Abstract
Dysbiosis in the periodontal microbiota is associated with the development of periodontal diseases. Little is known about the initiation of dysbiosis. It was hypothesized that some commensal bacteria suppress the outgrowth of pathobionts by H2O2 production. However, serum and blood components released due to inflammation can neutralize this suppressive effect, leading to the initiation of dysbiosis. Agar plate, dual-species and multi-species ecology experiments showed that H2O2 production by commensal bacteria decreases pathobiont growth and colonization. Peroxidase and blood components neutralize this inhibitory effect primarily by an exogenous peroxidase activity without stimulating growth and biofilm formation of pathobionts directly. In multi-species environments, neutralization of H2O2 resulted in 2 to 3 log increases in pathobionts, a hallmark for dysbiosis. Our data show that in oral biofilms, commensal species suppress the amounts of pathobionts by H2O2 production. Inflammation can neutralize this effect and thereby initiates dysbiosis by allowing the outgrowth of pathobionts.
Highlights
Promoting biofilm formation and inhibiting the adhesion of certain species[16]
It can be hypothesized that commensal bacteria suppress the overgrowth of pathobionts by H2O2 but some serum and blood components released during inflammation can neutralize this suppressive effect, leading to the initiation of dysbiosis
Hemin, serum, hemoglobin and peroxidase significantly lowered the inhibitory effect of commensal bacteria on P. intermedia, P. gingivalis and A. actinomycetemcomitans (Fig. 1)
Summary
Serum and blood components can have peroxidase activity[17]. This is of significance since these could interact with the H2O2 produced by commensal bacteria to suppress the outgrowth of pathobionts. It is known that absence of bleeding on probing is a good marker for periodontal stability[18]. It is shown that crevicular myeloperoxidase concentrations are highly correlated with periodontal disease severity[19]. It can be hypothesized that commensal bacteria suppress the overgrowth of pathobionts by H2O2 but some serum and blood components released during inflammation can neutralize this suppressive effect, leading to the initiation of dysbiosis. The objective of this study is to determine the neutralizing effect of serum, hemoglobin and hemin on the inhibitory effect of the commensal bacteria towards pathobionts
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