Dental Plaque - Dentalstudymaterial Blog

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Transcript Dental Plaque - Dentalstudymaterial Blog

Dental Plaque
According to Bowden, Dental plaque can be
defined as the soft tissue deposits that form the
biofilm adhering to the tooth surface or on the
other hard surfaces in the oral cavity, including
removable and fixed restorations.
According to Marsh, Dental plaque can be
defined as the diverse community of
microorganisms found on the tooth surface as a
biofilm, embedded in an extracellular matrix of
polymers of host and microbial origin.
Dental plaque must be differentiated from other
tooth deposits, like materia alba and calculus.
Materia Alba refers to soft accumulations of
bacteria and tissue cells that lack the organized
structure of dental plaque.
Calculus is hard deposits that form by
mineralization of dental plaque and is generally
covered by a layer of unmineralised plaque.
Plaque can be defined as a complex microbial
community, with greater than 1010 bacteria per
milligram. It has been estimated that as many as 400
distinct bacterial species may be found in plaque.
In addition to the bacterial cells, plaque contains a
small number of epithelial cells, leukocytes, and
macrophages. The cells are contained within an
extracellular matrix, which is formed from bacterial
products and saliva.
The extracellular matrix contains protein,
polysaccharide, lipids and glycoproteins
Inorganic components are also found in dental
plaque; largely calcium and phosphorus which
are primarily derived from saliva.
The inorganic content of plaque is greatly
increased with the development of calculus.
The process of calculus formation involves the
calcification of dental plaque.
The practical consequences of calculus
formation are that the deposit is significantly
more difficult to remove once calcified, and it
leaves a rough surface on the root which is
easily colonized by plaque..
Dental plaque can be classified
in several different ways.
Plaque is classified as supragingival or subgingival based on its
relationship to the gingival margin. Supragingival plaque is
evident on the tooth above the gingival margin
Plaque can also be classified by its relationship to the tooth
surface, as either attached or unattached plaque.
The unattached subgingival plaque is more closely associated
with the wall of the subgingival tissues than is the attached
Lastly, plaque has been classified by association with disease
state as "health-associated" or "disease-associated".
The latter classification is related to differences in the microbial
composition of dental plaque in health versus disease.
Development of dental plaque
The development of dental plaque has been studied in
humans as well as non-human animal model systems.
One of the most commonly used models of plaque
development is referred to as the "experimental
gingivitis" model (Loe, et al., 1965).
This protocol involves the examination of subjects
(usually dental students!) who abstain from any oral
hygiene measures for a period of three weeks.
These studies have provided much information on the
structural and microbiological characteristics of dental
The pellicle is evident as lightly stained material on a
tooth surface when patients use disclosing solution.
A newly cleaned tooth surface is rapidly covered with
a glycoprotein deposit referred to as "pellicle".
The pellicle is derived from salivary constituents which
are selectively adsorbed onto the tooth surface.
Components of the dental pellicle include albumin,
lysozyme, amylase, immunoglobulin A, proline-rich
proteins and mucins.
The formation of pellicle is the first step in plaque
The pellicle-coated tooth surface is colonized by Gram-positive
bacteria such as Streptococcus sanguis, Streptococcus
mutans, and Actinomyces viscosus. These organisms are
examples of the "primary colonizers" of dental plaque.
Bacterial surface molecules interact with components of the
dental pellicle to enable the bacteria to attach or adhere to the
pellicle-coated tooth surface.
For example, specific protein molecules found as part of the
bacterial fimbria (hair-like protein extensions from the bacterial
cell surface) on both Streptococcus sanguis and Actinomyces
viscosus interact with specific proteins of the pellicle (the
proline-rich proteins) with a "lock and key" mechanism that
results in the bacteria firmly sticking to the pellicle-coating on
the tooth surface (Mergenhagen et al. 1987).
Within a short time after cleaning a tooth, these Gram-positive
species may be found on the tooth surface.
