BackgroundParkinson'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.MethodsWe recruited 60 patients with Stage III, Grade B periodontitis (P) with and without PA (n = 20 for each). We also included systemically and periodontally healthy individuals as controls (n = 20). Clinical periodontal parameters were recorded. Serum, saliva, and gingival crevicular fluid (GCF) samples were collected to measure the inflammatory and neurodegenerative targets (YKL‐40, fractalkine, S100B, alpha‐synuclein, tau, vascular cell adhesion protein‐1 (VCAM‐1), brain‐derived neurotrophic factor (BDNF), neurofilament light chain (NfL).ResultsParkinson's patients in this study had mild to moderate motor dysfunctions, which did not prevent them from performing optimal oral hygiene control. Periodontal parameters and GCF volume were significantly higher in the P and P+PA groups than in the control group. PA was associated with significantly increased bleeding on probing (BOP) compared to P‐alone (p < 0.05), while other clinical parameters were similar between P and P+PA groups. In saliva and serum, YKL‐40 levels were higher in the P+PA group than in P and C groups (p < 0.001). GCF NfL levels from shallow sites were significantly higher in the P+PA group compared to the C group (p = 0.0462). GCF S100B levels from deep sites were higher in the P+PA group than in healthy individuals (p = 0.0194).ConclusionThe data suggested that PA is highly associated with increased periodontal inflammatory burden—bleeding upon probing and inflammatory markers—in parallel with PA‐related neuroinflammation.

ObjectivesCigarette consumption is common around the world and besides its negative effects on health, and its effects on periodontitis draw attention. Arginine metabolites are involved in the pathogenesis of several systemic inflammatory diseases' including cardiovascular diseases. Our aim was to determine periodontitis and healthy individuals' arginine metabolites and IL‐6 levels in saliva and serum and to evaluate those according to smoking status.Materials and MethodsThe study consisted of four groups: healthy individuals (control [C]; n = 20), smokers with healthy periodontium (S‐C; n = 20), nonsmokers with Stage‐III Grade‐B generalized periodontitis (P; n = 20) and smokers with Stage‐III Grade‐C generalized periodontitis (S‐P; n = 18). Periodontal parameters were measured. Analysis of methylated arginine metabolites was performed by LC–MS/MS, and IL‐6 levels were determined by ELISA kits.ResultsIn nonsmokers, salivary concentrations of asymmetric dimethylarginine (ADMA) and symmetrical dimethylarginine (SDMA) were higher in the periodontitis than control (p < 0.001, p = 0.010). Smokers with periodontitis exhibited higher ADMA (p = 0.033, p < 0.001) and arginine (p = 0.030, p = 0.001) saliva concentrations than smoking and nonsmoking controls.ConclusionsOur results demonstrated that salivary concentrations of ADMA and SDMA were associated with periodontitis. Smoking increased ADMA, SDMA and NG‐monomethyl L‐arginine (L‐NMMA) levels in serum only in periodontitis patients.