Oral and gut microbial profiling in periodontitis and Parkinson's disease.

Objectives: We tested the hypothesis that Parkinson's disease (PA) alters the periodontitis-associated oral microbiome.

Method: Patients with periodontitis with Parkinson's disease (PA+P) and without PA (P) and systemically and periodontally healthy individuals (HC) were enrolled. Clinical, periodontal and neurological parameters were recorded.

Modulating the sEH/EETs Axis Restrains Specialized Proresolving Mediator Impairment and Regulates T Cell Imbalance in Experimental Periodontitis.

Epoxyeicosatrienoic acids (EETs) and other epoxy fatty acids are short-acting lipids involved in resolution of inflammation. Their short half-life, due to its metabolism by soluble epoxide hydrolase (sEH), limits their effects. Specialized proresolving mediators (SPMs) are endogenous regulatory lipids insufficiently synthesized in uncontrolled and chronic inflammation.

Parkinson's disease alters the composition of subgingival microbiome.

Aim: The current study aimed to test the hypothesis that Parkinson's disease exacerbates periodontitis by altering its microbiome.

Materials And Methods: Clinical periodontal parameters were recorded. Subgingival samples from healthy controls, periodontitis patients (PD), and Parkinson's patients with periodontitis (PA+PD) were analyzed using the checkerboard DNA-DNA hybridization technique for targeting 40 bacterial species typically associated with periodontal disease and health.

Parkinson's disease is positively associated with periodontal inflammation.

Background: Parkinson's disease (PA) affects 1% of the global population above 60 years. PA pathogenesis involves severe neuroinflammation that impacts systemic and local inflammatory changes. We tested the hypothesis that PA is associated with periodontal tissue inflammation promoting a greater systemic inflammatory burden.