## 1 Introduction  
Dental plaque is regarded as one of the most common biofilm-related infectious dental problems reported in public health settings [1]. Plaque formation can cause dental caries, periodontitis, and endodontic infections [2; 3], with resultant infections leading to dental decay. The public health problem of dental plaques and disease of dental caries are known to cut across all strata of the entire human population [4]. This has been attributed to the consumption of dietary free sugars (sucrose), either as additives or preservatives, and they are linked to biofilm induced tooth decay [5; 6]. The phenomenon of biofilm formation is complex with its control suggested to be a critical approach in curtailing the challenges faced by healthcare professionals [7]. Generally, dental plaques occur when the oral microbial pH is lowered, thereby creating the presence of increased acid producing and acid tolerant bacteria in a structurally and functionally organized biofilm formation [8]. Subsequently, as plague develops over time, the low pH becomes dominant and demineralizes the enamel and dentin [9]. The resultant plaque develops in such an ordered way that it is of a diverse microbial composition. As plague formation evolves over time, a low pH becomes dominant, demineralizing the enamel and dentin [9]. One of most common bacteria associated with dental plaques and a major contributor to the breaking down of tooth enamel, causing tooth decay, is _Streptococcus mutans_ (_S. mutans_) [9]. The ability to cause dental plaque biofilm by this bacterium has been attributed to glucansucrase, an enzyme secreted extracellularly by _S. mutans_. Glucansucrase is reported to use fermentable carbohydrates to form high molecular-weight sticky glucan that is associated with the pathogenesis of biofilm production [10]. Extracellular glucan is a critical virulent element of _S. mutans_ and can either be water soluble or insoluble contributing to the development of dental biofilm [11]. The main component of these virulent genes is three glucanttransferase enzymes (_gtfB_, _gtfC_, _gtfD_). They catalyze the synthesis of extracellular glucans in concert with fermentable carbohydrates, all of which are important as virulence factor in biofilm formation. Therefore, the pathogenicity of _S. mutans_ is dependent on the virulence elements that enable it to adapt to low oral pH due to its characteristic aciduricity property [12]. The virulence characteristics such as mass, viscosity, and stickiness creating an adherent environment for the bacterium to survive and thrive on teeth surfaces, thus contributing to the stability of structural dental plaque integrity [10; 11; 12]. In addition to this, glucans possess binding proteins, an example of which is the glucan binding protein B (_GbpB_) that facilitates the binding of bacteria to secreted glucans [13]. Furthermore, _S. mutans_ produces two-component signal transduction system protein, _ComDE_[14], known to regulate the expression of virulent gene elements. As an environmental sensor, downregulation of this gene will result in biofilm defects [15]. Currently, the treatment of dental biofilm involves the mechanical removal of the plaque and the use of antimicrobial mouthwash such as chlorhexidine. However, these agents are non-specific in their action, and hence disrupt the oral microbiome by targeting commensals. Their reported side effects include teeth discoloration and gingival epithelial cells cytotoxicity [16; 17]. In view of these treatment limitations, coupled with the emergence of bacterial resistance, alternative molecules of natural origin with potential antibacterial activity that have been used as remedies could be evaluated. A recent study reported a number of natural compounds, such as anthraquinones, apigenin, chitosan, \(\alpha\)-mangostin, and myricetin to exhibit anti-biofilm activities. According to the report, most of these products are not selective in their action [18].