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 + 2SD 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.

The suspicion of an origin of Parkinson's disease (PD) at the periphery of the body and the involvement of environmental risk factors in the pathogenesis of PD have directed the attention of the scientific community towards the microbiota. The microbiota represents all the microorganisms residing both in and on a host. It plays an essential role in the physiological functioning of the host. In this article, we review the dysbiosis repeatedly demonstrated in PD and how it influences PD symptoms. Dysbiosis is associated with both motor and non-motor PD symptoms. In animal models, dysbiosis only promotes symptoms in individuals genetically susceptible to Parkinson's disease, suggesting that dysbiosis is a risk factor but not a cause of Parkinson's disease. We also review how dysbiosis contributes to the pathophysiology of PD. Dysbiosis induces numerous and complex metabolic changes, resulting in increased intestinal permeability, local and systemic inflammation, production of bacterial amyloid proteins that promote α-synuclein aggregation, as well as a decrease in short-chain fatty acid-producing bacteria that have anti-inflammatory and neuroprotective potential. In addition, we review how dysbiosis decreases the efficacy of dopaminergic treatments. We then discuss the interest of dysbiosis analysis as a biomarker of Parkinson's disease. Finally, we give an overview of how interventions modulating the gut microbiota such as dietary interventions, pro-biotics, intestinal decontamination and fecal microbiota transplantation could influence the course of PD.

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.

Diabetes mellitus (DM) poses a significant challenge to global health, with its prevalence projected to rise dramatically by 2045. This narrative review explores the bidirectional relationship between periodontitis (PD) and type 1 diabetes mellitus (T1DM), focusing on cellular and molecular mechanisms derived from the interplay between oral microbiota and the host immune response. A comprehensive search of studies published between 2008 and 2023 was conducted to elucidate the association between these two diseases. Preclinical and clinical evidence suggests a bidirectional relationship, with individuals with T1DM exhibiting heightened susceptibility to periodontitis, and vice versa. The review includes recent findings from human clinical studies, revealing variations in oral microbiota composition in T1DM patients, including increases in certain pathogenic species such as Porphyromonas gingivalis, Prevotella intermedia, and Aggregatibacter actinomycetemcomitans, along with shifts in microbial diversity and abundance. Molecular mechanisms underlying this association involve oxidative stress and dysregulated host immune responses, mediated by inflammatory cytokines such as IL-6, IL-8, and MMPs. Furthermore, disruptions in bone turnover markers, such as RANKL and OPG, contribute to periodontal complications in T1DM patients. While preventive measures to manage periodontal complications in T1DM patients may improve overall health outcomes, further research is needed to understand the intricate interactions between oral microbiota, host response, periodontal disease, and systemic health in this population.

Objective: The aim of the study is to compare the levels of Gingival Crevicular Fluid (GCF) interleukin 8 (IL‐8), matrix metalloproteinase 8 (MMP‐8) and advanced glycated‐end products (AGEs) in a cohort of type 1 diabetic (T1D) subjects and healthy controls.Material and methods: GCF samples and periodontal examination were assessed in 50 subjects with T1D (30 males and 20 females; mean age: 35.2 years) recruited from the Diabetology Unit of the Geneva University Hospitals and in 50 control subjects matched for gender, age and smoking status. Samples were assessed for IL‐8 and MMP‐8 using a bead array multianalyte detection system and for AGEs the ELISA. The two groups were compared using the Wilcoxon signed rank test.Results: The mean HbA1c differed significantly between the groups (8.3% for the T1D group vs. 5.2% for the control group, p < 0.001). T1D subjects had significantly more plaque and gingival inflammation and presented more sites with bleeding on probing compared to the controls. The GCF levels of IL‐8, MMP‐8 and AGEs did not differ significantly between the groups. Further analysis of the GCF markers in younger ( 8%), again no significant differences could be identified for any of the biochemical markers.Conclusions: T1D subjects, particularly the younger ones, exhibited more inflammation compared to the matched healthy controls. Results on the GCF expression of IL‐8, MMP‐8 and AGEs did not differ between the groups. The diabetic population of our cohort was for the most part fairly‐controlled, with little if any complications and with presence of only mild type of periodontal disease, as 68% had gingivitis.

The primary objective is to critically analyze approaches to local therapy for periodontal disease, particularly in light of its well‐established systemic implications. We specifically address common misconceptions and overestimations regarding the potential of local treatments in contrast to their actual clinical effectiveness. Historically, the therapeutic approach to periodontitis has concentrated on local intervention within periodontal pockets. Local drug delivery systems show potential for targeting periodontal infections with high drug concentrations while minimizing systemic side effects. This could potentially help overcome the challenges posed by microbial biofilms. However, evidence suggests that periodontitis is not a disease affecting only confined areas of a dentition. Currently, in the presence of multiple deep pockets, local therapy is less cost‐effective than systemic antibiotics due to the costs of products and the extensive professional chair time required for their application. Isolated deep pockets in otherwise stable dentitions are often caused by problems that cannot be resolved with antimicrobial agents. Finally, recurrent biofilm formation in residual pockets during the maintenance phase can be addressed through suitable physical rather than chemical procedures.