# _Stretococcus mutans_ Associated with Endo-Periodontal Lesions in Intact Teeh
## 4 Discussion  
Periodontal disease determines the exposure of anatomical communications between periodontal tissues and RC system. Alveolar bone resorption causes exposure and loss of cementing that exposes the dental tubules and allows bacterial entrance into the tooth [14]. \begin{table}
\begin{tabular}{l c c c c c c c c c c c c c c c c} \hline \hline  & **1** & **2** & **3** & **4** & **5** & **6** & **7** & **8** & **9** & **10** & **11** & **12** & **13** & **14** & **15** & **16** & **17** \\ \hline Tooth * & 33 & 41 & 16 & 32 & 27 & 15 & 28 & 28 & 46 & 36 & 31 & 17 & 33 & 42 & 25 & 26 & 36 \\ \hline \multicolumn{11}{c}{_S. mutans_ Cultivation and Biomolecular Investigation} \\ \hline _S. mutans_ & & & & & & & & & & & & & & & & & & & & \\ RC & \(-\) & \(++\) & \(-\) & \(+\) & \(-\) & \(++\) & \(++\) & \(-\) & \(+\) & \(-\) & \(+\) & \(-\) & \(+\) & \(-\) & \(-\) & \(++\) & \(-\) \\ RS & \(-\) & \(+\) & \(-\) & \(++\) & \(+\) & \(++\) & \(++\) & \(-\) & \(+\) & \(++\) & \(+\) & \(-\) & \(+\) & \(++\) & \(++\) & \(+\) & \(-\) \\ \hline \multicolumn{11}{c}{_S. mutans_ CBPs Genes Investigation} \\ \hline _cnm_ & & & & & & & & & & & & & & & & & & & \\ gene & & & & & & & & & & & & & & & & \\ RC & \(-\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(-\) & \(+\) & \(-\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) \\ RS & \(-\) & \(--\) & \(--\) & \(--\) & \(+\) & \(--\) & \(--\) & \(+\) & \(-\) & \(+\) & \(-\) & \(+\) & \(-\) & \(-\) & \(--\) & \(--\) \\ _cbm_ gene & & & & & & & & & & & & & & & & & \\ RC & \(-\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) \\ RS & \(-\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) & \(--\) \\ \hline \hline \end{tabular}  
* Type of tooth affected by EPL using FDI World Dental Federation notation. In the section “_S. mutans_ isolation and biomolecular investigation”: \(+=\) positive for the _S. mutans_ qPCR/no growth observed in traditional culture, \(++=\) positive for the _S. mutans_ qPCR/growth of _S. mutans_ isolate observed in traditional media and confirmed with biochemical identification. \(-=\) negative for the _S. mutans_ qPCR/no growth observed in traditional culture. In the section “_S. mutans_ CBPs genes investigation”: \(+=\) positive for the _S. mutans_ CBPs genes detection by specific PCR targeting the _cnm_ and _cbm_ genes, respectively. \(-=\) negative for the _S. mutans_ CBPs genes detection. RC: root canals; RS: root surface.  
\end{table} 
Table 1: _Streplococcus mutans_ and CBPs genes detection by cultivation method and qPCR and PCR, respectively, in teeth extracted from patients affected by EPL. Moreover, in severe periodontal disease where the depth of the periodontal pocket reach root apex, there is a direct communication between RC system and periodontal pocket with damage of neurovascular bundles and bacterial invasion from the pocket through the apex in the RC system. Over vascular supply, lateral and accessory canals may distribute bacteria and toxins from the periodontal apparatus into the dental pulp [15]. The formation of pathologic communication between the pulpal and periodontal tissues determines an EPL that can be classified according to periodontal probing, presence/absence of root damage and presence/absence of periodontitis. EPL can also be classified in three grades of severity. Grade 1 EPL presents a narrow deep (>6 mm) periodontal pocket that affects 1 tooth surface. In Grade 2 there is a wide, deep periodontal pocket in 1 tooth surface. In Grade 3, deep periodontal pockets are present in >1 tooth surface [4]. Primary involvement can originate from endodontic or periodontal tissues or with a combined origin. Pulpal pathology of periodontal origins is more controversial, because generally, negative caries teeth can present coronal leakages that make a clear diagnosis and etiopatho-genesis difficult.