Is the Oral Microbiome Involved in the Pathogenesis of Sjogren’s Syndrome?

Taco A van der Meulen¹, Frans G.M. Kroese², S.C. Liefers², Arnau Vich Vila³, Hermie J.M. Harmsen⁴, Hendrika Bootsma², Fred K.L. Spijkervet¹ and Arjan Vissink⁵, ¹Oral and Maxillofacial Surgery, University of Groningen, University Medical Center Groningen, Groningen, Netherlands, ²Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands, ³Gastroenterology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands, ⁴Medical Microbiology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands, ⁵Department of Oral and Maxillofacial Surgery, University of Groningen, University Medical Center Groningen, Groningen, Netherlands

Meeting: 2017 ACR/ARHP Annual Meeting

Date of first publication: September 18, 2017

Keywords: microbiome, oral and pathogenesis, Sjogren's syndrome

Session Information

Date: Sunday, November 5, 2017

Title: Sjögren's Syndrome Poster I: Translational Research

Session Type: ACR Poster Session A

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

Background/Purpose: Environmental factors involved in the pathogenesis of primary Sjögren’s syndrome (pSS) are still largely unknown. The oral cavity is the microbial habitat closest to the salivary glands – the most affected tissue in pSS. Hypofunction of the salivary glands is the major cause underlying symptoms of a dry mouth (xerostomia), occurring in over 90% of the patients with pSS. The aim of our study was to explore whether the oral microbiome, in particular the bacterial composition and/or the presence of bacterial species, is specific for the oral microbiome of patients with pSS.

Methods: To assess whether changes in the oral microbiome of pSS patients are a cause of pSS or an effect of oral dryness, we included two control groups: patients with oral dryness not diagnosed as pSS (non-SS sicca patients) and population based controls. We collected a swab from the buccal mucosa of 82 patients with oral dryness referred to our outpatient clinic for a complete diagnostic work-up for pSS. After completing the diagnostic workup, 32 patients could be classified as pSS according to the 2002 AECG classification criteria and 50 patients as non-SS sicca. The bacterial composition of the buccal mucosa samples was determined with 16S rRNA sequencing. Buccal mucosa swab samples from a population based cohort study were used as population controls (n=118).

Results: Mean unstimulated whole salivary flow rates in pSS and non-SS sicca patients were 0.09 and 0.17 mL/min respectively. Significantly less 16S rRNA reads per sample were obtained from the buccal swab samples of patients with oral dryness (pSS and non-SS sicca together) compared to population controls (p<0.0001). Also the diversity of the bacterial composition from the buccal mucosa was significantly lower in pSS and non-SS sicca patients than in population controls (p=0.01 and p<0.001 respectively), but no difference was observed between pSS and non-SS sicca patients. Principal coordinate analysis showed no evident separation of the individual samples between the three different study groups, but the buccal mucosa bacterial communities from pSS patients were significantly more dissimilar to those from population controls than non-SS sicca patients from population controls (p=0.028). Multivariate analysis showed highly significant associations between oral dryness and the genera Olsenella, Cryptobacterium and Fretibacterium – all which have been associated with periodontal disease – since these genera were only detected in samples from the buccal mucosa of patients with oral dryness and not in population controls (p-value <0.005). However, no oral bacterial taxa were specifically associated with pSS.

Conclusion: Patients with pSS have a dysbiosis of the oral microbiome, viz. a reduced diversity and increase of pathogenic bacteria. We presume that dysbiosis in the oral microbiome of patients with pSS is largely an effect of oral dryness and not a causal factor in the pathogenesis of pSS. On top of this dysbiosis as a consequence of oral dryness, there might be a specific effect of pSS on the diversity of the oral microbiome.

Disclosure: T. A. van der Meulen, None; F. G. M. Kroese, None; S. C. Liefers, None; A. Vich Vila, None; H. J. M. Harmsen, None; H. Bootsma, None; F. K. L. Spijkervet, None; A. Vissink, None.

To cite this abstract in AMA style:

van der Meulen TA, Kroese FGM, Liefers SC, Vich Vila A, Harmsen HJM, Bootsma H, Spijkervet FKL, Vissink A. Is the Oral Microbiome Involved in the Pathogenesis of Sjogren’s Syndrome? [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/is-the-oral-microbiome-involved-in-the-pathogenesis-of-sjogrens-syndrome/. Accessed .

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