Figure 4.

Oral biofilm infection model and proposed ABPs modes of action. (A) Dental caries infection model. In this model, some important factors are considered, including the use of newly weaned animals, pretreatment with antibiotics, confirmation of oral microbial depletion, and cariogenic diets in association with oral S. mutans infection. After the infection is confirmed, the topical treatment with ABPs is initiated. ABPs used in this model have been capable of preventing and eradicating biofilm-associated caries. ABPs can prevent tooth caries by inhibiting bacteria adherence to the tooth surface. In addition, ABPs also present direct antibacterial activity, significantly killing cariogenic pathogens before biofilm formation. When it comes to preformed biofilms, ABPs can interfere with the biofilm’s structure by avoiding EPS synthesis and reducing biofilm biomass. (B) Periodontitis murine model. Periodontitis mainly consists of inflammation of the periodontium due to biofilm formation. Particularly, S. gordonni and P. gingivalis have been shown to play a crucial role in this infection. Usually, the primary colonization of S. gordonni is followed by the infection with P. gingivalis, using carboxymethylcellulose (CMC) as a vehicle. P. gingivalis can also be used alone to induce oral infection. However, in this case, there is a subgingival thread in the first molars from the mice to allow biofilm formation. ABPs have demonstrated the ability to prevent biofilm formation by acting directly on free-floating bacteria or eradicating preformed biofilms. ABPs can also modulate cytokines regulation (e.g., IL-17, IL-1β, TNF-α), which significantly contributes to reducing alveolar bone loss, one of the main aggravating factors associated with periodontitis. All figures were made by the authors with a subscription version of BioRender.com.