# A Potential \"Vitaminic Strategy\" against Caries and Halitosis
## 1 Introduction
nucleatum_ stimulates the production of host matrix metalloproteinases, the increased levels of which concur to the initial periodontal inflammation in periodontal diseases [14]. This pathogen is also provided by significant hemolytic activity and, more interestingly, is the main producer of hydrogen sulfide (H\({}_{2}\)S) in the oral cavity. H\({}_{2}\)S, together with methyl mercaptan (CH\({}_{3}\)SH) and dimethyl sulfide (CH\({}_{3}\)SCH\({}_{3}\))\({}_{24}\), is one of the volatile sulfur compounds (VSCs) produced by periodonotrophic anaerobic bacteria and principally responsible for typical malador in halitosis [18, 19, 20, 21, 22]. Consistently, the uncomfortable phenomenon of halitosis is associated with an increase in VSCs producer species, principally _F. nucleatum_ but also _Porplyomonas gingivalis, Treponema denticola, Prevotella intermedia_, and _Eubacterium_[18,19,21,22]. On these assumptions, inhibiting _F. nucleatum_ in the oral cavity could represent an excellent double-sided strategy to reduce both the formation of the oral biofilm causative of oral diseases and the uneasiness of halitosis. An even more efficient approach to massively prevent/reduce oral pathologies could also be represented by the simultaneous inhibition of the main early colonizer, _S. mutans_. At present, rather than specific action against these key oral germs, lifestyle modulation and the use of innovative cosmetics are recognized as the only strategies to maintain a generally balanced microbiome in the oral cavity [2,4]. Indeed, mouthwashes and many dentistry products made by antimicrobial compounds, such as chlorhexiidine, triclosan, cetylpyridinium chloride, and chlorine dioxide, are often used against the oral biofilm to treat bad breath [19,20]. Nevertheless, the use of such products is more often associated with an increase in bacterial resistance, as well as with the undesirable killing of nonpathogenic commensal species and a dysbiosis state [23; 24]. Surely, the use of natural products is, at least conceptually, a more appreciable strategy to prevent and contrast oral pathologies, even more if these products can selectively impact the pathogenic species of the buccal microbiota. A potential \"natural therapy\" could also modify the applicability of the treatment, not only as curative but also as a preventive therapy, both in pediatric and old-aged patients. Natural derivatives such as propolis, cranberry, tea, _Galla chinensis_, grapes, coffee, and cacao-containing polyphenols have already demonstrated their activity against oral biofilms [20; 25; 26; 27; 28]. Similarly, hinokitiol, green tea powder, and eucalyptus extract have been beneficially used against oral malodor [19; 29; 30; 31]. Further, oxidative stress was found as an important causative factor of dysbiosis and oral disorders, and the action of diverse antioxidant substances against oral bacteria has also been studied. Fat-soluble vitamins (vitamin A, vitamin E-tocopherol and b-carotene), water-soluble vitamins (vitamin C and vitamin B complex), trace elements (zinc, magnesium), and bioflavonoids (plant derived) neutralize the reactive oxygen species (ROS) causative of many oral pathologies [32; 33; 34; 35; 36; 37; 38; 39]. These antioxidant compounds are generally consumed through fruits and vegetables, and they are maintained at an optimal level in individuals by a well-balanced diet [40; 41]. Conversely, the low quotes of these antioxidants found in individuals affected by oral diseases clearly suggest their potential role against oral pathogens [4; 32; 42]. Among all the known compounds, vitamin E is the major fat-soluble antioxidant in cell membranes [43; 44]. It exerts a considerable anti-inflammatory action and enhances the humoral immune response [43; 45; 46; 47; 48]. Its beneficial effect on oral health has already been documented through improvements in all periodontal parameters in patients treated with vitamin E (decrease in plaque and biofilm formation indexes, probing depth, clinical attachment level, and bleeding on probing) [32; 39; 42; 49].