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A previous longitudinal study about using microbiome as a caries indicator has successfully predicted early childhood caries (ECC) in healthy individuals, but there is no evidence to verify the composition of core microbiota and its pathogenicity in vitro and in vivo. Biofilm acidogenicity, S. mutans count, and biofilm composition were estimated by pH evaluation, colony-forming unit, and quantitative PCR, respectively. Extracellular polysaccharide production and enamel demineralization were observed by confocal laser scanning microscopy (CLSM) and transverse microradiography (TMR), respectively. A rat caries model was established for dental caries formation in vivo, and caries lesions were quantified by Keyes Scoring. We put forward that microbiota including Veillonella parvula, Fusobacterium nucleatum, Prevotella denticola, and Leptotrichia wadei served as the predictors for ECC may be the core microbiota in ECC. This study found that the core microbiota of ECC produced limited acid, but promoted growth and acidogenic ability of S. mutans. Besides, core microbiota could help to promote the development of biofilms. Moreover, the core microbiota enhanced the enamel demineralization in vitro and increased cariogenic potential in vivo. These results proved that core microbiota could promote the development of dental caries and plays an important role in the development of ECC.

Background Oral squamous cell carcinoma (OSCC) is the most common tumor in the oral cavity. Methicillin-resistant Staphylococcus aureus (MRSA) were highly detected in OSCC patients; however, the interactions and mechanisms between drug-resistant bacteria (MRSA) and OSCC are not clear. Aim The aim of this study was to investigate the promotion of MRSA on the development of OSCC. Methods MRSA and MSSA (methicillin-susceptible) strains were employed to investigate the effect on the proliferation of OSCC in vitro and vivo . Results All of the MRSA strains significantly increased the proliferation of OSCC cells and MRSA arrested the cell cycles of OSCC cells in the S phase. MRSA activated the expression of TLR-4, NF-κB and c-fos in OSCC cells. MRSA also promoted the development of squamous cell carcinoma in vivo. The virulence factor fnbpA gene was significantly upregulated in all MRSA strains. By neutralizing FnBPA, the promotions of MRSA on OSCC cell proliferation and development of squamous cell carcinoma were significantly decreased. Meanwhile, the activation of c-fos and NF-κB by MRSA was also significantly decreased by FnBPA antibody. Conclusion MRSA promoted development of OSCC, and the FnBPA protein was the critical virulence factor. Targeting virulence factors is a new method to block the interaction between a drug-resistant pathogen and development of tumors.