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  • A. actinomycetemcomitans
  • Transcript

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