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.

In periodontitis patients, high levels of several inflammatory markers may be expressed in serum, reflecting the effect of local disease on the general health. The objective of the present analysis was to compare cytokine levels assessed in peripheral blood with those in the gingival crevicular fluid (GCF) and evaluate the impact of nonsurgical periodontal therapy on the incidence of high levels of 12 biomarkers in serum. Twenty‐four patients with chronic periodontitis (Group P) contributed with serum and GCF samples at baseline (BL) and 1 and 3 months after periodontal treatment (M1 and M3). Samples were assessed for 12 cytokines using the Bio‐Plex bead array multianalyte detection system. For each analyte, peak values were calculated as greater than the mean + 2 SD of the one found in 60 periodontally healthy participants. Significant correlations between serum and GCF values were obtained in the periodontitis group for interleukin (IL) 1ra, IL‐6, and interferon γ at BL and for macrophage inflammatory protein 1β at M3 after treatment. Periodontitis subjects were found to exhibit high peaks for several inflammatory markers in serum. The highest incidence of peaks at BL was found for interferon γ (37.5% of the periodontitis subjects). For the four biomarkers with a detection frequency of >75% at BL (IL‐1ra, IL‐8, macrophage inflammatory protein 1β, and vascular endothelial growth factor), no significant difference was observed over time for the P group or between the two groups at BL. The significant correlation found between the serum and the GCF for certain cytokines and the fact that periodontitis subjects exhibit high peaks for several inflammatory markers in serum may support the hypothesis that the inflammatory reaction due to periodontitis is not restricted to the diseased sites. Within the limitations of the study, periodontal therapy did not seem to have any significant impact on the systemic cytokine levels.

No abstract

Cytokines are thought to play an important role in the pathogenesis of periodontal disease. Because periodontal disease is known for its inhomogeneous distribution within the dentition, it is unclear to what extent the detection of various cytokines at different sites correlates with presence of disease. We evaluated whether levels of 12 cytokines in gingival crevicular fluid (GCF) discriminated periodontally diseased sites from healthy ones, or periodontally diseased persons from healthy ones, and assessed the impact of nonsurgical periodontal therapy on these readings. This study included 20 periodontally healthy persons (H) and 24 patients with chronic periodontitis (P). In every participant, we measured the plaque index, gingival index, probing pocket depth (PD), bleeding on probing, and recession at six sites of every tooth. GCF was collected with Durapore® filter strips from two healthy sites (PD<4 mm; HH) in group H, and from two periodontally diseased sites (PD≥5 mm; PP) and two periodontally healthy sites (PD≤3 mm; PH) in group P. The periodontally diseased participants underwent comprehensive nonsurgical periodontal therapy including deep scaling and root planing under local anesthesia. In these participants, GCF samples were again collected at the same sites 1 and 3 months after therapy. Twelve cytokines (il‐1β, il‐1ra, il‐6, il‐8, il‐17, b‐fgf, g‐csf, gm‐csf, ifn‐γ, mip‐1β, vegf, and tnf‐α) were assessed using the Bio‐Plex suspension array system. Mean plaque index, gingival index, bleeding on probing, PD, and recession were significantly different between groups H and P. Differences between PP and PH sites were not significant for any of the cytokines. Il‐1ra, il‐6, il‐17, b‐fgf, gm‐csf, mip‐1β, and tnf‐α differed significantly between HH sites and both PH and PP sites, whereas il‐8 was significantly higher only at PP sites. Periodontal treatment increased gm‐csf and decreased il‐1ra levels in PP sites. Il‐1ra, il‐6, il‐8, il‐17, b‐fgf, gm‐csf, mip‐1β, and tnf‐α identified patients with chronic periodontitis, rather than diseased sites, suggesting a generalized inflammatory state that is not limited to clinically diseased sites only.

To evaluate oral health conditions in pediatric liver transplant recipients, with special focus on caries, green staining of the teeth, gingival bleeding, and gingival overgrowth. 40 patients (mean age 11.6 years) were examined at a routine follow-up visit, 6 months to 16 years after liver transplantation at the Swiss Center for Liver Disease in Children. After the medical examination, participants were further examined for the presence of dental caries, periodontal disease, GE, and GTC. The mean decay, missing, and filled teeth (dmft/DMFT) score was 3.8. 45% of the participants presented at least one carious lesion. Two-third of the participants had more than 20% of sites with the presence of plaque and gingival inflammation. Signs of GE were found in 18% and GTC in 30% of the participants. A positive correlation was identified between GTC and peak serum bilirubin (P<.001) and primary diagnosis of cholestatic disease (P=.04). Gingival inflammation was associated with plaque (P<.001), use of immunosuppressive medication (P=.04), and was more pronounced in children with cholestatic disease (P=.007). Children and young adults with liver transplants presented a rather poor oral health status. Liver transplant physicians should counsel patients for regular dental follow-up in order to avoid serious dental infections.