Behçet's disease modifies the gingival inflammatory response.

BACKGROUND: Behçet's disease (BD) pathogenesis involves severe outcomes such as blindness, central nervous system manifestations, and deep venous thrombosis that impacts systemic and local inflammatory changes. We tested the hypothesis that BD negatively affects gingival health and increases the severity of gingivitis. METHODS: The study included 37 BD patients with gingivitis without any sign of periodontitis. Systemically healthy 19 patients with gingivitis (G) and 20 periodontally and systemically healthy individuals (C) were recruited as controls. BD patients were further grouped as stable and unstable based on their responses to BD treatment. Clinical periodontal parameters were measured to determine the impact of BD on gingival health. Serum and saliva levels of ELA-2 (neutrophil elastase-2), SLPI (secretory leukocyte protease inhibitor), α1-AT (alpha1-anti-trypsin), VEGF (vascular endothelial growth factor), IL-6 (interleukin-6), IL-8 (interleukin-8), and TNF-α (tumor necrosis factor alpha) were analyzed using multiplex immunoassay to measure the systemic and local inflammatory impact of BD. RESULTS: Plaque index (PI), probing pocket depth (PPD), and bleeding on probing (BOP) were significantly higher in the BD group than in the controls (p < 0.05). IL-6 was higher in both serum and saliva in the BD group than in the G group (p < 0.05). ELA-2 levels in saliva were higher in the stable BD group than in the controls, while TNF-α and SLPI were statistically significantly higher in BD than in the control (p < 0.05). Salivary α1-AT level was statistically lower in the BD group compared to the control group. CONCLUSION: Our study suggested that the gingival inflammatory profile was impaired in patients with BD.

Sirtuin6 and Lipoxin A4 levels are decreased in severe periodontitis.

OBJECTIVE: Sirtuin6 plays an important role in the regulation of inflammation, homeostasis, and apoptosis, and it has anti-inflammatory effects on several diseases. Lipoxin A4 is a pro-resolving lipid mediator of inflammation and inhibits hypoxia-induced apoptosis and oxidative stress. Considering that Lipoxin A4 and Sirtuin6 have protective effects on inflammatory diseases, the aim of this study is to determine the possible roles of these molecules on periodontitis inflammation in saliva and serum and to reveal the relationship of these data with clinical periodontal parameters. MATERIAL AND METHODS: A total of 20 stage III/grade B periodontitis and 20 periodontally healthy subjects were included in this cross-sectional study (all never smokers and systemically healthy). Clinical periodontal parameters (plaque index, probing pocket depth, bleeding on probing, clinical attachment loss) were recorded. Saliva and serum levels of Sirtuin6 and Lipoxin A4 were analyzed by enzyme-linked immunosorbent assay. RESULTS: Serum Sirtuin6 and saliva Lipoxin A4 levels were significantly lower in the periodontitis group than the control group (respectively, p = 0.0098, p = 0.0008). There were negative correlations between all periodontal clinical parameters and saliva Lipoxin A4 level (p < 0.05) and between probing pocket depth, clinical attachment loss, and serum and saliva Sirtuin6 levels (respectively, r = - 0.465 and r = - 0.473, p < 0.05). CONCLUSIONS: Decreased levels of serum Sirtuin6 and saliva Lipoxin A4 in periodontitis patients and their correlation with clinical periodontal parameters suggest that serum Sirtuin6 and saliva Lipoxin A4 may be related with periodontal inflammation. CLINICAL RELEVANCE: Scientific rationale for the study: Sirtuin6 is one of seven members of the family of NAD + dependent protein that played an important role in the regulation of inflammation, energy metabolism, homeostasis, and apoptosis. Sirtuin6 is associated with the pathogenesis of several diseases. Lipoxin A4 is a lipid mediator that inhibits hypoxia-induced apoptosis and oxidative stress, and it has an active role in the resolution of periodontal inflammation. No studies that investigated the potential role Sirtuin6 and its relationship with inflammation resolution and apoptosis mechanisms in severe periodontitis patients. PRINCIPAL FINDINGS: the serum Sirtuin6 and saliva Lipoxin A4 levels were significantly lower and negatively correlated with clinical periodontal parameters in the patients with periodontitis than the healthy controls. PRACTICAL IMPLICATIONS: this study shows that serum Sirtuin6 and saliva Lipoxin A4 may be candidate biomarkers related with periodontal inflammation and estimating to periodontal status. CLINICAL TRIAL REGISTRATION: NCT05417061.

Potential biomarkers reflecting inflammation in patients with severe periodontitis: Fractalkine (CX3CL1) and its receptor (CX3CR1).

OBJECTIVE: The aim of this study was to determine differences in GCF and serum levels of fractalkine/CX3CL1 and its receptor/ CX3CR1 between the patients with stage III/grade B periodontitis and periodontally healthy subjects. BACKGROUND: Fractalkine (CX3CL1), the only member of CX3C chemokine family, is involved in the pathogenesis of several systemic inflammatory diseases' disorders including rheumatoid arthritis, cardiovascular diseases, tonsillitis, and diabetes mellitus. It has critical functions in inflammatory cell migration, adhesion, and proliferation. METHODS: 20 stage III/grade B periodontitis (P) and 20 healthy individuals (control; C) were included in this clinical study (all never smokers and systemically healthy). Clinical periodontal parameters were measured. Serum and GCF levels of CX3CL1, CX3CR1, and IL-1ß were quantified by enzyme-linked immunosorbent assay and reported as total amounts and concentration. RESULTS: The GCF concentrations and also total amount of CX3CL1, CX3CR1, and IL-1ß were statistically significantly higher in the patients with periodontitis compared with control group (P < 0.05). CX3CL1, CX3CR1, and IL-1ß levels in the GCF were significantly and positively correlated with all the clinical periodontal parameters (PI, PPD, BOP, and CAL; P < 0.01, P < 0.05). There was a significant correlation between IL-1ß, CX3CL1, and CX3CR1 concentrations in the GCF (respectively; r = 0.838 and r = 0.874, P < 0.01). CONCLUSION: Fractalkine and its receptor may play role in mechanisms through the regulation of inflammation or on the pathogenesis of periodontal disease.