After the initial colonization of the tooth surface, plaque
increases by two distinct mechanisms:
the multiplication of bacteria already attached to the
tooth surface, and
the subsequent attachment and multiplication of new
bacterial species to cells of bacteria already present in
the plaque mass.
The secondary colonizers include Gram-negative
species such as Fusobacterium nucleatum, Prevotella
intermedia, and Capnocytophaga species. A key
property of these microorganisms appears to be the
ability to adhere to Gram-positive species already
present in the existing plaque mass. These organisms
would typically be found in plaque after 1 to 3 days of
After one week of plaque accumulation, other Gramnegative species may also be present in plaque.
These species represent what is considered to be
the "tertiary colonizers", and include Porphyromonas
gingivalis, Campylobacter rectus, Eikenella
corrodens, Actinobacillus actinomycetemcomitans,
and the oral spirochetes (Treponema species).
The structural characteristics of dental plaque in this
time period reveal complex patterns of bacterial cells
of cocci, rods, fusiform, filaments, and spirochetes.
In particular, specific associations of different
bacterial forms have been observed.
The structural interactions of the bacteria probably
are a reflection of the complex metabolic
interactions that are known to occur between
different plaque microorganisms.
One example of this is the production of succinic
acid from Campylobacter species that is known to
be used as a growth factor by Porphyromonas
gingivalis. Streptococcus and Actinomyces species
produce formate, which may then be used by
Campylobacter species.
Fusobacterium species produce both thiamine and
isobutyrate that may be used by spirochetes to
support their growth.
The metabolic and structural interactions between
different plaque microorganisms are a reflection of
the incredible complexity of this ecological niche.
Plaque in health and disease
The overall pattern observed in dental plaque development
is a very characteristic shift from the early predominance of
Gram-positive facultative microorganisms to the later
predominance of Gram-negative anaerobic microorganisms,
as the plaque mass accumulates and matures.
This developmental progression is also reflected in the shifts
in predominant microorganisms that are observed in the
transition from health to disease.
Studies of plaque taken from sites of health or disease and
examined either microscopically or by culturing have
demonstrated distinct differences in health versus diseaseassociated microbial populations.
Microscopic studies of plaque have examined the
presence of different morphological types
("morphotypes") of bacteria.
studies reveal an increase in the presence of motile
rods and spirochetal organisms in gingivitis and
periodontitis as compared to gingival health.
A major limitation of studies of bacterial morphotypes
is that many "health-associated" microorganisms are
indistinguishable from "disease-associated"
microorganisms (for example, Streptococcus species
and Porphyromonas gingivalis, respectively).
However, cultural studies also reveal characteristic
distinctions between health- and disease-associated
The percentage of Gram-positive rods and cocci
decrease in gingivitis- and periodontitis-associated
plaque as compared to health-associated plaque.
Similarly, the percentage of microbiota comprised of
Gram-negative anaerobic species is greatly
increased in gingivitis (approximately 25%) and
periodontitis (approximately 75%) as compared to
health (approximately 13%, Slots, 1979).
Specific microbial species that are important in
plaque development and disease development are
outlined below based on their categorization by cell
wall morphology (Gram-positive, Gram-negative, or
spirochetal) and their physiological status (facultative
or anaerobic).
Facultative Anaerobic Gram-Positive
Streptococcus mutans
Streptococcus sanguis
Actinomyces viscosus
Actinobacillus actinomycetemcomitans
Capnocytophypa species
Eikenella corrodens
Porphyromonas gingivalis
Fusobacterium nucleatum
Prevotella intermedia
Bacteroides forsythus
Campylobacter rectus
Treponema denticola
(Other Treponema species)
Relationship of Specific Microorganisms to
Periodontal Diseases
Our understanding of the relationship between the
microorganisms found in dental plaque and the
common dental disease of periodontitis has
undergone numerous phases historically
Early in the 19th century, it was felt that, like the
situation with diseases such as tuberculosis, a specific
bacterial species was responsible for the disease
The criteria by which a given bacterial species was
associated with disease historically has been through
the application of Koch's Postulates.
