Debate over Bacteria as Etiologic Agents

R. S. Hirsch and N. G. Clarke.
Rev Infect Dis 1989; 11: 707-715

 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.

 Dense population of the oral surfaces provides a protective screen against potentially harmful bacteria.
 These bacteria must compete for both site and nutrients.

 Dual and paradoxical roles.
 Protection against pathogens.
 Causation of chronic disease.
 Periodontal disease.
 Caries.

 To test the widely help assumption that severe localized periodontal lesions are infections caused by specific bacteria of the indigenous oral flora.

 Gingivitis:
 Inflammation that is confined to the gingival tissues.
 Periodontitis:
 Inflammation of the supporting structures of the tooth.
O’Leary TJ et al. 1988.

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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

 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

 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.

 Is thought to result from the activity of mixed cultures of predominantly anaerobic gramnegative 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

 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

 Longitudinal studies have measured attachment loss rates that are too fast or too slow to fit the continuously progressive model.
Grant et al. 1988

 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.

 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.

1) Localized lesions are either created by sitespecific 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.

 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

 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.

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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

 Neither commensal nor pathogenic bacteria have the facility to create environments suitable for their proliferation.

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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

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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.

 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.

1) 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.
2) The organisms show periodontopathogenicity in animal models.

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.

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.

1) Microbes are able to colonize and proliferate in only those sites that meet their nutritional and metabolic demands.
2) Animals models for testing periodontopathogenicity have failed to provide any evidence of a primary role for bacteria in human periodontal destruction.
3) Virulence factors enable bacteria to colonize deep periodontal defects by providing protection against host defenses.

4) The immune system may be triggered by contact with microbes through the ulceration of epithelium of the periodontal pocket.
5) 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.

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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.

Modified from Clarke NG, Hirsch RS. Personal Risk Factors for
Generalized Periodontitis . J Clin Periodontol 1995, 22(2): 136-142