These results support the notion that the clinical outcome of some types of severe periodontal infection depends on the presence of specific herpesviruses and bacterial pathogens. Our findings open the door to testing a variety of hypotheses regarding the deleterious aspects of combined herpesviral-bacterial infections in periodontal sites.

The elevated occurrence of HCMV and EBV DNA copies in periodontal pockets and in the gingival tissue of aggressive periodontitis lesions relative to chronic periodontitis lesions, and the increase in herpesvirus counts with increasing severity of periodontitis lend substantial support to a periodontopathic role of the two viruses. Real-time PCR determination of herpesvirus DNA in periodontal sites may become a promising marker to monitor the course of destructive periodontal disease. Herpesviruses and bacteria, now mostly studied in isolation, may cooperate synergistically in the development of periodontitis, and should probably be considered as a pathogenetic consortium in future investigations of periodontal infections.

The present study provides compelling evidence of a periodontitis source for salivary HCMV and EBV. The potential of periodontal therapy to decrease herpesvirus salivary counts may help diminish herpesvirus transmission from person to person and herpesvirus-related diseases in exposed individuals. Further research is warranted to determine the relationship between periodontal herpesvirus counts and the risk of viral transmission to close acquaintances.

Findings of the present study confirm the frequent presence of HCMV in crevicular samples of chronic periodontitis lesions, and suggest a strong relationship between the presence of HCMV and EBV-1 in subgingival areas and the measurements of probing depth and probing attachment loss.

The TaqMan real-time PCR technology seems to provide a rapid and sensitive method for quantifying HCMV in periodontal pockets. The present findings confirm the frequent presence of HCMV in aggressive periodontitis lesions. Determining HCMV levels in different types of periodontitis may help elucidate the periodontopathic role of the virus and advance our understanding of the disease pathogenesis.

HCMV and EBV-1 genomes are commonly found in periodontal abscesses. These data favor a model in which a herpesvirus infection of the periodontium impairs the host defense and serves as a platform for the entrance of bacterial pathogens into gingival tissue with subsequent risk of abscess development.

Hyaline or amyloid-like substances may be seen in several oral lesions. Some of these originate from epithelial cells and some from connective tissue components. In this study, amyloid-like material causing gingival enlargement in three patients, with eyelid involvement in two, was examined using histochemistry, immunohistochemistry and electron microscopy. These accumulations did not share the classical features of amyloid such as green birefringence under polarized light after Congo red staining. Our findings suggest that epithelial degeneration plays an important role in the pathogenesis of these amyloid-like accumulations. These substances may be the result of defective amyloidogenesis and our cases may represent an oral counterpart of ligneous conjunctivitis or colloid milium of the skin.

These findings indicate that subgingival presence of EBV-1 HCMV is strongly associated with aggressive periodontitis, and coinfection with HCMV and EBV-1 appears to be particularly deleterious to periodontal health.