These criteria were developed by Robert Koch in
the late 1800's. The criteria are as follows:
A specific organism can always be found in
association with a given disease.
The organism can be isolated and grown in
pure culture in the laboratory.
The pure culture will produce the disease
when inoculated into a susceptible animal.
It is possible to recover the organism in pure
culture from the experimentally infected
Non-Specific Plaque Hypothesis
However, the concept that a specific bacterial
species was responsible for periodontal diseases fell
out of favor for several reasons. First, despite
numerous attempts, a specific bacterial agent was
not isolated from diseased individuals. Rather, the
organisms found associated with disease were also
found associated with health.
Good experimental animal model systems of
periodontal disease were not available to test the
pathogenicity of specific microorganisms (this, in fact,
remains problematic today).
Further, in the mid 1900's, epidemiological
studies indicated that the older an individual
was, the more likely they were to have
periodontal disease. This led to the concept that
the bacterial plaque itself, irrespective of the
specific bacteria found in plaque, was
associated with disease. This concept, known as
the Non-Specific Plaque Hypothesis (Loesche,
1976), held that all bacteria were equally
effective in causing disease.
Specific Plaque Hypothesis
Several important developments caused a change in
this thinking.
First, it was realized that organisms that are found as
part of the "normal" bacterial flora (i.e., found in
health), may function as pathogens under certain
conditions. These organisms may be altered, or
increase significantly in numbers relative to other nonpathogenic species, to function as pathogens.
This type of bacterial pathogen is referred to as an
endogenous pathogen, in contrast to an organism that
is not normally found in healthy states which is termed
an exogenous pathogen.
Secondly, tremendous advances were made in the
1960's and 1970's in techniques used to culture
anaerobic microorganisms (bacterial species that
cannot grow in the presence of oxygen).
These advances were related to the anaerobic
culturing conditions as well as the nutrients required in
media to grow anaerobic species, which are typically
very fastidious in their nutrient requirements
The growth of anaerobic microorganisms, and
examination of their properties using in vitro and in
vivo model systems, has now led us back to the
understanding that different microorganisms have
varying potential to cause disease.
Thus, the current concept of the processes involved in
the development of periodontal diseases fall under the
Specific Plaque Hypothesis (Loesche,1976
The Specific Plaque Hypothesis states that disease
results from the action of one or several specific
pathogenic species and is often associated with a
relative increase in the numbers of these organism
found in plaque.
A form of Koch's Postulates specifically oriented to the
situation in periodontal diseases has been proposed
by a microbiologist by the name of Socransky
(Socransky & Haffajee, 1992).
Socransky's criteria for periodontal pathogens are as
ASSOCIATION: A pathogen should be found more
frequently and in higher numbers in disease states
than in healthy states
ELIMINATION: Elimination of the pathogen should
be accompanied by elimination or remission of the
HOST RESPONSE: There should be evidence of a
host response to a specific pathogen which is
causing tissue damage.
VIRULENCE FACTORS: Properties of a putative
pathogen that may function to damage the host
tissues should be demonstrated.
ANIMAL STUDIES: The ability of a putative
pathogen to function in producing disease should be
demonstrated in an animal model system.
The two periodontal pathogens that have most
thoroughly fulfilled Socransky's criteria are
Actinobacillus actinomycetemcomitans in the
form of periodontal disease known as Localized
Juvenile periodontitis (LJP), and Porphyromonas
gingivalis in the form of periodontal disease
known as adult periodontitis.
Selected properties of these microorganisms
that have been associated with disease are
summarized in the following tables.
