgarner R, Stevens A. Oral Microbiota in New-Onset Juvenile Idiopathic Arthritis [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 9). https://acrabstracts.org/abstract/oral-microbiota-in-new-onset-juvenile-idiopathic-arthritis/. Accessed .
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