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Herpesviral–bacterial interactions in periodontal diseases
Author(s) -
Slots Jørgen
Publication year - 2010
Publication title -
periodontology 2000
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.725
H-Index - 122
eISSN - 1600-0757
pISSN - 0906-6713
DOI - 10.1111/j.1600-0757.2009.00308.x
Subject(s) - tannerella forsythia , immune system , porphyromonas gingivalis , periodontitis , immunology , treponema denticola , virus , virology , medicine , microbiology and biotechnology , biology , honeysuckle , alternative medicine , pathology , traditional chinese medicine
Periodontitis is one of the most complex infectious diseases of the human body. Individual periodontal lesions may harbor millions of genomic copies of herpesviruses (179) as well as papillomaviruses, human immunodeficiency virus (HIV), human T-lymphotropic virus type 1, torquetenovirus, and hepatitis B and C viruses (190). Herpesvirus-infected periodontal sites tend to exhibit more breakdown than herpesvirus-free sites, and a herpesviral active infection is associated with an elevated risk of progressive periodontal disease (189). Furthermore, the oral cavity supports more than 700 bacterial species, and the periodontal pocket area harbors more than 400 bacterial species (148). Periodontopathic bacteria, such as Porphyromonas gingivalis and Tannerella forsythia, possess virulence factors involved in colonizing periodontal sites, neutralizing local host defenses and destroying periodontal tissues (78, 192). The host immune response attempts to control both pathogenic viruses and bacteria in periodontal sites. However, it is unclear if various immune mediators, such as certain cytokines and chemokines, exert primarily a protective or a destructive role in periodontal disease. Also, some immune mechanisms that are active against viruses may diminish antibacterial immune responses, and vice versa. It may be that periodontitis is the result of extensive and partly opposing immune responses against viral– bacterial combined infections (179). Major advances in the diagnosis, prevention and treatment of periodontitis probably depend upon a better understanding of the pathogenic infections and the associated host responses. This review article presents evidence that viruses and bacteria in aggregate produce a greater pathogenic effect than the sum of the individual agents, and discusses how the concept of a herpesviral– bacterial combined infection may change our understanding of the pathogenesis, and possibly the management, of destructive periodontal disease. Emphasis is placed on synergistic interactions between periodontal Epstein–Barr virus and cytomegalovirus, and major suspected periodontopathic bacteria.