Khadija. K.

Al-Dulaimy Microbiology /College Of Dentistry

B.Sc., M.Sc., Med. Microbiol. Al- Anbar University

Dental plaque and Dental caries.

Dental plaque is a general term for the complex microbial community

that develops on the tooth surface, embedded in a matrix of polymers of
bacterial and salivary origin. Plaque is composed of organic, inorganic
materials derived from saliva, gingival crevicular fluid & bacterial
products. The organic constituents of plaque include polysaccharides,
proteins, glycoproteins & lipid material. The inorganic constituents of
plaque include primarily of calcium & phosphorus & traces of sodium,
potassium. Plaque that becomes calcified is referred to as calculus or
tartar. The majority of plaque is found associated with the protected and
stagnant regions of the tooth surface such as fissures, approximal regions
between teeth, and the gingival crevice .

Plaque causes cavities when the acids from plaque attack teeth after
eating. With repeated acid attacks, the tooth enamel can break down and a
cavity may form. Plaque that is not removed can also irritate the gums
around the teeth, leading to gingivitis (red, swollen, bleeding gums),
periodontal disease and tooth loss.

 Specific plaque hypothesis states that, not all plaque is pathogenic

and its pathogenicity depends on the presence of certain specific
microbial pathogens in the plaque.

Types of Dental Plaque:

Dental plaque is broadly classified based on its position as:
a) Supragingival plaque: is found at or above the gingival margin
b) Sub gingival plaque: is found below the gingival margin.

The process of plaque formation can be divided into three phases:

a) Formation of Dental Pellicle
b) Initial colonization of bacteria
c) Secondary colonization & plaque maturation.

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 What is Dental Pellicle?
Pellicle is a glycoprotein, derived from components of saliva and
crevicular fluid as well as from bacteria and host tissue cell products and
debris. Pellicle is formed on all surfaces of the oral cavity, including all
tissue surfaces as well as surfaces of teeth and fixed and removable
restorations if any. Pellicle functions as a protective barrier but pellicle
provides a substrate on which bacteria progressively accumulate to form
Dental Plaque. Pellicle provides a medium or base on which bacteria in
the oral cavity attach. Pellicle gets easily stained & may display many
colors ranging from white to dark brown due which the teeth appear
discolored.

Mechanism of Pellicle formation:

The enamel surface has predominance of negatively charged phosphate
groups that interact directly or indirectly with positively charged
components of salivary & crevicular fluid macromolecules. Within few
hours bacteria are found on the pellicle. These initial bacteria colonizing
the pellicle-coated tooth surface are predominantly gram-positive
microorganisms such as Actinomyces viscosus & Streptococcus sanguis.
These initial colonizers adhere to the pellicle through specific molecules
termed adhesins, on the bacterial surface that interact with receptors in
dental pellicle. The major constituents of pellicle are salivary
glycoproteins, phosphoproteins and lipids, including statherin, amylase,
proline-rich peptides (PRPs) .For example, cells of Actinomyces viscosus
possess fibrous protein structures called Fimbriae that extend from the
bacterial cell surface. Protein adhesins on these Fimbriae specifically bind
to proline-rich proteins that are found in dental pellicle, resulting in the
attachment of the bacterial cell to the pellicle-coated tooth surface.
The plaque mass then matures through the growth of attached species as
well as colonization & growth of additional species. Microorganisms are
generally transported passively to the tooth surface by the flow of saliva;
few oral bacterial species are motile (e.g. possess flagella), and these are
mainly located subgingivally. Plaque may be readily visualized on teeth
after 1 to 2 days with no oral hygiene measures. Plaque is white, grayish
or yellow & has a globular appearance. With good oral hygiene practices
one can remove this pellicle & plaque layers. There are different types of
treatments which are extensively aim at removal of plaque &stains;
patient friendly methods are practically more acceptable than clinical
treatment .Certain chemical toothpastes remove stains by altering the
surface environment of the teeth thereby inhibiting the adherence of
plaque. For example hydrogen peroxide in the toothpaste acts by
releasing nascent oxygen, abrasive characteristic of baking soda or silica
is said to cleanse the tooth surface. Some toothpaste contains specific

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enzymes which are believed to remove plaque, stain & thereby improving
the gingival health. These toothpastes are biologically compatible with
the tooth surface & the surrounding soft tissues.

