Dental plaque and calculus

Roy 52852
 Bacteria
In health, the bacteria are predominantly Gram
positive and include: streptococci (with
Streptococcus sanguis, S. oralis and S. mitis being
pioneer species), Neisseria, Nocardiaand
Actinomyces.
Milleri streptococci (S. anginosus, S. constellatus
and S. intermedius) are believed to contribute to
disease progression.
 Biofilm
A biofilm is any group of microorganisms in which
cells stick to each other and often these cells adhere
to a surface.
Mechanisms of pathogenicity

1. Colonise, achieved by:

Attaching to one or more surfaces: (i) adhesins
enable binding to host tissue, and (ii) co-aggregation to
bacteria attached to surface.
Multiplying using available nutrients.
Competing successfully against other species trying
to inhabit the site.
Defending itself from host defences.
2. Produce factors that damage the host tissue directly or
indirectly (by causing host tissue to damage itself).
3. Release and spread.
Relationship between Biofilm
and disease
Biofilm involved in a lot of type of microbial
infection in the body.
Such as dental plaque, gingivitis , chronic sinusitis,
middle-ear infection.
Less common but fatal disease like endocarditis,
infection in heart valves, infection in joint
prostheses. Because of the intrinsic resistance of
these structures to antibiotics and host defence
systems, such diseases are very difficult to treat
effectively.
 Dental Plaque.
Dental plaque is
a biofilm which
builds up on and
surrounding the
teeth. Plaque is
sticky and usually
colorless. It forms
every day on teeth.
Contents of plaque.
Plaque is formed by microorganisms embedded in
the matrix made up of saliva. Most of the
microorganisms are bacteria(mainly streptococcus
mutants and anaerobes). The anaerobes include
fusobacterium and actinobacteria . The
composition varies by the location of plaque.
Fusobacterium is a genus of anaerobic, Gram-
negative bacteria. Fusobacterium cause several
human diseases, including periodontal diseases.
How the plaque causes harm.
The microorganisms found in plaque are usually
seen in mouth at all times and are harmless. They
feed on many of the foods we eat. Carbohydrates
and sugars are their favorite. Plaque sticks to the
teeth. If not removed properly by tooth brushing it will
build up in thick layers. Those microorganisms which
are nearest to the tooth convert to anaerobic
respiration. In this stage they produce acids.
Bacteria in dental plaque
Dental plaque formation stage
Accumulation of a Dental
Plaque Biofilm
 Formation of the Pellicle
All surfaces in the oral cavity, including the hard
and soft tissues, are coated with a layer of organic
material known as the acquired pellicle. The pellicle
on tooth surfaces consists of more than 180
peptides, proteins, and glycoproteins, including
keratins, mucins, proline-rich proteins, histidine-rich
proteins, and other molecules that can function as
adhesion sites for bacteria. The salivary pellicle can
be detected on clean enamel surfaces within 1
minute after their introduction into the mouths of
volunteers.By 2 hours, the pellicle is essentially in
equilibrium between adsorption and detachment,
although further pellicle maturation can be
observed for several hours.
Initial Adhesion of Bacteria
The initial steps of transport and interaction with the
surface are essentially nonspecific. The proteins and
carbohydrates that are exposed on the bacterial
cell surface become important when the bacteria
are in loose contact with the acquired enamel
pellicle. The specific interactions between microbial
cell surface adhesin molecules and receptors in
the salivary pellicle determine whether a bacterial
cell will remain associated with the surface. Only a
relatively small proportion of oral bacteria possess
adhesins that interact with receptors in the host
pellicle, and these organisms are generally the most
abundant bacteria in biofilms on tooth enamel
shortly after cleaning. Over the first 4 to 8 hours, 60%
to 80% of bacteria present are members of the
genus Streptococcus.
Colonization and Plaque
Maturation
The primary colonizing bacteria adhered to the
tooth surface provide new receptors for
attachment by other bacteria as part of a process
known as coadhesion. Together with the growth
of adherent microorganisms, coadhesion leads to
the development of microcolonies and eventually
to a mature biofilm. Cellcell adhesion between
genetically distinct oral bacteria also occurs in the
fluid phase.
Different speciesor even different strains of a
single species have distinct sets of coaggregation
partners . Fusobacteria coaggregate with all other
human oral bacteria, whereas Veillonella spp.,
Capnocytophaga spp.and Prevotella spp. bind
with streptococci and/or actinomyces. Each newly
accreted cell becomes itself a new surface and
therefore may act as a coaggregation bridge to
the next potentially accreting cell type that passes
by. Many coaggregations between strains of
different genera are mediated by lectin like
adhesins and can be inhibited by lactose and other
galactosides or by amino acids such as L-arginine.
The significance of coaggregation in oral
colonization has been documented in studies of
biofilm formation in vitro as well as in animal model
studies.
Coaggregation
Coaggregation is a direct interaction. At least 18
genera from the oral cavity have shown some form
of coaggregation.All oral bacteria possess surface
molecules that foster some sort of cellcell
interaction .The initial stages of coaggregation or
coadhesion are essentially the same as the first
steps involved in bacterial binding to surfaces:
bacterial cells come into contact through passive
or active transport and bind weakly through
nonspecific hydrophobic, electrostatic, and van
der Waals forces.These steps can be dramatically
accelerated in vitro by vigorously mixing dense
suspensions of bacterial cells.Strong cellcell
binding is then determined by the presence of
adhesin proteins or carbohydrates on one partner
and complementary receptor proteins or
carbohydrates on the other.
Positive interactions

