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Evaluation of microbiota associated with Herpesviruses in active sites of generalized aggressive periodontitis.
Annali di Stomatologia 2017 April
Aims: The present study aimed to investigate microbial patterns associated with disease progression and coinfection by different Herpesviruses in generalized aggressive periodontitis (GAP).
Methods: Microbiological samples were obtained from active (AS) and non-active (n-AS) sites in 165 subjects affected by GAP and were analyzed for 40 bacterial species by the Checkerboard DNA-DNA Hybridization technique and for Herpes simplex 1 (HSV-1), Human Cytomegalovirus (CMV), and Epstein Bar virus (EBV) by PCR.Common Factor Analysis and Multiple Regression Analysis were applied to disclose specific microbial patterns associated with the three viruses.
Results: Herpesviruses were detected in 37.6% of subjects. Detection of each of the searched viruses was associated with specific patterns of subgingival biofilm in AS. Logistic regression analyses evidenced several virus/bacteria associations: i) EBV with Aggregatibacter actinomycetemcomitans ; ii) CMV with A. actinomycetemcomitans , Veillonella parvula, Parvimonas micra and Fusobacterium nucleatum subsp . polymorphum ; iii) HSV-1 with Porphyromonas gingivalis , Tannerella forsythia , Fusobacterium periodonticum and Staphylococcus aureus .
Conclusions: Microbiological data suggest that Herpesviruses are probably not mere spectators of disease progression and that specific patterns of subgingival plaque are correlated with the presence of different Herpesviruses.
Methods: Microbiological samples were obtained from active (AS) and non-active (n-AS) sites in 165 subjects affected by GAP and were analyzed for 40 bacterial species by the Checkerboard DNA-DNA Hybridization technique and for Herpes simplex 1 (HSV-1), Human Cytomegalovirus (CMV), and Epstein Bar virus (EBV) by PCR.Common Factor Analysis and Multiple Regression Analysis were applied to disclose specific microbial patterns associated with the three viruses.
Results: Herpesviruses were detected in 37.6% of subjects. Detection of each of the searched viruses was associated with specific patterns of subgingival biofilm in AS. Logistic regression analyses evidenced several virus/bacteria associations: i) EBV with Aggregatibacter actinomycetemcomitans ; ii) CMV with A. actinomycetemcomitans , Veillonella parvula, Parvimonas micra and Fusobacterium nucleatum subsp . polymorphum ; iii) HSV-1 with Porphyromonas gingivalis , Tannerella forsythia , Fusobacterium periodonticum and Staphylococcus aureus .
Conclusions: Microbiological data suggest that Herpesviruses are probably not mere spectators of disease progression and that specific patterns of subgingival plaque are correlated with the presence of different Herpesviruses.
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