Human viruses in periodontitis

Periodontitis affects the majority of adults worldwide (4), but relatively few patients receive adequate treatment for the disease (9). Conventional periodontal therapy includes a stabilization phase and a maintenance phase. Stabilization of the disease is accomplished by periodontal mechanical depuration and the removal of calculus and other biofilmretentive factors, and may involve adjunctive antimicrobial medication and ⁄ or surgery. The long-term goals in the maintenance stage are to have patients exercise proper plaque control and to commit to professional antimicrobial treatment in order to minimize the likelihood of a clinical relapse. Current periodontal therapy is successful in combating initial and moderate types of periodontitis, but may show limited efficacy in resolving late-stage disease. Optimal periodontal care is often impeded by the lack of patient cooperation and by affordability issues. Periodontal treatment can entail substantial costs attributed to direct healthcare expenses and to loss of income during the time of professional therapy. A greater understanding of the etiopathogeny of periodontal disease seems to be a prerequisite for the development of preventive and therapeutic strategies that are more efficacious and less burdensome for patients. The task of determining the periodontopathic importance of suspected disease determinants is hampered by difficulty in identifying the initial stage of periodontitis and in distinguishing between progressive and stable phases of the disease. Differences in case definitions and diagnostic methods also complicate the interpretation of epidemiological findings in periodontal research. Periodontitis typically occurs in otherwise healthy individuals and is statistically associated with various environmental and demographic factors (3). The disease can also be linked to rare immunogenetic defects or be part of systemic diseases that primarily affect nonoral tissues (75). It is not clear if some of the proposed risk factors for periodontal disease reflect true genetic or immunological variations, or merely poor healthseeking behavior related to socioeconomic factors, lifestyles or cultural differences. Microbiological culture and culture-independent molecular studies have identified more than 1,200 bacterial species (140) and 19,000 phylotypes (91) in the oral cavity. At least 400 bacterial species inhabit subgingival sites (141), but despite the long list of different bacteria in periodontitis, fewer than 20 species are considered to be major periodontal pathogens (175, 185). Healthy periodontal sites harbor a scant microbiota of predominantly gram-positive facultative bacteria, whereas periodontitis lesions contain a large variety of gram-negative anaerobic species (171). The shift in the periodontal microbiota with disease development is the result of a multifaceted interaction of microbial-specific traits, host immune responses and ecosystem-based factors. It is not known why fastidious gram-negative anaerobic bacteria outcompete common oral gram-positive bacteria, and why relatively few suspected periodontopathogens are surging in numbers in periodontitis sites. Periodontopathogenicity is assessed primarily on the basis of an elevated occurrence of a given bacterial species in advanced periodontitis lesions. However, many anaerobic bacteria benefit from proteinaceous components that are present in the gingival crevice fluid and may merely be secondary invaders of periodontitis sites. Also, the cross-sectional design of most bacteria–periodontitis association studies prevents the pathogenetic importance of specific microorganisms from being firmly established. An important exception to this is Aggregatibacter actinomycetemcomitans in localized aggressive (juvenile) periodontitis (184). As expected for a true pathogen, the subgingival counts of A. actinomycetemcomitans have, in longitudinal studies, shown a dramatic increase immediately prior to clinical attachment loss and a marked decrease at the time of disease remission (16, 64). Theories proposed so far to explain the etiopathogeny of periodontitis have not been able to