Fusobacterium nucleatum provides survival advantage of

other bacteria, for example: Porphyromonas gingivalis
Fusobacterium nucleatum reduces oxidative potential of
environment and provides protection for others anaerobic
bacteria
Positive interactions

Production of grow-factors for example:

fatty acids
analogues of K vitamin
hydrogen
Grow-factors can be used by another species of bacteria
Production of substances that expose receptors involved in
colonization
Negative interactions

Bacteria concurrency in substances for nutrition

Bacteria concurrency in receptors
Growth-inhibition substances, for example S. sanguis
inhibits growth A. actionomycetemcomitans
Synthesis of bacteriocins by A. actionomycetemcomitans
inhibits growth S. sanguis
Specific plaque hypothesis
The specific plaque hypothesis underlines the importance of
the qualitative composition of the resident microbiota. The
pathogenicity of dental plaque depends on the presence
of or an increase in specific microorganisms. This concept
encapsulates that plaque that harbors specific bacterial
pathogens may provoke periodontal disease because key
organisms produce substances that mediate the
destruction of host tissues. The association of specific
bacterial species with disease came about during the early
1960s, when the microscopic examination of plaque
revealed that different bacterial morphotypes were found
in healthy versus periodontally diseased.At about the same
time, major advances were made in the techniques used to
isolate and identify periodontal microorganisms.
These included improvements in procedures to
sample subgingival plaque, in the handling of
samples to prevent killing the bacteria, and in the
media used to grow the bacteria in the
laboratory.The result was a tremendous increase in
the ability to isolate periodontal microorganisms
and considerable refinement in bacterial
taxonomy.Acceptance of the specific plaque
hypothesis was spurred by the recognition of A.
actinomycetemcomitans as a pathogen in
localized aggressive periodontitis.These advances
led to a series of association studies focused on
identifying specific periodontal pathogens by
examining the microbiota associated with states of
health and disease in cross-sectional and
longitudinal studies.
 Non-specific plaque hypothesis
During the mid-1900s, periodontal diseases were thought to
result from an accumulation of plaque over time, eventually
in conjunction with a diminished host response and
increased host susceptibility with age. This theory, which is
called the nonspecific plaque hypothesis, was supported by
epidemiologic studies that correlated both age and the
amount of plaque with evidence of periodontitis. According
to the nonspecific plaque hypothesis, periodontal disease
results from the elaboration of noxious products by the
entire plaque flora. When only small amounts of plaque are
present, the noxious products are neutralized by the host.
Similarly, large amounts of plaque would cause a higher
production of noxious products, which would essentially
overwhelm the hosts defenses.
Several observations contradicted these
conclusions. First, some individuals with
considerable amounts of plaque and calculus as
well as gingivitis never developed destructive
periodontitis. Furthermore, individuals who did
present with periodontitis demonstrated
considerable site specificity with regard to the
pattern of disease. Some sites were unaffected,
whereas advanced disease was found in adjacent
sites. In the presence of a uniform host response,
these findings were inconsistent with the concept
that all plaque was equally pathogenic.
Dental calculus
Its the form of Hardened dental plaque

Caused by deposition of minerals form saliva and

gingival crevicular fluid in plaque.
The components of dental
calculus
It composed of inorganic (mineral ) and organic
(cellular and extracellular) components

Bacteria

Salivary proteins, milk proteins, and smoke

particles.
Stage of calculus formation
1. No calculus

2. Trace

3. Slight: about 1
mm or less.

4. Moderate: about
1~2mm

5. Heavy: grater the

2mm, may extend
over soft tissue.
Supragingival and
Subgingival calculus
Supragingival calculus
Its above the gum line.
Also called salivary calculus.
Can easily find on the buccal surface of maxillary
molars and on the lingual surface of the
mandibular incisors.
Colour: white or whitish yellow.
Obtain the nutrition from saliva and diet in oral
cavity.
Subgingival calculus
Calculus below the gum line.
Also called seruminal calculus.
Usually seen in proximal surfaces of tooth.
Colour: dark brown or green black
Acquires nutrition from gingival cervicular fluid
and host cells.
Differences between supragingival
and subgingival calculus.
Thank you for your
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