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Herpesviruses in human periodontal disease
Author(s) -
Contreras Adolfo,
Slots Jørgen
Publication year - 2000
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1034/j.1600-0765.2000.035001003.x
Subject(s) - treponema denticola , prevotella intermedia , periodontitis , porphyromonas gingivalis , gingivitis , human cytomegalovirus , immunology , biology , treponema , actinobacillus , cytomegalovirus , human herpesvirus 6 , virology , herpesviridae , microbiology and biotechnology , medicine , virus , viral disease , dentistry , syphilis , human immunodeficiency virus (hiv)
Recent studies have identified various herpesviruses in human periodontal disease. Epstein–Barr virus type 1 (EBV‐1) infects periodontal B‐lymphocytes and human cytomegalovirus (HCMV) infects periodontal monocytes/macrophages and T‐lymphocytes. EBV‐1, HCMV and other herpesviruses are present more frequently in periodontitis lesions and acute necrotizing ulcerative gingivitis‐lesions than in gingivitis or periodontally healthy sites. Reactivation of HCMV in periodontitis lesions tends to be associated with progressing periodontal disease. Herpesvirus‐associated periodontitis lesions harbor elevated levels of periodontopathic bacteria, including Acrinobacillus actinomycetemcomitans , Porphyromonas gingivalis , Bacteriodes forsythus , Prevotella intermedia , Prevotella nigrescens and Treponema denticola . It may be that active periodontal herpesvirus infection impairs periodontal defenses, thereby permitting subgingival overgrowth of periodontopathic bacteria. Alteration between latent and active herpesvirus infection in the periodontium might lead to transient local immunosuppression and explain in part the episodic progressive nature of human periodontitis. Tissue tropism of herpesvirus infections might help explain the localized pattern of tissue destruction in periodontitis. Absence of herpesvirus infection or viral reactivation might explain why some individuals carry periodontopathic bacteria while still maintaining periodontal health. Further studies are warranted to delineate whether the proposed herpesvirus‐periodontopathic bacteria model might account for some of the pathogenic features of human periodontal disease.