ABSTRACT
AIM: To characterize and map temporal changes in the biological and clinical phenotype during a 21-day experimental gingivitis study. MATERIALS AND METHODS: Experimental gingivitis was induced over 21 days in healthy human volunteers (n = 56), after which normal brushing was resumed (resolution phase). Gingival and plaque indices were assessed. Gingival crevicular fluid was collected from four paired test and contra-lateral control sites in each volunteer during induction (Days 0, 7, 14 and 21) and resolution (Days 28 and 42) of experimental gingivitis. Fluid volumes were measured and a single analyte was quantified from each site-specific, 30s sample. Data were evaluated by analysis of repeated measurements and paired sample tests. RESULTS: Clinical indices and gingival crevicular fluid volumes at test sites increased from Day 0, peaking at Day 21 (test/control differences all p < 0.0001) and decreased back to control levels by Day 28. Levels of four inflammatory markers showed similar patterns, with significant differences between test and control apparent at Day 7 (substance P, cathepsin G, interleukin-1ß, elastase: all p < 0.03) and peaking at Day 21 (all p < 0.002). Levels of α-1-antitrypsin showed no pattern. CONCLUSIONS: Levels of substance P, cathepsin G, interleukin-1ß and neutrophil elastase act as objective biomarkers of gingival inflammation induction and resolution that typically precede phenotypical changes.
Subject(s)
Cathepsin G/metabolism , Gingival Crevicular Fluid/metabolism , Gingivitis/metabolism , Interleukin-1beta/metabolism , Leukocyte Elastase/metabolism , Substance P/metabolism , Adolescent , Adult , Biomarkers/metabolism , Dental Plaque , Female , Gingival Crevicular Fluid/immunology , Gingivitis/immunology , Gingivitis/pathology , Humans , Inflammation/immunology , Inflammation/pathology , Male , Middle Aged , Oral Hygiene , Reference Values , Single-Blind Method , Young AdultABSTRACT
AIM: To quantify reduced and oxidized glutathione (GSH and GSSG) levels in gingival crevicular fluid (GCF) of periodontitis patients pre-therapy (versus periodontally healthy controls) and ascertain whether successful non-surgical therapy alters glutathione levels. MATERIALS AND METHODS: Thirty-second GCF samples (6/subject) were collected on Periopaper() strips from starved, non-smokers (n=20; mean age 43.6 years) with chronic periodontitis, before and 3 months after non-surgical therapy, and periodontally healthy, age- and gender-matched controls (n=20). GSH and GSSG levels were determined using reversed-phase high-performance liquid chromatography with fluorescence detection. RESULTS: Lower concentrations of GSH (p<0.01) and GSSG (p<0.05) were detected in GCF from patients (pre- and post-therapy) than controls and treatment had no significant effect. Amounts per 30-second sample did not differ between patients and controls. However, the amount of GSSG per 30-second sample decreased in patients after therapy (p<0.05). Consequently, therapy increased the GSH:GSSG ratio (p<0.05) in patients compared with the controls (p=0.8). CONCLUSION: These data demonstrate high concentrations of GSH within GCF, which are compromised in chronic periodontitis. While therapy does not appear to fully restore GSH concentrations in GCF, it does restore the redox balance (GSH:GSSG ratio), suggesting that the abnormal redox balance arises secondary to oxidative stress resulting from periodontal inflammation.
