Background and purpose: The role of the gut microbiome in the pathogenesis of Parkinson disease (PD) is under intense investigation, and the results presented are still very heterogeneous. These discrepancies arise not only from the highly heterogeneous pathology of PD, but also from widely varying methodologies at all stages of the workflow, from sampling to final statistical analysis. The aim of the present work is to harmonize the workflow across studies to reduce the methodological heterogeneity and to perform a pooled analysis to account for other sources of heterogeneity.Methods: We performed a systematic review to identify studies comparing the gut microbiota of PD patients to healthy controls. A workflow was designed to harmonize processing across all studies from bioinformatics processing to final statistical analysis using a Bayesian random‐effects meta‐analysis based on individual patient‐level data.Results: The results show that harmonizing workflows minimizes differences between statistical methods and reveals only a small set of taxa being associated with the pathogenesis of PD. Increased shares of the genera Akkermansia and Bifidobacterium and decreased shares of the genera Roseburia and Faecalibacterium were most characteristic for PD‐associated microbiota.Conclusions: Our study summarizes evidence that reduced levels of butyrate‐producing taxa in combination with possible degradation of the mucus layer by Akkermansia may promote intestinal inflammation and reduced permeability of the gut mucosal layer. This may allow potentially pathogenic metabolites to transit and enter the enteric nervous system.

Aim: To explore whether adjunctive antibiotics can relevantly influence long‐term microbiota changes in stage III–IV periodontitis patients.Materials and Methods: This is a secondary analysis of a randomized clinical trial on periodontal therapy with adjunctive 500 mg amoxicillin and 400 mg metronidazole or placebo thrice daily for 7 days. Subgingival plaque samples were taken before and 2, 8, 14 and 26 months after mechanical therapy. The V4‐hypervariable region of the 16S rRNA gene was sequenced with Illumina MiSeq 250 base pair paired‐end reads. Changes at the ribosomal sequence variant (RSV) level, diversity and subgingival‐microbial dysbiosis index (SMDI) were explored with a negative binomial regression model and non‐parametric tests.Results: Overall, 50.2% of all raw reads summed up to 72 RSVs (3.0%) that were generated from 163 stage III–IV periodontitis patients. Of those, 16 RSVs, including Porphyromonas gingivalis, Tannerella forsythia and Aggregatibacter actinomycetemcomitans, changed significantly over 26 months because of adjunctive systemic antibiotics. SMDI decreased significantly more in the antibiotic group at all timepoints, whereas the 2‐month differences in alpha and beta diversity between groups were not significant at 8 and 14 months, respectively.Conclusions: Mechanical periodontal therapy with adjunctive antibiotics induced a relevant and long‐term sustainable change towards an oral microbiome more associated with oral health.

This study examines the relationship between supragingival plaque control and subgingival microbiota during periodontal therapy, focusing on microbial clusters associated with plaque levels. Data were drawn from a 26-month multicenter, double-blinded, randomized, placebo-controlled trial. Supragingival plaque was measured using the O’Leary index, and subgingival microbiota were profiled via Illumina 16S rRNA gene sequencing. A novel topic modelling approach using cross-validated Latent Dirichlet Allocation (LDA) identified microbial clusters, and negative binomial mixed models evaluated their association with plaque levels. Supragingival plaque was positively associated with bleeding on probing (BOP) and microbial diversity, but not with dysbiosis. A specific subgingival microbial cluster dominated by Selenomonas and Leptotrichia was linked to elevated plaque levels and increased in abundance following both antibiotic and placebo treatments. The odds ratio for plaque associated with this cluster was 1.20 (95% CI: 1.07–1.35). Stratified analyses showed this association was reduced in the antibiotic group but remained in the placebo group. Ineffective supragingival plaque control correlates with increased BOP and microbial diversity, though not necessarily with dysbiosis. Adjunctive antibiotics may promote a more cariogenic subgingival microbiota by disrupting the association between plaque accumulation and the abundance of acidogenic taxa such as Selenomonas and Leptotrichia.

