# _Stretococcus mutans_ Associated with Endo-Periodontal Lesions in Intact Teeh
## 1 Introduction  
The oral cavity houses the second largest and most complex microbial communities after the gut, harboring about \(10^{10}\) microorganisms [1]. It hosts a huge variety of microorganisms, which include bacteria, fungi, viruses, and protozoa. The mouth, which has a large composition of ecology, is a sophisticated ecosystem where microbes could colonize the hard surfaces of the teeth and the soft tissues of the oral mucosa [1, 2]. Moreover, the resident bacterial species cannot arrive to the pulpal tissues thanks to the external hard tissues and may become pathogenic only after they breach the barrier of the commensals, causing infection and disease [3]. Therefore, the pulpal tissue of healthy subjects is sterile. However, in pathological situations, which can affect the enamel and/or the the ementrum, the pulpo-dential complex could be exposed to the bacterial aggression, and it could be placed at risk of colonization and infection [3]. Caries are the most common cause of pulp exposure and subsequent endodontic bacterial infection, resulting from a complex interaction of specific host immunity, bad oral care and hygiene, diet, and resident microbial composition [1, 3]. Moreover, a massive periodontal destruction can secondarily affect the root canal (RC), forming a pathologic communication between pulpal and periodontal tissues with the proliferation of bacteria, which can result in pulpal inflammation and necrosis. Periodontal and endodontic tissues have strict anatomical correlation through lateral and accessory canals, apical foramen, and dental tubules, where bacteria may migrate from one tissue to the other [4]. Over local manifestations and loss of tooth-periodontiumintegrity, periodontal and endodontic infections may evolve into potential life-threatening infections such as abscesses or disseminating infections with systemic involvement, especially in some categories of patients (immunocompromised subjects, with high risk of infective endocarditis, patients with organic dysfunctions) [5; 6]. _Streptococcus mutans_ is generally considered to be a major pathogen of human caries [7] and is also involved in periodontal diseases [8]. _S. mutans_ strains are classified into serotypes c, e, f, and k on the basis of the biochemical composition of serotype-specific polysaccharides. From the literature, it is known that approximately 70-80% of strains found in the human oral cavity are classified as serotype c, followed by the serotype e (~20%), and the serotypes f and k (less than 5% each) [7]. The virulence of _S. mutans_ as a dental pathogen mostly resides in its ability to (i) adhere and form biofilms on tooth surfaces, (ii) produce large quantities of organic acids, and (iii) tolerate low pH and oxidative stress. The oral host tissue attachment could be due to a group of glycoproteins, which act as a cell surface protein antigen, recognized to have a collagen-binding activity [9]. The most described collagen-binding proteins (CBPs), described only in the _S. mutans_ strains, are the Cnm and Cbm proteins [10]. These act as adhesins, i.e., they have the ability to adhere to type I collagen, thus promoting the biofilm formation, the development, and the duration of the periodontal pathologies [11]. In addition, _S. mutans_ strains can became invasive, and the _cnm_ gene is required for _S. mutans_ adherence to endothelial and epithelial cells and intracellular invasion, also being an important virulence factor for systemic disease secondary to bacteremia such as endocarditis [10; 11; 12]. The distribution frequency of the strains carrying the _cnm_ gene among oral isolates has been estimated to be approximately 10-20% and the detection of _S. mutans_ in the oral sites has been subject of interest, not only due to its primary role in caries onset but also due to its association with extra-oral infections.