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Updated: Jul 14, 2026
Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network
Published on: February 16, 2016
Comparison of experimental gingivitis with persistent gingivitis: differences in clinical parameters and cytokine
R Deinzer1, U Weik, V Kolb-Bachofen
1Institute of Medical Psychology, University of Duesseldorf, D-40001 Düsseldorf, Germany. renate.deinzer@uni-duesseldorf.de
Background And Objective:
Experimental gingivitis has been studied extensively as a well-controlled laboratory model of gingivitis. It is unclear, however, how experimental gingivitis compares with persistent plaque and gingivitis in more naturalistic settings. The present study compares both conditions in a randomized controlled design.
Material And Methods:
Twenty-six students suffering from plaque and gingivitis were randomly assigned to either a persistent gingivitis or an experimental gingivitis condition. Subjects with persistent gingivitis continued their habitual (i.e. insufficient) oral hygiene behaviour, resulting in persistence of plaque and gingivitis. Experimental gingivitis consisted of initial prophylaxis and subsequent total neglect of oral hygiene. Crevicular interleukin-1beta and interleukin-8 and clinical data were assessed weekly.
Results:
After 4 wk, subjects with experimental gingivitis showed significantly more plaque accumulation (p = 0.005), higher interleukin-1beta (p = 0.037), and lower interleukin-8 (p = 0.043) concentrations than subjects with persistent gingivitis. Whereas in experimental gingivitis we observed considerable fluctuations in clinical and immunological parameters over the 4-wk period, persistent gingivitis was characterized by little fluctuation, indicating that we were monitoring an inflammatory steady state.
Conclusion:
The data indicate that conditions observed after 4 wk of experimental gingivitis are not comparable with persistent gingival inflammation in a naturalistic setting. Results are discussed with respect to current studies, indicating that chronic inflammation may reflect a stage of down-regulated pro-inflammatory response.
