The Bacterial Etiology Of Destructive Periodontal Disease
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Transcript The Bacterial Etiology Of Destructive Periodontal Disease
Infectious agents causing periodontal
diseases
Periodontal Disease
Definition
An inflammatory disease of the supporting tissues
of the teeth caused by specific microorganism,
resulting in progressive destruction of the
periodontal ligament and alveolar bone with
pocket formation, recession or both.
Periodontal Structures
Attachment
Apparatus:
Cementum
Bone
Periodontal ligament
Periodontal Microbiology
1960’s
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.
Periodontal Microbiology
Complexity of the problem
Technical difficulties
Taking of the plaque samples
Uncontaminated samples
Laboratory diagnosis
Cultivation
Inadequate understanding of Disease
Pathogenesis
Misclassification of the disease type and status
Disease due to different species at different sites
Succesive episodes of disease due to different species
Mistaken conclusion of samples taken from sites in
remission
Complexity of the Problem
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
Approach to Determining Etiologic
Agents
Koch’s Postulates:
1) The agent must be routinely isolated from diseased individuals and
recovered from cases of other forms of disease or healthy individuals
2) The agent must be isolated as a pure culture
3) Produce a similar disease when inoculated into susceptible laboratory
animals
4) The agent must be re-isolated from infected animal
Approach to Determining Etiologic
Agents
In recent years, periodontal researchers have extended
Koch’s 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 stop
disease progression
Host response
the organism must have high levels of serum, salivary and gingival
fluid antibody against it in periodontally diseased subjects
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
Evolving Concepts
Susceptible Host
Active Disease
Presence of Pathogens
Absence of Beneficial Species
Destructive Periodontal Disease
Evolving Concepts
Susceptible Host
Impaired Neutrophils
Inadequate or unregulated immunological response
LPS Responsiveness
AIDS
Diabetes
Smoking
Drugs
Evolving Concepts
Presence of Pathogens
Actinobacillus actinomycetemcomitans
T. forsythus
Eikenella corrodens
Fusobacterium nucleatum
Peptostreptococcus micros
Porphyromonas gingivalis
Prevotella intermedia
Campylobacter rectus
Selenomonas sp.
Eubacterium sp.
Spirochetes
Evolving Concepts
Absence of Beneficial species
Actinomyces sp
Capnocytophaga ochracea
[] C. ochracea; [] P. gingivalis
Diminished attachment loss
S. mitis
S. mitis produces H2O2
Kills A. a.
Streptococcus sanguis
Veillonella parvula
Veillonella parvula
Actinomyces odontolyticus
S. mitis
S. oralis
S. sanguis
S. gordonii
S. intermedius
Campylobacter rectus
Campylobacter. showae
Porphyromonas
gingivalis
Capnocytophaga spp.
Eubacterium nodatum
Eikinella corrodens
Fusobacterium nucleatum
Treponema denticola
A. actinomycetemcomitans
Prevotella intermedia
Tannerella forsythensis
Peptostreptococcus micros
(Bacteroides forsythus )
Prevotella nigrescens
Microbial Complexes in Subgingival Plaque
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
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
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
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
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