Oral Dysbiosis and Inflammation in Parkinson's Disease

Abstract

Background: Oral microbiota has largely escaped attention in Parkinson's disease (PD), despite its pivotal role in maintaining oral and systemic health.

Objective: The aim of our study was to examine the composition of the oral microbiota and the degree of oral inflammation in PD.

Methods: Twenty PD patients were compared to 20 healthy controls. Neurological, periodontal and dental examinations were performed as well as dental scaling and gingival crevicular fluid sampling for cytokines measurement (interleukine (IL)-1β, IL-6, IL-1 receptor antagonist (RA), interferon-γ and tumor necrosis factor (TNF)-α). Two months later, oral microbiota was sampled from saliva and subgingival dental plaque. A 16S rRNA gene amplicon sequencing was used to assess bacterial communities.

Results: PD patients were in the early and mid-stage phases of their disease (Hoehn & Yahr 2-2.5). Dental and periodontal parameters did not differ between groups. The levels of IL-1β and IL-1RA were significantly increased in patients compared to controls with a trend for an increased level of TNF-α in patients. Both saliva and subgingival dental plaque microbiota differed between patients and controls. Streptococcus mutans, Kingella oralis, Actinomyces AFQC_s, Veillonella AFUJ_s, Scardovia, Lactobacillaceae, Negativicutes and Firmicutes were more abundant in patients, whereas Treponema KE332528_s, Lachnospiraceae AM420052_s, and phylum SR1 were less abundant.

Conclusion: Our findings show that the oral microbiome is altered in early and mid-stage PD. Although PD patients had good dental and periodontal status, local inflammation was already present in the oral cavity. The relationship between oral dysbiosis, inflammation and the pathogenesis of PD requires further study.

Keywords: Oral microbiome; Parkinson’s disease; biomarker; cytokine; inflammation; microbiota; non-motor symptoms.

Fig. 1

Differential bacterial community composition between controls and PD patients assessed in saliva (A) and dental plaque samples (B). Participant’s number is indicated next to her/his location point.

Fig. 2

zOTU richness (A) and Shannon bacterial diversity index (B) in saliva and dental plaque samples in PD patients and controls.

Fig. 3

Bacterial taxa significantly different in abundance between patients and controls in both saliva and dental plaque.