Identification of inflammatory response patterns in experimental gingivitis studies

Abstract

We used novel analytical approaches to identify inflammatory response patterns to plaque accumulation in experimental gingivitis studies in humans. Data from two experimental gingivitis studies [Dataset I (n = 40) and Dataset II (n = 42)], which differed in design and recording methods, were used. Both studies comprised a three‐phase program as follows: pre‐induction period (oral hygiene as usual for Dataset I; professional tooth cleaning for Dataset II); induction period (plaque accumulation); and resolution period (oral hygiene as usual). Clinical recordings of plaque and gingival inflammation were made on days 0, 4, 9, and 14 for Dataset I and on days −14, 0, 7, 21, and 35 for Dataset II. Group‐based‐trajectory and growth curve modeling were used for data analysis. In Dataset I, gingival response to plaque accumulation was found to be lagged in time. Different group‐based response patterns for gingival inflammation were not identified. However, in Dataset II, ‘fast’ and ‘slow’ gingival inflammation responders were identified. ‘Slow’ responders had lagged inflammation responses, whereas ‘fast’ responders seemed to respond immediately to plaque. The findings show that analytical approaches which consider the data structure allow investigation of the dynamics of the relationship between plaque accumulation and gingival inflammation and facilitate the identification of differential patterns of gingival inflammation development.

To what extent does smoking affect gingival bleeding response to supragingival plaque? Site‐specific analyses in a population‐based study

“…Finally, the host‐dependent variation in gingivitis susceptibility should be considered. In several studies, a subject‐specific gingival inflammatory response has been reported, and “high and low responders” or “fast and slow responders” were identified …”

“…In several studies, a subject-specific gingival inflammatory response has been reported, and "high and low responders" 53 or "fast and slow responders" were identified. 54 With increased focus on the inflammatory nature of periodontitis, host modulation therapy is an emerging treatment strategy for managing periodontitis, aiming to control the inflammation in order to control the infection. 55 In this respect, smoking's effect on periodontal disease should be considered, where gingival inflammation is reduced, but periodontal destruction is enhanced.…”

Label‐Free Quantitative Proteomics versus Antibody‐Based Assays to Measure Neutrophil‐Derived Enzymes in Saliva

“…Overall, samples and data of ten individuals (6 females, 4 males, mean age 23.1 y (range: 21–24 y) from the original study were included in the current study. Figure illustrates TQHPI and MGI scores ( n = 50) during the I‐ and R‐phases, with mean (± SD) TQHPI of 0.1 ± 0.1, 1.3 ± 0.2, 2.2 ± 0.4, 2.9 ± 0.4, and 0.6 ± 0.3, and MGI of 0.0 ± 0.0, 0.5 ± 0.1, 1.3 ± 0.3, 1.9 ± 0.1, and 0.3 ± 0.4, respectively on day 0, +7, +14, +21, and +35.…”

“…The current study included a subset of participants ( n = 10) from a larger human experimental gingivitis study conducted between 2015 and 2016 at the Department of Dentistry and Oral Health, Aarhus University . The study was ethically approved by the Ethics Committee of Central Denmark (number 1‐10‐72‐402‐14) according to MOUTH guidelines as described earlier .…”

“…Fifty saliva samples, collected from ten individuals at day 0, +7, +14, +21, and +35 between 8 and 10 a.m. and after fasting for 2 h prior to the sample collection were selected from the entire cohort and stored at − 80 °C until analysis . For further analysis, whole saliva samples were thawed on ice and centrifuged at 4000 rpm (5943 g , 4 °C, 20 min) to separate saliva supernatants (SN) from pellets.…”