the initial colonizers constitute a highly selected part of the oral

microflora. Within minutes, coccal bacteria appear on the surface , and
these pioneer organisms are mainly streptococci, especially members of
the mitis-group of streptococci(e.g. S. sanguinis, S. oralis and S. mitis
biovar ) . Streptococcus sanguinis and S. oralis produce an IgA1 protease
which may help them to survive and overcome a key element of the host
defences during the early stages of plaque formation. Actinomyces spp.
are also commonly isolated after 2 hours, as are Haemophilus spp. and
Neisseria spp., while obligately anaerobic species are detected only rarely
at this stage and are usually in low numbers. Some aggregates of mixtures
of cells may also attach .Once attached, these pioneer populations start
to divide and form microcolonies; these early colonizers become
embedded in bacterial extracellular slimes and polysaccharides together
with additional layers of adsorbed salivary proteins and glycoproteins.
The early streptoccocal colonizers (mitis-group of streptococci) possess a
range of glycosidase activities that enable them to interact and use
salivary glycoproteins as substrates . The fastest rates of multiplication
occur during these early stages of plaque formation.

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The initial bacteria that colonize the pellicle surface are mostly;

 gram+ve
 Facultative microorganism such as actinomyces viscosus and
streptococcus sanguis.

The adhesion of organisms to the ‘conditioned’ tooth surface is a

complex process involving, initially, weak electrostatic attractive
forces, followed by a variety of specific molecular interactions
between bacterial adhesins and receptors adsorbed to the surface
(acquired pellicle). These latter processes together with the synthesis
of extracellular polysaccharides (EPS) from, for example, sucrose
serve to increase the probability of permanent attachment. EPS also
contributes to the plaque matrix. Pioneer species interact directly with
the acquired pellicle while subsequent biofilm formation is dependent
on intra and intergeneric coadhesion between bacteria (involving
lectin-mediated binding) and the subsequent growth of the attached
microorganisms. If conditions become unfavourable, some cells are
able to actively detach,
providing the opportunity to
colonize other sites.

The pattern of plaque biofilm

development can be divided
into three phases:
1. Attachment of bacteria to a
solid surface;
2. Formation of microcolonies
on the surface; and
3. Formation of the mature,
subgingival plaque biofilms.
The bi adhere to the previously
attached cells. The bacteria
cluster together to form
sessile,mushroom-shaped micro
colonies that are attached to the
tooth surface at a narrow base.

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In particular, specific associations of different bacterial forms have been
observed. For example, the adherence of cocci to filaments results in a
typical form referred to as "test-tube brushes" or "corn-cob" arrays and
these structures can be seen in Figure 6.The result of coaggregation is the
formation of a complex array of different bacteria linked to one another.
Following a few days of undisturbed plaque formation, the gingival
margin becomes inflamed and swollen. These inflammatory changes
result in the creation of a deepened gingival sulcus. The biofilm extends
into this subgingival region and flourishes in this protected environment,
resulting in the formation of a mature subgingival plaque biofilm.
Gingival inflammation does not appear until the biofilm changes from
one composed largely of gram-positive bacteria to one containing gram-
negative species such as Fusobacterium nucleatum, Prevotella
intermedia, and Capnocytophaga species. A subgingival bacterial
microcolony, predominantly composed of gram-negative anaerobic
bacteria, becomes established in the gingival sulcus between 3 and 12
weeks after the beginning of supragingival plaque formation. Most
bacterial species currently suspected of being periodontal pathogens are
anaerobic, gram-negative bacteria.

Synergistic interactions

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.

Antagonistic interactions
Antagonism is a major contributing factor in determining the composition
of microbial ecosystems such as dental plaque . The production of
antagonistic compounds (such as bacteriocins or bacteriocin-like
substances, BLIS) can give an organism a competitive advantage when
interacting with other microbes. Bacteriocins are relatively high
molecular weight proteins that can inhibit the growth of related bacteria

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while the producer strains are resistant to the action of the bacteriocins
they produce. Bacteriocins are produced by most species of oral
streptococci (e.g. mutacin by S. mutans and sanguicin by S. sanguinis), as
well as by C. matruchotii, black-pigmented anaerobes, and A.
actinomycetemcomitans; in contrast, Actinomyces species are not
generally bacteriocinogenic. Although bacteriocins are usually limited in
their spectrum of activity, many of the streptococcal bacteriocins are
broad spectrum, inhibiting species belonging to Gram positive(including
Actinomyces) and Gram negative genera. The production of bacteriocins
may give strains a competitive advantage during colonization.Other
inhibitory factors produced by plaque bacteria include organic acids,
hydrogen peroxide, and enzymes. The production of hydrogen peroxide
by members of the mitis-group of streptococci has been proposed as a
mechanism whereby the numbers of periodontal pathogens are reduced in
plaque to levels at which they are incapable of initiating disease. Some
periodontal pathogens (e.g. A. actinomycetemcomitans) produce factors
inhibitory to oral streptococci, might result from an ecological imbalance
between dynamically-interacting groups of bacteria. The low pH
generated from carbohydrate metabolism is also inhibitory to many
plaque species, particularly Gram negative organisms and to some
streptococci associated with sound enamel.

