Objective: Our goal is to bridge the mechanistic knowledge gap on the Microbiota-Gut-Oral-Brain-Axis (MGOBA)’s role in Parkinson’s disease (PD) pathogenesis through a case-control, proof-of-concept, observational study.

Background: Understanding mechanisms underlying PD is essential to developing prevention strategies, new therapies, and prediction of disease progression. Reports demonstrate that alpha-synuclein (ASYN) aggregates in PD can spread from the gut to the brain via the vagal-pharyngeal nerve, with increasing interest in ASYN deposition in oral mucosa and saliva. Both we and others have documented pro-inflammatory intestinal, oral, and nasal microbial dysbiosis in PD that may trigger neuroinflammation, ASYN aggregation, and neurodegeneration by disrupting the MGOBA.

Method: A multidisciplinary team from the University of Illinois Chicago College of Dentistry and Rush University Medical Center proposed a case-control study with plans to enroll 60 PD participants and their individually matched, age-similar household controls (dyad). To minimize confounding effects of motor disability on oral hygiene, we will only recruit mild (non-medicated) and moderate (medicated) PD participants all with similar, high-level motor function (Hoehn and Yahr stages I/II). All participants will meet the minimal American Dental Association oral hygiene standards. We will record attachment loss, periodontal indices, oral manifestations of PD, and collect oral samples (brush cytology, saliva, gingival crevicular fluid). Oral motoric dysfunction that may promote ASYN pathology will be examined. Dental examiners and lab personnel who analyze samples will be blinded to case-control status.

Results: Currently, we consented and completed the study on seven dyads. PD participants significantly (p<0.05) present with moderate to severe gingivitis or potential periodontitis. They also exhibited higher rates of xerostomia, tooth loss, and worsened periodontal disease indicators, including gingival inflammation, periodontal attachment plus alveolar bone loss, increased plaque, and bleeding on probing.

Conclusion: Our pilot data suggests that PD participants: (1) exhibit higher rates of gingival and localized bone inflammation than age-similar household controls and (2) may benefit from more rigorous dental care. Analysis of oral microbiota, ASYN aggregates and inflammation/immune activation markers in these seven dyads and additional dyads will be presented during the meeting.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/monitoring-parkinsons-disease-in-the-dental-chair/