Yazar "Rivas, Carla Alvarez" seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim
    Öğe
    Oral and gut microbial profiling in periodontitis and parkinson's disease
    (Taylor & Francis Ltd, 2024) Yay, Ekin; Yılmaz, Melis; Toygar, Hilal; Balcı, Nur; Rivas, Carla Alvarez; Bolluk Kılıç, Başak; Zırh, Ali; Paster, Bruce J.; Kantarcı, Alpdoğan
    ObjectivesWe tested the hypothesis that Parkinson's disease (PA) alters the periodontitis-associated oral microbiome.MethodPatients 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. The severity of PA motor functions was measured. Unstimulated saliva samples and stool samples were collected. Next-generation sequencing of 16S ribosomal RNA (V1-V3 regions) was performed.ResultsPA patients had mild-to-moderate motor dysfunction and comparable plaque scores as those without, indicating that oral hygiene was efficient in the PA+P group. In saliva, there were statistically significant differences in beta diversity between HC and PA+P (p = 0.001), HC and P (p = 0.001), and P and PA+P (p = 0.028). The microbial profiles of saliva and fecal samples were distinct. Mycoplasma faucium, Tannerella forsythia, Parvimonas micra, and Saccharibacteria (TM7) were increased in P; Prevotella pallens, Prevotella melaninogenica, Neisseria multispecies were more abundant in PA+P group, Ruthenibacterium lactatiformans, Dialister succinatiphilus, Butyrivibrio crossotus and Alloprevotella tannerae were detected in fecal samples in P groups compared to healthy controls.ConclusionsNo significant differences were detected between Parkinson's and non-Parkinson's gut microbiomes, suggesting that Parkinson's disease modifies the oral microbiome in periodontitis subjects independent of the gut microbiome.
  • Küçük Resim
    Öğe
    Parkinson's disease is positively associated with periodontal inflammation
    (Wiley, 2023) Yılmaz, Melis; Yay, Ekin; Balcı, Nur; Toygar, Hilal; Bolluk Kılıç, Başak; Zırh, Ali; Rivas, Carla Alvarez; Kantarcı, Alpdoğan
    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.