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  • A. actinomycetemcomitans
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    1. 1. Debate over Bacteria as Etiologic Agents
    2. 2. <ul><li>R. S. Hirsch and N. G. Clarke. </li></ul><ul><ul><li>Rev Infect Dis 1989; 11: 707-715 </li></ul></ul>
    3. 4. <ul><li>Oral cavity: </li></ul><ul><ul><li>Densely populated by site-specific biofilm. </li></ul></ul><ul><ul><li>Progressively acquired. </li></ul></ul><ul><ul><li>Developed during the early months of life. </li></ul></ul><ul><ul><li>Oral sites: </li></ul></ul><ul><ul><ul><li>Different ecologic conditions. </li></ul></ul></ul><ul><ul><ul><li>Populated by different commensal bacterial groups. </li></ul></ul></ul>
    4. 5. <ul><li>Dense population of the oral surfaces provides a protective screen against potentially harmful bacteria. </li></ul><ul><li>These bacteria must compete for both site and nutrients. </li></ul>
    5. 6. <ul><li>Dual and paradoxical roles. </li></ul><ul><ul><li>Protection against pathogens. </li></ul></ul><ul><ul><li>Causation of chronic disease. </li></ul></ul><ul><ul><ul><li>Periodontal disease. </li></ul></ul></ul><ul><ul><ul><li>Caries. </li></ul></ul></ul>
    6. 7. <ul><li>To test the widely help assumption that severe localized periodontal lesions are infections caused by specific bacteria of the indigenous oral flora. </li></ul>
    7. 8. <ul><li>Gingivitis: </li></ul><ul><ul><li>Inflammation that is confined to the gingival tissues. </li></ul></ul><ul><li>Periodontitis: </li></ul><ul><ul><li>Inflammation of the supporting structures of the tooth. </li></ul></ul><ul><ul><li>O’Leary TJ et al. 1988. </li></ul></ul>
    8. 9. <ul><li>Is caused by nonspecific bacterial plaque (dental). Löe H et al. 1988 </li></ul><ul><li>Microbial colonization: </li></ul><ul><ul><li>Streptococcal sp </li></ul></ul><ul><ul><li>Gram + rods </li></ul></ul><ul><li>As plaque matures, its ecology becomes more complex: </li></ul><ul><ul><li>Specific proliferate (environment becomes suitable). Hardie & Bowden 1976 </li></ul></ul><ul><ul><li>Facultative. </li></ul></ul><ul><ul><li>Anaerobes (environment changes). Grant et al. 1988 </li></ul></ul>
    9. 10. <ul><li>The nonspecific plaque hypothesis. </li></ul><ul><ul><li>Emerged in 1960 s </li></ul></ul><ul><ul><li>Propose: accumulation of microbes at of below gingival margin. </li></ul></ul><ul><ul><li>The number rather than the type of bacteria was considered critical in triggering tissue destruction. </li></ul></ul><ul><ul><li>Theilade E. 1986 </li></ul></ul>
    10. 11. <ul><li>However, it soon became evident that the periodontal diseases failed to fit the nonspecific plaque hypothesis. </li></ul><ul><ul><li>It was observed that the distribution of plaque and gingivitis in most populations was widespread. </li></ul></ul><ul><ul><li>Severe destruction of alveolar bone occurred in localized areas. </li></ul></ul>
    11. 12. <ul><li>Is thought to result from the activity of mixed cultures of predominantly anaerobic gram-negative bacteria. Marsh PD 1986 </li></ul><ul><li>The association of specific microbial species with localized forms of disease has greatly strengthened the belief that the periodontal diseases are opportunistic infections. </li></ul><ul><li>Van Palenstein Helderman WH 1981; Slots J & Listgarten MA 1988 </li></ul>
    12. 13. <ul><li>The burst theory of the loss of periodontal attachment challenges the former idea that periodontitis was progressive. </li></ul><ul><li>Socransky SS, Haffajee AD, Goodson JM, Lindhe J 1984 </li></ul>
    13. 14. <ul><li>Longitudinal studies have measured attachment loss rates that are too fast or too slow to fit the continuously progressive model. </li></ul><ul><li>Grant et al. 1988 </li></ul>
    14. 15. <ul><li>Burst of disease activity: </li></ul><ul><ul><li>Brought under control (without Tx) by unknown mechanism. Grant DA et al. 1988 </li></ul></ul><ul><ul><li>Initiated by proliferation of one or more members of the subgingival biofilm. </li></ul></ul><ul><ul><li>Control of this process may occur by the host or by interaction of the biofilm with other microorganisms. </li></ul></ul>
    15. 17. <ul><li>Site-specific microbes cause localized periodontal lesions. </li></ul><ul><li>Fundamental conflict: </li></ul><ul><ul><li>Oral microbes can cause deep pockets. </li></ul></ul><ul><ul><li>Bacteria are unable to create an environment conductive to their proliferation. </li></ul></ul><ul><ul><li>All bacteria are able to flourish only when their required conditions already exist. </li></ul></ul>
    16. 18. <ul><li>1) Localized lesions are either created by site-specific bacteria; or </li></ul><ul><li>2) Populated by the oral bacteria selected by the conditions of a deep pocket that has been established by a different pathologic process. </li></ul>
