The trefoil factor family 1 (TFF-1) and 3 (TFF-3) are upregulated in the saliva, gingival crevicular fluid and serum of periodontitis patients.

OBJECTIVE: This study aimed to investigate the levels of trefoil factor family (TFF)-1, TFF-3 and interleukin (IL)-1ß in gingival crevicular fluid (GCF), saliva and serum of patients with gingivitis, stage 3 periodontitis and healthy individuals. MATERIALS AND METHODS: A total of 100 individuals consisting of 25 periodontally healthy, 25 gingivitis and 50 stage 3 periodontitis, were enrolled in the study. Clinical periodontal examinations were recorded and GCF, saliva and serum samples were obtained. TFF-1, TFF-3 and IL-1ß were measured by ELISA. RESULTS: TFF-1 and TFF-3 levels in both GCF, saliva and serum were higher in periodontitis patients than healthy controls (p < .001) and gingivitis group (p < .01). The levels of these peptides in all biofluids were similar between gingivitis and healthy control groups (p > .05). GCF, saliva and serum IL-1ß levels were also higher in periodontitis patients than the controls (p < .01). Periodontitis patients had elevated GCF and saliva IL-ß levels than gingivitis group (p < .001). CONCLUSION: Elevated TFF-1 and TFF-3 levels both locally and systemically in periodontitis in parallel to increased IL-1ß levels might suggest that these peptides are involved in host response during the periodontal tissue destruction.

Effect of non-surgical periodontal treatment on gingival crevicular fluid hypoxia inducible factor-1 alpha, vascular endothelial growth factor and tumor necrosis factor-alpha levels in generalized aggressive periodontitis patients.

BACKGROUND: Hypoxia-inducible angiogenic pathway involving hypoxia inducible factor-1 alpha (HIF-1α), vascular endothelial growth factor (VEGF) and tumor necrosis factor-alpha (TNF-α) may regulate several biological processes related to inflammation. The present study aimed to assess the effect of non-surgical periodontal treatment on gingival crevicular fluid (GCF) HIF-1α, VEGF, and TNF-α levels in generalized aggressive periodontitis (G-AgP). METHODS: Twenty G-AgP patients and 20 periodontally healthy individuals were included. G-AgP patients received scaling and root planning (SRP), per quadrant at a 1-week-interval, performed with ultrasonic and periodontal hand instruments. GCF samples were collected and clinical periodontal parameters including probing depth, clinical attachment level, gingival index and plaque index were recorded at baseline, 1 and 3 months after treatment. Biomarker levels in GCF were analyzed by ELISA. RESULTS: At baseline all clinical parameters and GCF HIF-1α, VEGF, and TNF-α levels were significantly higher in G-AgP patients compared to healthy control (P < 0.05). All clinical parameters improved over the 3-month-period in G-AgP patients (P < 0.05). GCF HIF-1α levels in G-AgP reduced at 1 and 3 months post-treatment, however, this did not reach to statistical significance (P > 0.05). GCF VEGF and TNF-α levels remained unchanged throughout the study period (P > 0.05). CONCLUSIONS: Within the limitations of the present study, although HIF-1α seems to possess a potential diagnostic value for G-AgP, it might not be a proper predictor of clinically favorable treatment outcome. SRP plus different adjunctive therapies could provide better information about the prognostic role of hypoxia-inducible angiogenic pathway in G-AgP.