Anticoagulant rodenticides (ARs) are highly effective, but can be of environmental concern due to primary and secondary non-target exposure, with the latter possible being relevant to domestic cats. Therefore, liver residues of ARs and an alternative rodenticide, α-chloralose, were systematically monitored in domestic cats for the first time in the current study. In 2021 and 2022, the carcasses of 99 cats were collected in Slovenia and liver residues were measured by using solid supported liquid–liquid extraction and LC-MS/MS. The results show that 65% of cats carried at least one rodenticide. The second-generation ARs brodifacoum and bromadiolone were most prevalent and found in 53.5 and 25.3% of the samples, respectively. Of first-generation ARs, coumatetralyl was the most prevalent (21.2% of cats). More compounds were detected at high human population density, low farm density and in rural versus intermediate landscapes, but no effect was found for livestock density. Similar trends were found for the presence of brodifacoum, bromadiolone and all rodenticides combined. Farm density was negatively correlated with brodifacoum liver concentration. Individual factors (cat age, sex, outdoor activity) did not matter. The results indicate that a reasonably populated rural landscape, and not the rural or intermediate environment as such, is the main driver of cat exposure to ARs. The risk quotient (RQ) of worst-case acute brodifacoum poisoning was 1506. In summary, a potential environmental problem is globally highlighted for cats that is probably related to secondary exposure to ARs, with a pattern different to that seen in wild predators. Cats are an appropriate sentinel species for assessing rodenticide exposure and endangerment in the environment.

Aim: To evaluate the effect of prolonged fasting on the oral microbiome in patients with metabolic syndrome (MetS).Materials and Methods: This follow‐up study evaluated changes in the oral microbiome in a sub‐cohort of 42 patients with MetS during prolonged fasting. Periodontal parameters such as bleeding on probing (BOP), plaque index (PI) and gingival crevicular fluid (GCF) measured in Periotron units (PU) as well as supra‐ and subgingival plaque samples were taken at baseline (T1), after 5–10 days of prolonged fasting (T2) and at 4–5‐month follow‐up (T3). Sequencing of the V4 hypervariable region of the 16S rRNA gene was performed to analyse the microbiome composition.Results: Significant reductions were observed in BOP: 36.4% ± 18.2% to 30.4% ± 15.6% (p = 0.01), PI: 66.9% ± 19.5% to 58.8% ± 23.4% (p < 0.01) and GCF: 83.6 ± 27.8 PU to 67.9 ± 30.3 PU (p < 0.01) post fasting. Microbiome α‐ and β‐diversity did not change significantly. However, significant changes in specific bacterial genera were noted: Lachnospiraceae [G‐3] increased only in subgingival samples; Eikenella and Peptostreptococcaceae [XI][G‐7] increased; while Mitsuokella and Atopobium decreased in both sub‐ and supra‐gingival samples.Conclusion: Within the constraints of this analysis, prolonged fasting was found to be associated with reduced periodontal inflammation and selected shifts in the oral microbial composition. Larger controlled trials are needed to confirm these exploratory findings and determine their clinical relevance.

Aim: To investigate whether exhaled carbon monoxide (CO) is dose‐dependently associated with subgingival polymicrobial clusters before and after non‐surgical periodontal therapy. Material and Methods: We followed 163 adults with periodontitis, measuring CO before and at 2, 14 and 26 months after therapy. Subgingival plaque samples were analysed using 16S rRNA gene sequencing. We applied topic models and regression analysis, adjusted for age, sex, treatment group, pocket probing depth and plaque levels. Results: Smokers had generally higher mean CO levels at every visit and showed significant declines at 14 and 26 months after therapy ( p < 0.01). Before therapy, CO was not associated with dysbiosis; after therapy, higher levels were positively associated. In sensitivity analyses, self‐reported smoking status explained more variance in dysbiosis than CO alone, with only marginal gains when both were combined. Among smokers, a distinct polymicrobial cluster dominated by Fusobacterium and Prevotella increased with higher exhaled CO. Every 10 parts per million increase in CO was associated with an estimated 16% increase in cluster abundance (95% confidence interval: 8%–26%). Conclusion: Exhaled CO may help monitor persistent dysbiosis and select an anaerobe‐dominated subgingival community after periodontal therapy among smokers.