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Clinical concentrations of peroxidases cause dysbiosis in in vitro oral biofilms

Authors :
Marc Quirynen
Vera Slomka
Esteban Rodriguez Herrero
Tim Verspecht
Kristel Bernaerts
Nico Boon
Wim Teughels
Source :
Journal of Periodontal Research. 53:457-466
Publication Year :
2018
Publisher :
Wiley, 2018.

Abstract

Background and Objective Little is known about the initiation of dysbiosis in oral biofilms, a topic of prime importance for understanding the etiology of, and preventing, periodontitis. The aim of this study was to evaluate the effect of different concentrations of crevicular and salivary peroxidase and catalase on dysbiosis in multispecies biofilms in vitro. Material and Methods The spotting technique was used to identify the effect of different concentrations of myeloperoxidase, lactoperoxidase, erythrocyte catalase, and horseradish peroxidase in salivary and crevicular fluid on the inhibitory effect of commensals on pathobiont growth. Vitality–quantitative real-time PCR was performed to quantify the dysbiotic effect of the peroxidases (adjusted to concentrations found in periodontal health, gingivitis, and periodontitis) on multispecies microbial communities. Results Agar plate and multispecies ecology experiments showed that production of hydrogen peroxide (H2O2) by commensal bacteria decreases pathobiont growth and colonization. Peroxidases at concentrations found in crevicular fluid and saliva neutralized this inhibitory effect. In multispecies communities, myeloperoxidase, at the crevicular fluid concentrations found in periodontitis, resulted in a 1-3 Log increase in pathobionts when compared with the crevicular fluid concentrations found in periodontal health. The effect of salivary lactoperoxidase and salivary myeloperoxidase concentrations was, in general, similar to the effect of crevicular myeloperoxidase concentrations. Conclusions Commensal species suppress pathobionts by producing H2O2. Catalase and peroxidases, at clinically relevant concentrations, can neutralize this effect and thereby can contribute to dysbiosis by allowing the outgrowth of pathobionts.

Details

ISSN :
00223484
Volume :
53
Database :
OpenAIRE
Journal :
Journal of Periodontal Research
Accession number :
edsair.doi.dedup.....a37fcdbb9a524158b5287a5e27ae7519
Full Text :
https://doi.org/10.1111/jre.12534