Estimation of N‑terminal telopeptides of type I collagen in periodontal health, disease and after nonsurgical periodontaltherapy in gingival crevicular fluid: A clinico ‑ biochemical study.

Aim: This study explored gingival crevicular fluid (GCF) N‑terminal telopeptides of type I collagen (NTx) levels in periodontal health, disease and after nonsurgical periodontal therapy along with its association with the clinical parameters. Materials and Methods: Study comprised of three groups of 10 subjects each: Healthy (Group I), gingivitis (Group II), and periodontitis (Group III), while Group III patients after scaling and root planning (SRP) constituted Group IV. Gingival index (GI), probing pocket depth (PPD), clinical attachment loss (CAL), and radiological parameters were recorded. GCF samples were analyzed by competitive‑enzyme‑linked immunosorbent assay. Results: Samples in Group III and Group IV tested positive for NTx whereas in Group I and Group II, NTx was not detected. Mean NTx levels were higher in Group III (6.79 ± 0.94 nanomole bone collagen equivalents per liter [nm BCE/L]) compared to Group IV (5.73 ± 0.95 nm BCE/L) which was statistically significant. Positive correlation was seen between the clinical parameters and the NTx levels in Group III and IV. Conclusion: As NTx is specific bone turnover marker, it is detected only in periodontitis Group and the values decline after SRP. Failure to detect NTx in Group I and II, relates to the minimum or no resorption at the sample sites.

Use of minimally invasive gingival biopsies in the study of inflammatory mediators expression and their correlation with gingival fluid in patients with chronic periodontitis.

Background: There are no studies comparing the gingival crevicular fluid (GCF) cytokines expression with its corresponding values from the same tissue’s sites. Such comparison might be of great value since most of the cytokine function is related to cell and/or tissue receptors. Aims: Our aim was to use minimally invasive biopsies to evaluate the expression of interferon‑gamma, interleukin 1 (IL‑1) β, IL‑6, IL‑17A, IL‑17F, and their correlation with the expression in gingival fluid in patients with chronic periodontitis. Materials and Methods: The collection of gingival fluid comprised 22 samples from 11 patients (mean age 46.73 ± 10.16 standard deviation years) with chronic periodontitis. The collection of biopsies comprised 22 samples from the same patients. Gingival fluid and biopsy were taken from the same site in one shallow and one deep site per patient. Gingival fluid samples were collected with periopaper® and analyzed using Luminex®. Biopsies were taken with a 2 mm diameter punch and analyzed for the same mediators using immunohistochemistry. Results: The gingival fluid showed higher amounts for IL‑1‑β in deep sites. Immunohistochemical markers were observed in the analyzed cells groups, both in deep and shallow sites, without significant differences between them. In the comparative analysis between immunohistochemical markers and GCF, IL‑1‑β showed high concordance in shallow and deep sites. Conclusions: The use of a standardized punch of 2 mm diameter for periodontal tissue biopsies seems to be suitable for immunohistochemistry analysis and showed that the GCF may not express all the markers in the same proportion at the corresponding tissue.

Estimation of the level of tumor necrosis factor-α in gingival crevicular fluid and serum in periodontal health and disease: A biochemical study.

Tumor Necrosis Factor-α(TNF-α), a "major inflammatory cytokine" not only plays an important role in periodontal destruction, but also is extremely toxic to the host. Till date, there are not many studies comparing the levels of TNF-α in GCF and serum and its relationship to periodontal disease. Aim: Hence, an attempt is made to estimate the level of TNF-α in GCF and serum, its relationship to periodontal disease, and to explore the possibility of using the level of TNF-α in GCF as a biochemical "marker" of periodontal disease. Materials and Methods: 60 subjects participated in the study and were grouped into control, gingivitis and periodonititis groups. The GCF and serum samples were assayed for TNF-α levels by Enzyme Linked Immunosorbent Assay (ELISA) method. Results: Showed elevated levels of TNF-α in group II and III subjects as compared to healthy controls in both GCF and serum, suggesting an association between periodontal disease and levels of TNF-α. Conclusion: It remains a possibility that the absence or low levels of TNF-α in GCF might indicate a stable lesion and elevated levels might indicate an active site but only longitudinal studies taking into account, the disease "activity" and "inactivity" could suggest the possibility of using TNF-α in GCF as an "Indicator" of periodontal disease.

[Relationships between smoking and IL-1 beta concentrations in chronic periodontal patients]

Cigarette smoking is a significant risk factor in pathogenesis and progression of periodontal diseases. Smoking could interfere with pro-inflammatory cytokines in inflammatory process. IL-1 beta is a main inflammatory cytokine in gingival crevicular fluid [GCF] which contributes in periodontitis. In fact it is a key molecule in pathogenesis of periodontitis. This study aimed to investigate the correlation between cigarette smoking and concentration of cytokine interleukin [IL]-1 beta in GCF of patients with moderate-to-sever chronic periodontitis. Sixty subjects were entered into this analytical case-control study, divided equally into smokers and non smokers. Two groups were matched in clinical parameters, age and sex. GCF samples were collected in one diseased and one healthy site from each subject. The IL-1 beta concentration in all 120 samples was determined by ELISA kits, specific for IL-1 beta. The observed data were analysed with SPSS 13 software using T, Paired T, Chi-square and Mann-whitney tests. Mean concentration of GCF IL-1 beta in healthy sites of the smokers was significantly more than non smokers [p<0.01]. But in diseased sites no significant differences were shown between the two groups. The differences between concentration of IL-1 beta in smokers and nonsmokers were not significant. Although no significant differences were found in concentration of IL-1 beta between all smokers and all non smokers, there were significant differences between two groups in healthy sites, which require more investigations