# A Potential \"Vitaminic Strategy\" against Caries and Halitosis
## 1 Introduction  
The oral cavity is one of the most complex environments in the human body due to the continuous variation of homeostasis conditions. Over 700 diverse bacterial species have been identified as potential colonizers of the oral niches [1, 2, 3]. The bacterial composition of the oral microbiota is responsive to different intrinsic and extrinsic factors. These intrinsic factors are not changeable by the host, related to genetic factors (e.g., ethnicity, gender, immune response, medical conditions, etc. ), characteristics of the oral cavity such as temperature and saliva composition (pH, buffer capacity, hormones, and secreted substances), and characteristics of adhesion surfaces (e.g., roughness of tooth surface). Extrinsic factors are modifiable by the host, related to the environment, habits and lifestyle, and regard hygiene, diet, the use of drugs, smoking, medications, sex, access to dental care, etc. [4, 5, 6, 7]. Intrinsic and extrinsic factors contribute, together with host aging, to colonization by different microbial pools of the oral cavity. As a result of this complex interaction, the balancebetween beneficial and pathogen species is continuously altered, passing from eubiosis to a dysbiosis state and, as a consequence, to the onset of oral pathologies such as caries, gingivitis, and periodontitis [2,4]. Innovative metagenomic approaches have greatly benefited researchers and clinicians to correlate the modulation of the diverse bacterial species in the oral cavity with all possible stimuli acting in this body environment [3,8]. Through sequencing methods, the relationships between beneficial and pathogenic species have been extensively studied, and the composition of the polymicrobial biofilms on teeth, gingiva, tongue surface, and other soft tissues has been deeply characterized [7]. As is now well known, the biofilm structure constitutes a protected sub-environment in which various bacterial species interact to protect themselves from possible surrounding perturbations, as a kind of \"mutualist survival strategy\" of the microbial community. This microbial assembly is quite difficult to inhibit and remove from the adhesion surface, and this is also verified for the biofilms formed in the oral cavity [9, 10, 11]. Indeed, the most common oral pathologies, such as plaque and dental caries, gingivitis, and periodontitis, are due to biofilm deposition [7,12]. The process of biofilm formation in the oral cavity occurs in three subsequent steps, i.e., first, adhesion to the surface; then, the colonization step; and finally, biofilm assemblage and maturation [13]. Diverse bacterial species participate in biofilm development as \"early\" or \"late\" colonizers [14]. The \"early\" colonizers are involved in the first two steps of biofilm formation. Because of their ability to bind salivary proteins, they adhere to hard or soft tissues, colonize the oral niches, and provide an adhesive substratum for the \"late\" colonizers [6,13, 14, 15]. The early colonizers belong mainly to the _Streptococcus_ genus. _S. mutans_ is the most represented species in supragingival plaque, childhood caries, and dental and root lesions. Due to its rapid metabolism and strong acid tolerance, it is recognized as the most carigenic bacteria in the oral cavity [6,12,13]. On the other hand, the Gram-negative anaerbe _F. nucleatum_, acting halfway between the early and late colonizers, can be considered a key player of the oral biofilm maturation stage. Due to its coating adhesion molecules and polysaccharide receptors, it co-aggregates both with the early and late streptococcal colonizers; these latter, mainly Gram-negative, anaerbes belong to the genera of _Bacteroides_ and _Spirocheates_[13, 14, 15]. In addition to this bridging role in the biofilm network, the enhanced prevalence of _F. nucleatum_ within the deep periodontal pockets suggests that this germ also plays an active role as a periodontal pathogen [16,17]. In this niche, _F.