Platelet aggregation promoted by biofilms of oral bacteria and the effect of mouth rinses in vitro

Abstract

Introduction: The purpose of this study was to observe platelet aggregation promoted by biofilms of Streptococcus sanguinis and Porphyromonas gingivalis and to evaluate the effect of two different mouth rinses on this process. Methodology: In the first experiment, the same amount of S. sanguinis, P. gingivalis, and the S. sanguinis + P. gingivalis mixed solution was added to an equivalent amount of platelet-rich plasma (PRP). Aggregation was measured using a recording platelet aggregometer. In the second experiment, S. sanguinis, P. gingivalis, S sanguinis + P. gingivalis mixed solutions were pretreated with either Listerine antiseptic mouth rinse or Xipayi mouth rinse for 3 minutes, 6 minutes, and 10 minutes, respectively. The same amount of solution was added to the PRP, and the inhibition of aggregation was measured. Results: In the first experiment, S. sanguinis and P. gingivalis were able to induce platelet aggregation. The aggregation rate of S. sanguinis + P. gingivalis was significantly lower than that of either S. sanguinis or P. gingivalis. In the second experiment, when S. sanguinis, P. gingivalis, and the S. sanguinis + P. gingivalis mixed solutions were pretreated with Listerine antiseptic mouth rinse for 3 minutes and Xipayi mouth rinse for 10 minutes, there was no significant platelet aggregation. Conclusions: Platelets could adhere to S. sanguinis or P. gingivalis, but when S. sanguinis was mixed with P. gingivalis, the aggregation rate was reduced significantly. Treatment with Listerine antiseptic mouth rinse or Xipayi mouth rinse inhibited the ability of the bacteria to induce platelet aggregation.

Oral hygiene might prevent cancer

“…S. gordonii, also amongst the common pathogens isolated from subjects with infective endocarditis, is ubiquitous within the human oral cavity. Two of their cell surface proteins mediate adherence and activation of platelets, binding to cellular fibronectin and vitronectin, and also promote formation of biofilms [ 141 , 142 ]. Platelet aggregation was promoted by biofilms of oral bacteria in vitro, including P. gingivalis [ 142 , 143 , 144 ].…”

“…Two of their cell surface proteins mediate adherence and activation of platelets, binding to cellular fibronectin and vitronectin, and also promote formation of biofilms [ 141 , 142 ]. Platelet aggregation was promoted by biofilms of oral bacteria in vitro, including P. gingivalis [ 142 , 143 , 144 ]. Interestingly, some commercially known antiseptic mouth rinses inhibited the aggregation [142] .…”

“…Platelet aggregation was promoted by biofilms of oral bacteria in vitro, including P. gingivalis [ 142 , 143 , 144 ]. Interestingly, some commercially known antiseptic mouth rinses inhibited the aggregation [142] . Other biofilm-associated and platelet-binding bacteria described are Aerococcus urinae and Enterococcus faecalis [ 145 , 146 ].…”

“…One is a systemic dissemination from the ulcerated gingival pockets into the bloodstream that allows P. gingivalis or F. nucleatum access to the colon. In this context a biofilm-platelet complex make sense [ 133 , 139 , 140 , 141 , 142 , 143 , 144 , 145 , 146 ]. These species have been implicated in other diseases such as adverse pregnancy outcomes including stillbirth, liver cirrhosis, and rheumatoid arthritis [151] .…”

Effects of the periodontal pathogens Porphyromonas gingivalis and Tannerella forsythia on platelets

“…Periodontal pathogens in the form of bioflims have been reported to induce platelet aggregation (Tu et al, 2016). More specifically, P. gingivalis been shown to induce both platelet aggregation and activation (Curtis et al, 1993b;Afrodite Lourbakos et al, 2001;Li et al, 2008;Assinger et al, 2012;Klarström Engström et al, 2015) which may suggest a possible role of periodontitis in CVD.…”