    17. 19. <ul><li>All species of oral bacteria probably have access to a periodontal pocket. </li></ul><ul><li>Only those supported by pocket’s conditions are able to flourish and be identified. </li></ul><ul><li>Christersson LA, Genco RJ et al. 1985 </li></ul>
    18. 20. <ul><li>Anecdotal evidence for the inability of oral bacteria to promote periodontitis may be obtained from human experience: </li></ul><ul><ul><li>No form of human periodontal disease can be initiated or promoted by: </li></ul></ul><ul><ul><ul><li>Inoculation with bacteria; </li></ul></ul></ul><ul><ul><ul><li>Disease transmission; </li></ul></ul></ul><ul><ul><ul><li>When probing healthy sites after probing a severe lesion. </li></ul></ul></ul>
    19. 21. <ul><li>Those that are true pathogens not normally found in humans and that always cause disease when first experienced; </li></ul><ul><li>Bacteria indigenous to one habitat but that can cause disease when relocated to another site; </li></ul><ul><li>Commensal (indigenous) microbes that may occasionally promote disease if a change occurs in their habitat. </li></ul><ul><li>Sherris JC, 1984 </li></ul>
    20. 22. <ul><li>Neither commensal nor pathogenic bacteria have the facility to create environments suitable for their proliferation. </li></ul>
    21. 23. <ul><li>The assumption that untreated gingivitis generally progresses to periodontitis is unproven. Ivanyi L, Newman HN, 1986 </li></ul><ul><li>In fact, periodontitis is an unusual consequence of gingivitis. Cutress et al. 1982; Baelum et al. 1986; Lembarti et al. 1988; Gaengler et al. 1988 </li></ul><ul><li>The role of bacteria in the progression of gingivitis to horizontal or angular alveolar bone loss is not established. Kornam KS 1986 </li></ul>
    22. 24. <ul><li>With no evidence of: </li></ul><ul><ul><li>Intratissue bacterial multiplication; </li></ul></ul><ul><ul><li>Disease transmission between persons; or </li></ul></ul><ul><ul><li>Spread from diseased to healthy sites in affected patients. </li></ul></ul><ul><li>Aggressive periodontitis cannot be considered to be infectious. </li></ul><ul><li>There is no definitive evidence that it is a specific infection initiated by Aa. </li></ul>
    23. 25. <ul><li>Conventional views: </li></ul><ul><ul><li>Characteristics are used to classify oral microbes as periodontopathogens. </li></ul></ul><ul><li>Alternative views: </li></ul><ul><ul><li>Explanations account for the presence of periodontopathogens in angular alveolar lesions in concordance with the principles of medical microbiology. </li></ul></ul>
    24. 26. <ul><li>Specific bacteria are found in high numbers in periodontal pockets, whereas their numbers are low at healthy sites. Different species are associated with the different forms of periodontal disease. </li></ul><ul><li>The organisms show periodontopathogenicity in animal models. </li></ul>
    25. 27. <ul><li>3) Periodontopathogens have numerous virulence factors that enhance their colonization, disable host defenses, and cause tissue destruction directly or by activations of an inflammatory response. </li></ul><ul><li>4) The presence of antibodies to periodontopathogens antigens in serum, saliva, and gingival crevicular fluid in patients with severe periodontal lesions. </li></ul>
    26. 28. <ul><li>5) Antibody levels are low in periodontally healthy persons and in patients treated for periodontitis. </li></ul><ul><li>6) Therapy directed at elimination of periodontopathogens from diseased sites is usually followed by improvement in the clinical signs of disease. </li></ul>
    27. 29. <ul><li>Microbes are able to colonize and proliferate in only those sites that meet their nutritional and metabolic demands. </li></ul><ul><li>Animals models for testing periodontopathogenicity have failed to provide any evidence of a primary role for bacteria in human periodontal destruction. </li></ul><ul><li>Virulence factors enable bacteria to colonize deep periodontal defects by providing protection against host defenses. </li></ul>
    28. 30. <ul><li>The immune system may be triggered by contact with microbes through the ulceration of epithelium of the periodontal pocket. </li></ul><ul><li>No periodontal therapy can selectively eliminate specific bacteria from deep pockets. Mechanical therapy may disturb the subgingival ecosystem as a whole. The role of antibiotic therapy in the Tx of periodontitis concluded that no additional benefit could be measured over and above mechanical Tx in the long term. </li></ul>
    29. 31. <ul><li>The site has to exist before adapted microbes are able to colonize. </li></ul><ul><li>The conventional view of a gingival etiology for the initiation of angular alveolar lesion is inconsistent. Chronic dental diseases need to be incorporated into a chronic disease model in which the host defenses and their interaction with environmental agents determine the physiopathologic outcomes in the tissues. </li></ul>
    30. 32. Modified from Clarke NG, Hirsch RS. Personal Risk Factors for Generalized Periodontitis . J Clin Periodontol 1995, 22(2): 136-142