Evidence implicating Actinobacillus actinomycetemcomitans as
a periodontal pathogen(Adapted from Socransky, 1992)
Association Elevated in lesions of Juvenile Periodontitis, and
some lesions of Adult Periodontitis
Elevated in "active" Localized Juvenile Periodontitis (LJP)
Detected in apical region of periodontal pocket or in tissues of
LJP lesions
Unusual in health or gingivitis
Elimination Elimination associated with clinical resolution of
Species found in recurrent lesions
Host Response Elevated systemic and local antibody levels in
Juvenile Periodontitis
Virulence Factors Leukotoxin, collagenase, endotoxin,
epitheliotoxin, fibroblast inhibitory factor, bone resorptioninducing factor
Animal Studies Disease induced in gnotobiotic rats
Evidence implicating Porphyromonas gingivalis as a periodontal
pathogen (Adapted from Socransky, 1992)
Association Microorganism is elevated in periodontitis lesions
Unusual in health or gingivitis
Elimination Suppression or elimination results in clinical
Species found in recurrent lesions
Host Response Elevated systemic and local antibody in
Virulence Factors Collagenase, trypsin-like enzyme,
fibrinolysin, immunoglobulin degrading enzymes, other
proteases, phospholipase A, phosphatases, endotoxin,
hydrogen sulfate, ammonia, fatty acids and other factors that
compromise PMN function
Animal Studies Onset of disease correlated with colonization in
monkey model
Key role in mixed infections in animal models
Other species that have been implicated as
pathogens, including Fusobacterium nucleatum,
Prevotella intermedia, Eikenella corrodens,
Campylobacter rectus, Bacteroides forsythus, and
the oral spirochetes of the genus Treponema.
It is important to note that the disease processes
involve not only pathogenic microorganisms, but also
a susceptible host.
Further, many microorganisms function to the benefit
of the host, by inhibiting the growth of potential
pathogenic species. One example of such an
interaction is Streptococcus sanguis, which produces
hydrogen peroxide that is lethal for Actinobacillus
"Ecological Plaque Hypothesis"
The data from the mixed cultures studies described
above, and from other work, provide an argument for
plaque mediated diseases being viewed as a
consequence of imbalances in the resident microflora
resulting from an enrichment within the microbial
community of these "oral pathogens.".
Potentially cariogenic bacteria may be found naturally
in dental plaque, but these organisms are only weakly
competitive at neutral pH, and are present as a small
proportion of the total plaque community
In this situation, with a conventional diet, the levels of
such potentially cariogenic bacteria are clinically
insignificant,and the processes of de- and remineralization are in equilibrium.
If the frequency of fermentable carbohydrate intake increases,
then plaque spends more time below the critical pH for enamel
demineralization (approximately pH 5.5). The effect of this on
the microbial ecology of plaque is two-fold.
Conditions of low pH favor the proliferation of acid-tolerating
(and acidogenic) bacteria (especially mutans streptococci and
lactobacilli), while tipping the balance towards demineralization.
Greater numbers of bacteria such as mutans streptococci and
lactobacilli in plaque would result in more acid being produced
at even faster rates, thereby enhancing demineralization still
Other bacteria could also make acid under similar conditions,
but at a slower rate. These bacteria could be responsible for
some of the initial stages of demineralization or could cause
lesions in the absence of other (more overt) cariogenic species
in a more susceptible host.
If aciduric species were not present initially, then the repeated
conditions of low pH coupled with the inhibition of competing
organisms might increase the likelihood of successful
colonization by mutans streptococcior lactobacilli.
Key features of this hypothesis are that
(a) the selection of "pathogenic" bacteria is directly coupled to
changes in the environment and
(b) diseases need not have a specific etiology; any species with
relevant traits can contribute to the disease process.
