In our study too, despite the homogenous population, several species were site-specific, while others were subject-specific and undergo succession from health to disease. Hence, even a slight distinction in bacterial community at non-tumor and tumor sites has significance as the samples were from two adjoining sites of same OSCC subject. The underlying species-specific shift implicates alterations in bacterial colonization at tumor sites. The translocation of bacteria from oral cavity to cervical lymph nodes and more in metastatic than in uninvolved nodes in oral cancer patients has

been reported by Sakamoto et al. [35]. Conclusions Together, the results indicate that certain bacterial species/phylotypes detected in this study may play a role in triggering chronic inflammation in oral cavity and possibly be associated at different stages selleck chemical of cancer [95]. This may be due to disrupted oral mucosal surface allowing bacterial invasion and perhaps serve as point of entry to the regional lymph nodes [33, 35]. This indicates that though the bacterial biota were commensals of oral cavity and may become pathogenic when their balance is disturbed.

Microbial shift or dysbiosis has been implicated in some diseases due to unequal ratio of beneficial symbionts to pathogens [96]. This study recognized association of some new bacterial species, like J. ignava not detected earlier in tumor samples by culture- dependent

or independent methods. However, these studies were performed with limited sample XL765 nmr size. Therefore, further investigation with larger sample size using high throughput sequencing would validate these findings and broaden our perspective on bacterial association and oral cancer. Acknowledgements This work was supported by NIDCR Grants DE019178 and DE020891. Electronic supplementary material Additional file 1: Figure S1. Distribution of pentoxifylline relative abundance of classes detected by HOMD and RDP in tissue samples from non-tumor and tumor sites of OSCC subjects. (DOC 79 KB) Additional file 2: Figure S2. Distribution of relative abundance of order detected by HOMD and RDP in tissue samples from non-tumor and tumor sites of OSCC subjects. (DOC 100 KB) Additional file 3: Figure S3. Distribution of relative abundance of families detected by HOMD and RDP in tissue samples from non-tumor and tumor sites of OSCC subjects. (DOC 124 KB) Additional file 4: Figure S4. (a) Individual-based rarefaction; and (b) Rank abundance curves for bacterial species associated with non-tumor tissue and tumor tissue libraries. (DOC 80 KB) References 1. Bagan J, Sarrion G, Jimenez Y: Oral cancer: clinical features. Oral Oncol 2010,46(6):414–417.PubMedCrossRef 2. Rosenquist K: Risk factors in oral and oropharyngeal squamous cell carcinoma: a population-based case-control study in southern Sweden. Swed Dent J Suppl 2005, 179:1–66.PubMed 3.