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The Epidemiologic Triangle

The Triangle has three corners: Agent (microbe)


that causes the disease (the “what” of the
Triangle); Host (organism) harboring the disease
(the “who” of the Triangle); Environment (those
external factors that cause or allow disease
transmission (the “where” of the Triangle)
Host

Agent Envir.

Agent : is the cause of the disease.


Host : are organisms, usually humans or
animals, which are exposed to and
harbor a disease.
Environment: the favorable surroundings and
conditions external to the host that
cause or allow the disease to be
transmitted.

Disease-causing microbes are bacteria, virus, fungi,


and protozoa

In the center of the Triangle is time.


Time between when the host is infected and when
disease symptoms occur. Or, time may describe the
duration of the illness or the amount of time a
person can be sick before death or recovery occurs.
CAUSES OF CARIES
HOST- AGENT INTERACTION
• Bakteri di sulkus gingiva berinteraksi dengan sel-sel epitel ----►
pertahanan awal IgA yang banyak terdapat pada sel epitel----► LPS
dari bakteri yang melekat pada dinding sel epitel mengakibatkan
gingiva menjadi permiabel ----► sel epitel rusak ----► fbroblast
membentuk kolagen ----►bakteri mengeluarkan kolagenase ----►
kolagen dirusak ----► attachment loss ----►awal proses infamasi
----►netrofl masuk ke jaringan
• Interaksi LPS dengan sel epitel ----►sel epitel mensekresi IL-1β, TNF-
α, IL-6 dan IL-8
• Bakteri di sulkus gingiva berinteraksi dengan sel-sel epitel ----►
pertahanan awal IgA yang banyak terdapat pada sel epitel----► LPS
dari bakteri yang melekat pada dinding sel epitel mengakibatkan
gingiva menjadi permiabel ----► sel epitel rusak ----► fbroblast
membentuk kolagen ----►bakteri mengeluarkan kolagenase ----►
kolagen dirusak ----► attachment loss ----►awal proses infamasi
----►netrofl masuk ke jaringan
• Interaksi LPS dengan sel epitel ----►sel epitel mensekresi IL-1β, TNF-
α, IL-6 dan IL-8
CAUSES OF PERIODONTAL DESEASE

• The most common forms of human periodontal


disease are gingivitis and periodontitis.
• Gingivitis is defned as an infammation of the
gingiva. Gingivitis is reversible
• The defnition of periodontium includes
cementum, periodontal ligament, alveolar bone,
and the gingiva; and periodontitis includes loss of
attachment of periodontal tissues from the tooth
and net loss of alveolar bone height, while
regeneration after the destruction during
periodontitis is not predictably achievable.
- The role of dental plaque
The presence of bacteria in the oral cavity has
been known
- The bacterial etiology of periodontal diseases
has been explored for over 100 years, evolving
along with technologic advances in
identifcation and characterization.
- Early studies indicated that periodontal
diseases occurred in response to plaque mass
BIOFILM
- Cell–cell communication.
An important characteristic seen only in
bioflm associated bacteria is quorum sensing,
This process is mediated by two groups of
compounds known as autoinducer 1 and
autoinducer 2. Gram-positive and gram-
negative cells secrete molecules known as
autoinducer-2
- Gene transfer.
Bioflm-associated bacteria communicate with
each other by way of horizontal gene transfer. In S
mutans, quorum sensing is mediated by
competence-stimulating peptide. Genes of the
competence-stimulating peptide signaling system
(comC, comD, comE, and comX) are responsible
for multiple functions: bioflm formation,
competence (ability to accept foreign DNA), and
acid tolerance
- Antimicrobial resistance. The bioflm provides a
protected environment against antimicrobial
agents. The bioflm acts as a barrier to diffusion
due to the presence of neutralizing enzymes (b-
lactamase, IgA protease) and a diffusion-resistant
matrix.
- Cells in the bioflm can develop antibiotic
resistance from horizontal gene transfer and
mutations and by expressing efflux pumps.
- Thus, it has been argued that ‘‘bioflm inhibitory
concentration’’ is a more realistic estimate of
antimicrobial activity than the current measures [
- Regulation of gene expression.
Bioflm living has been shown to regulate gene
expression in certain bacteria. For example,
exposure of S gordonii to saliva results in the
induction of genes (sspA/B) that mediate host-
surface binding and coaggregation with
Porphyromonas gingivalis and Actinomyces.
Similarly, genes encoding glucan (gtf) and
fructan (ftf) synthesis are differentially
regulated in bioflm-associated S mutans
-The last decade or so has brought signifcant
advances to the understanding of periodontal
disease pathogenesis.
-The recognition of dental plaque as a bioflm; the
identifcation and characterization of genetic
defects that predispose to periodontitis; the role
of risk factors in disease susceptibility; and the
discovery of new host-derived cellular and
molecular mechanisms implicated in periodontal
tissue destruction.
-Many of these discoveries hold promise for the
future as foundation for the engineering of new
prevention and treatment modalities.

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