Thus, mutans streptococci are among the best adapted
organisms to the cariogenic environment (high sugar/low pH),
but such traits are not unique to these bacteria. Strains of other
species, such as members of the S. mitis-group, also share
some of these properties and therefore will contribute to enamel
A key element of the ecological plaque hypothesis is that
disease can be prevented not only by targeting the putative
pathogens directly, e.g. by antimicrobial or anti-adhesive
strategies, but also by interfering with the selection pressures
responsible for their enrichment
Strategies that are consistent with the prevention of disease via
the principles of the ecological plaque hypothesis include the
(a) Inhibition of plaque acid production, e.g. by fluoride
containing products or other metabolic inhibitors. Fluoride not
only improves enamel chemistry but also inhibits several key
enzymes, especially those involved in glycolysis and in
maintaining intracellular pH. Fluoride can reduce the pH fall
following sugar metabolism in plaque biofilms,prevent the
establishment of conditions that favor growth of acid-tolerating
cariogenic species.
(b) avoidance between main meals of foods and drinks
containing fermentable sugars and/or the consumption of
foods/drinks that contain non-fermentable sugar substitutes
such as aspartame or polyols, thereby reducing repeated
conditions of low pH in plaque.
(c) the stimulation of saliva flow after main meals, e.g. by
sugar-free gum. Saliva will introduce components of the host
response, increase buffering capacity, remove fermentable
substrates, promote re-mineralization, and more quickly
return the pH of plaque to resting levels.
Benefits of dental plaque
They play a critical role in the normal development of
physiology of the host.
Germ free animals have altered mucosal surfaces, poor
nutrient absorption, suffer from nutritional deficiencies
and have impaired host defenses.
In mineralization of early carious lesions (white spot)
Resident microflora also reduces the risk of infection
by acting as a barrier to colonization by exogenous
species termed colonization resistance.
Reduction of colonization resistance can result in
overgrowth of minor components of microflora,
establishment of exogenous species which can lead to
pathological changes.
Plaque in children
In Children as in adults the cause of gingivitis is
plaque, local conditions and poor oral hygiene favor its
In preschool children the gingival response to bacterial
plaque has been found to be markedly less than that
in adults.
Dental plaque appears to form more rapidly in children
age 8 to 12 years than in adults
Calculus is uncommon in infants; it occurs approx
9%of children 4 to 6 years of age
In 18 % of those 7 to 9 years and in 33% to 43% of
those 10 to 15 years
Plaque as a biofilm
Biofilm is a well-organized ,co-operating
community of microorganisms. they form
under fluid conditions.
bacteria in the biofilms produce compounds
that the same bacteria do not produce in
cultures. also the matrix surrounding the
colonies acts as a protective barrier.
substances produced by bacteria within the
biofilm are retained and concentrated which
fosters metabolic interactions among the
different bacteria
Properties of a biofilm
cooperating community of various types of
microrganisms are arranged in microcolonies
microrganisms are surrounded by protective
within the micromolecules are differing
microrganisms have a primitive
communication system
microrganisms in biofilms are resistant to
antibiotics, antimicrobials and host response.
Significance of plaque as a biofilm
Some bacteria alter their pattern of gene expression when
cells encounter a surface. Attached cells up-regulate genes
associated with expolymer synthesis and can modify upto30%
of surface proteins
Increased resistance of biofilms to antimicrobial agents upto 21000 fold.
The surface of a biofilm may restrict the penetration of an
antimicrobial agent; some charged inhibitors can bind to
oppositely charged polymers that make up the biofilm matrix
Environment in the depth may be unfavorable for optimal
action of certain drugs
A susceptible pathogen may be rendered resistant if
neighboring cells produce a neutralizing or drug degrading
In addition biofilms provide an ideal environment for transfer of
resistance genes.
Despite tremendous increases in our understanding
of the pathogenic properties of specific plaque
microorganisms and the role of specific
microorganisms in the disease process, current
therapy in periodontics is largely non-specific.
The treatments that we utilize (e.g., oral hygiene
measures, debridement by scaling and root planning,
or even the currently available mouthwashes) are
oriented towards reducing the accumulation of plaque
on the teeth.
Future developments in periodontics will involve the
development of therapies which prevent the
colonization or growth of specific microorganisms that
are known to function as pathogens in this