IADR Abstract Archives

High or Low Gingival Crevicular Fluid Response After Experimental Gingivitis

Objectives: Exudation of gingival crevicular fluid (GCF) after experimental gingivitis (EG) for one week is an initial response to biofilm accumulation, but a clinical response, gingival index (GI), usually takes 2 – 3 weeks. At 3 weeks, differences in biofilm microbiome composition indicate differences in GI (PMID:24646694), whereas at only 1 week, GCF exudation rates depend on how much lysine remains unconverted to cadaverine by lysine decarboxylase (LDC) in the biofilm, not on biofilm accumulation (PMID:22141361). The relationship to biofilm lysine content fits an arch-shaped quadratic regression curve in which GCF exudation rates at lysine extremes (<0.025 or >0.185 μmol/g) are half that in the middle (0.123±0.047 vs 0.253±0.093 uL/min). Individual rates lie exclusively above (strong) or below the regression line (weak). We therefore examined whether strong or weak GCF responses to biofilm lysine remaining from LDC action are another consequence of LDC activity, or whether an unrelated GCF response is involved.
Methods: A quadratic polynomial regression model was fitted using GCF exudation as the outcome. Significance of strong or weak GCF responder status (main effect), and its interactions with lysine content and lysine content-squared were determined using an F-ratio test with 3 degrees of freedom to compare the sum of squares explained by the independent terms relative to the sum of squares error.
Results: A much stronger fit of the parallel high and low responder curves (R2≥0.90) compared to the combined data (R2 =0.37) was found, indicating a highly significant difference between the curves (F Ratio 41.77, p<0.0001). Yet the interaction of high or low GCF responses with biofilm lysine and lysine-squared contents was not significant.
Conclusions: Two factors therefore determine a host’s GCF response to biofilm accumulation after 7 days of EG: a bacterial factor resulting from biofilm LDC depleting GCF lysine by conversion to cadaverine, and perhaps an intrinsic host alarmin response.
IADR/PER General Session
2018 IADR/PER General Session (London, England)
London, England
2018
2343
Periodontal Research-Pathogenesis
  • Levine, Martin  ( University of Oklahoma Health Science Center , Oklahoma City , Oklahoma , United States )
  • Keremi, Beata  ( Semmelweis University , Budapest , Central Hungary , Hungary )
  • Aresti, Mikaela  ( Semmelweis University , Budapest , Central Hungary , Hungary )
  • Szoko, Eva  ( Semmelweis University , Budapest , Central Hungary , Hungary )
  • Tabi, Tamas  ( Semmelweis University , Budapest , Central Hungary , Hungary )
  • Szabo, Csaba  ( University of Texas Medical Branch , Galveston, , Texas , United States )
  • Lohinai, Zsolt  ( Semmelweis University , Budapest , Central Hungary , Hungary )
  • Hungarian National Office of Research and Technology Grant ALAP2-9/2006, Hungarian Scientific Research Development & Innovation Office –NKFIH (K112364, T049708) & MinDent 1987 to Z. Lohinai; NIDCR Award 1R21DE14583 to M Levine.
    NONE
    Oral Session
    Periodontal Pathogenesis: Inflammation and Biomarkers
    Friday, 07/27/2018 , 02:00PM - 03:30PM