The Bacterial Etiology Of Destructive Periodontal Disease: Current Concepts

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The Bacterial Etiology Of Destructive Periodontal
Disease Current Concepts

• Sigmund S. Socransky and Anne D. Haffajee
• J periodontol 1992 63322-331
• Cecilia Perera O.
• Department of Perio

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Periodontal Disease

• Definition
• An inflammatory disease of the supporting tissues
  of the teeth caused by specific microorganism or
  group of specific microorganism, resulting in
  progressive destruction of the periodontal
  ligament and alveolar bone with pocket formation,
  recession or both.
• (Carranzas Clinical Periodontology 2002)

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Periodontal Structures

• Attachment Apparatus
• Cementum
• Bone
• PDL

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100 Years of Periodontal Microbiology

• The time line is divided into three phases
• Initial phase
• Specificity in the etiology of disease was the
  prominent concept
• A period of Disillusionament
• Non-specificity in bacterial etiology
• A return to the concept of specificity in the
  etiology of periodontal disease ( 1970s)

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100 years of Periodontal Microbiology

• 1960s
• Spirochete might be the cause of acute
  necrotizing ulcerative gingivitis (ANUG)
• Actinobacillus actinomycetemcomitans (A.A.)
  possible pathogen in localized aggressive
  periodontitis
• Porphyromonas Gingivalis suggested to be
  important in chronic periodontitis.

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100 years of Periodontal Microbiology
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Prospective Studies

• Haffajee, Socrasky, Smith, Dibart 1992
• 67 subjects
• Active disease state if gt 2.5 mm Attachment loss
• 14 species determined in SubGing samples
• 10 suspected pathogens
• 4 suspected beneficial species

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Complexity of the problem

• Technical difficulties
• Taking of the plaque samples
• Uncontaminated samples is extremely challenging
  to obtain
• Discriminating pathogens from those encountered
  is difficult
• Problems growing and maintaining the pathogens.

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Complexity of the Problem

• Inadequate understanding of Disease Pathogenesis
• Misclassification of the disease type and status
• Disease due to different species at different
  sites
• Consecutive episodes of disease due to different
  species
• Erroneous conclusion of samples taken from sites
  in remission
• Pathogens may result from the disease rather than
  the cause
• Two or more species act together and cause
  disease
• The carrier state of disease can represent a long
  lag phase prior to detection of disease
• Differences in clonal types

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Approach to Determining Etiologic Agents

• Kochs Postulates
• The agent must be routinely isolated from
  diseased individuals
• The agent must not be recovered from cases of
  other forms of disease or non-pathogenically
• Produce a similar disease when inoculated into
  susceptible laboratory animals

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Approach to Determining Etiologic Agents

• In recent years, periodontal researchers have
  extended Kochs postulates including
• Association
• Requires that suspected pathogenic species be
  more frequently detected and at higher level in
  cases than in the controls
• Elimination
• Successful therapy will diminish the level of a
  pathogen and halt disease progression
• Host response
• the organism must have high levels of serum,
  salivary and gingival crevicular fluid antibody
  against it in periodontally diseased subjects

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Approach to Determining Etiologic Agents

• Virulence factors
• the organism must be found to produce virulence
  factors in vitro which can be correlated with
  clinical histopathology
• Animal Pathogenicity
• the organism must mimic similar pathogenic
  properties in an appropriate animal model

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Evolving Concepts
Susceptible Host
Active Disease
Presence of Pathogens
Absence of Beneficial Species
Destructive Periodontal Disease
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Evolving Concepts

• Susceptible Host
• Impaired Neutrophils
• Inadequate or unregulated immunological response
• LPS Responsiveness
• AIDS
• Diabetes
• Smoking
• Drugs

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Evolving Concepts

• Presence of Pathogens
• A. actinomycetemcomitans
• T. forsythus
• E. corrodens
• F. nucleatum
• P. micros
• P. gingivalis
• P. intermedia
• C. rectus
• Selenomonas sp.
• Eubacterium sp.
• Spirochetes

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Evolving Concepts

• Absence of Beneficial species
• Actinomyces sp
• C. ochracea
• ? C. ochracea ? P. gingivalis
• Diminished attachment loss
• S. mitis
• S. mitis procduces H2O2
• Kills A. a.
• S. sanguis
• V. parvula

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Microbial Complexes in Subgingival Plaque

• Yellow
• Green
• Purple
• Orange
• Red

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Veillonella parvula Actinomyces odontolyticus
S. mitis S. oralis S. sanguis S. gordonii S.
intermedius
C. rectus C. showae E. nodatum F. nucleatum P.
intermedia P. micros P. nigrescens
P. gingivalis T. denticola T. forsythensis
Capnocytophaga spp. Eikinella corrodens A.
actinomycetemcomitans
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Role of Disease Susceptibility

• Microbial species unevenly distributed from
  subject to subject and from site to site
• Subjects with widespread disease had more sites
  showing new attachment loss than subjects with
  fewer affected sites at baseline
• Percentages of suspected pathogens is highest in
  subjects with localized destruction and lowest in
  widespread disease subjects
• Subjects with widespread disease and high levels
  of suspected pathogens had a greater number of
  active sites than subjects in other groups

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Bacterial interactions

• Different types of microorganisms existing in
  periodontal pockets may act synergistically to
  induce disease progression
• Bacterial interactions may be beneficial to the
  host

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Virulent Clonal Types of Pathogens

• Multiple clonal types within a pathogenic species
• Clonal types differ in pathogenicity (A.a.)
• Some clonal types are associated with health and
  others with disease

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Regulation by the Local Environment

• Strains of many species may turn virulence
  factors on/off, depending on the nature of
  their environment
• Temperature
• ? subgingival
• ? new attachment loss (appears)
• Iron
• Calcium
• Magnesium
• Osmolarity

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Conclusions

• For a disease to result from a pathogen
• Be a virulent clonal type
• Must possess chromosomal/extrachromosomal genetic
  factors to initiate disease
• Host must be susceptible to pathogens
• Pathogen must be in numbers sufficient to exceed
  threshold for the host
• Must be located in the right place
• Other bacterial species must foster or at least
  not to inhibit the process
• Local environment must be favorable to disease
  expression