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      A new causal model of dental diseases associated with endocarditis.

      Annals of periodontology / the American Academy of Periodontology
      Animals, Bacteremia, etiology, physiopathology, Chronic Disease, Dental Care, adverse effects, Endocarditis, Bacterial, epidemiology, prevention & control, Heart Valve Diseases, microbiology, Humans, Incidence, Risk Factors, Staphylococcal Infections, complications, Streptococcal Infections, United States

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          Abstract

          Infective endocarditis (IE) is a serious disease that is associated with dental diseases and treatment. The objective of this study was to summarize the epidemiological information about IE and reevaluate previous causal models in light of this evidence. The world biomedical literature was searched from 1930 to 1996 for descriptive and analytic epidemiological studies of IE. Multiple searching strategies were performed on 9 databases, including MEDLINE, CATLINE, and WORLDCAT. Results show that: 1) the incidence of IE varies between 0.70 to 6.8 per 100,000 person-years: 2) the incidence of IE increases 20 fold with advancing age: 3) over 50% of all IE cases are not associated with either an obvious procedural or infectious event 3 months prior to developing symptoms; 4) about 8% of all IE cases are associated with periodontal or dental disease without a dental procedure: 5) the time from the diagnosis of heart valve deformities to the development of IE approaches 20 years: 6) the median time from identifiable procedures to the onset of IE symptoms is about 2 to 4 weeks: 7) the risk of IE after a dental procedure is probably in the range of 1 per 3,000 to 5,000 procedures: and 8) over 80% of all IE cases are acquired in the community, and the bacteria are part of the host's endogenous flora. The synthesis of these data demonstrates that IE is a disorder with the epidemiological picture of a chronic disease such as cancer, instead of an acute infectious disease, with a long latent period and possibly several definable intermediates or stages. A new causal model is proposed that includes early bacteremias that may "prime" the endothelial surface of the heart valves over many years, and a late bacteremia over days to weeks that allows adherence and colonization of the valve, resulting in the characteristic fulminant infection.

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