Oral Health and Microbiome in Juvenile Idiopathic Arthritis

Objectives: Juvenile idiopathic arthritis (JIA) occurs in 1of 1000 children and can cause significant disability. Children with polyarticular JIA tend to have more aggressive arthritis, similar to adult rheumatoid arthritis (RA) patients. Oral pathogens that cause periodontitis have been implicated as triggers for RA. Altered oral microbiota has been found to be associated with an abnormal humoral immune response in RA. Our hypothesis was that inflammation due to dysbiosis of the oral microbiome may play a role in JIA.

We tested for associations between oral health, expression of peripheral blood monocyte (PBMC) co-stimulatory molecules, and plaque bacterial communities in JIA patients compared to healthy child controls.
Methods: This study included 85 JIA patients, 62 dental patients and 11 healthy controls prospectively enrolled in Seattle Children’s Hospital Rheumatology and Dental Clinics. JIA disease activity, plaque index, gingival index and bleeding on probing (BOP) were recorded during exams. Plaque and blood samples were obtained at the same appointment. Flow cytometry was used to profile co-stimulatory molecules in PBMC. The plaque sample microbiome was analyzed using ultra-high throughput sequencing.
Results: JIA patients had lower gingiva and plaque indices than dental patients, but had significantly more bleeding on probing score (mean percentage of sites bleeding 17% vs 8%, p = 0.007). Monocyte PD-L1, an inflammatory marker, was elevated in JIA and dental patients compared to healthy controls. A significantly greater percentage of monocytes expressed CD16 (a marker of activation) in JIA patients compared to dental patients. Among patients with JIA, BOP was associated with a significantly greater percentage of monocytes expressing CD16. The plaque microbiome in JIA patients clustered apart from healthy controls.
Conclusions: Gingival inflammation as detected by BOP was associated with JIA and systemic monocyte activation. Oral microbiome dysbiosis in JIA patients may be responsible for this activated inflammatory state.