The Importance of Bacteria in Periodontal Disease

1
The Importance of Bacteria in Periodontal Disease
???

• Debate over Bacteria as Etiologic Agents

2
Infection and Periodontal Diseases

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

3
Introduction
4
Infection and Periodontal Diseases

• 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
Oral sites

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

6
Oral microbes

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

7
Objective

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

8
Concepts

• Gingivitis
• Inflammation that is confined to the gingival
  tissues.
• Periodontitis
• Inflammation of the supporting structures of the
  tooth.
• OLeary TJ et al. 1988.

9
Gingivitis

• 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
Chronic Periodontitis

• 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
Deficiencies of Contemporary Periodontal Theory
17
Site-specificity

• 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
Two possible explanations for the presence of
specific bacteria in severe periodontal defects

• 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 pockets 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
Bacteria capable of inducing disease

• 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
Periodontitis

• 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
Aggressive Periodontitis

• 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
How to classify oral microbes as
periodontopathogens

• 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
Conventional views

• 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
Alternative views

• 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
Conclusions

• 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