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).

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The major differences between supragingival and subgingival

EFFECTS ON THE PERIODONTIUM

 Supragingival plague if allowed to grow can lead to gingivitis and
it influences the growth, accumulation and pathologic potential of
subgingival plaque.
 Subgingival plaque is associated with enlarged gingiva, calculus
formation, periodontitis etc.

CARIOGENICITY OF PLAQUE
 The presence of cariogenic bacteria
 The ability of the plaque to adhere to the tooth surface.
 Its ability to resist dissolution by saliva
 Its protection of bacterial acids from salivary buffering.

Examination.
You can rely on your dentist to tell you if you have dental plaque, but
you can also take the do-it-yourself route. Disclosing tablets, swabs and
solution are plaque-revealing products that can be used at home. These
products temporarily stain dental plaque so that you can see where it is
and how much there is on your teeth.

How It Is Done

You will brush and floss your teeth. Then you will use the disclosing
product. Follow the instructions on the package. Gently rinse your mouth
with water. Check your teeth for plaque that has been colored with the
dye. Your gums also may be stained and appear red, but this is not a
problem. Use a dental mirror, if you have one, to help see behind teeth
and the areas in the back of your mouth. If you find stained plaque, brush
and floss again until it is gone. This helps you find areas you are missing.

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Disclosing tablets
Chew a disclosing tablet and allow it to mix with your saliva. Swish the
mixture around in your mouth with your tongue for about 30 seconds and
then spit it out.
Disclosing solution
Put some disclosing solution in your mouth, swish it around for about 30
seconds, and then spit the solution out.
Disclosing swabs
Apply the swab to all tooth surfaces in your mouth. Use these products
regularly until you find no more areas of stained plaque after you brush
and floss. You may want to test for plaque once a month to be sure you
are getting rid of the plaque.

Prevention

Follow these tips on how to remove plaque from teeth :

Brush thoroughly at least twice a day, with a fluoride toothpaste, to
remove plaque from your teeth
Use dental floss daily to remove plaque from between your teeth and
under your gum line, where your toothbrush may not reach
Check your teeth with plaque disclosing tablets to ensure removing
tooth plaque.
Control your diet. Limit sugary or starchy foods, especially sticky
snacks
Ask your dentist or dental hygienist if your plaque removal techniques
are ok.
Visit your dentist regularly for professional cleanings and dental
examinations
Ask your dentist if a dental sealant is appropriate for you. Dental
sealants are a thin, plastic coating that are painted on the chewing
surfaces of teeth to protect them from cavities and decay.
Use of an antibacterial mouth rinse can reduce bacteria that cause
plaque and gum disease, according to the American Dental Association.

Due to the structure of biofilms, physical removal of bacterial plaque

biofilms is the most effective means of control. Subgingival plaque within
pockets cannot be reached by brushes, floss, or oral rinses. Therefore,
frequent periodontal debridement of subgingival root surfaces by a dental
hygienist or dentist is an essential component in the treatment of
periodontitis.

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Calculus

Calculus, or tartar, is the term used to describe calcified dental plaque. It

consists of intra- and extracellular deposits of mineral, including apatite,
brushite, and whitlockite, as well as protein and carbohydrate. Mineral
growth can occur around any bacteria; areas of mineral growth can then
coalesce to form calculus which may become covered byan
unmineralized layer of bacteria. Calculus can occur both supragingivally
(especially near the salivary ducts) and subgingivally, where it may act as
an additional retentive area for plaque accumulation, thereby increasing
the likelihood of gingivitis and other forms of periodontal disease.
Calculus can be porous leading to the retention of bacterial antigens and
the stimulation of bone resorption by toxins from periodontal pathogens.
Over 80% of adults have calculus, and its prevalence increases with age.
An elevated calcium ion concentration in saliva may predispose some
individuals to be high calculus formers. Once formed, huge removal
forces are required to detach calculus; this removal takes up a
disproportionate amount of clinical time during routine visits by patients
to the dentist. Consequently, a number of dental products are now
formulated to restrict calculus formation. These products contain
pyrophosphates, zinc salts, or polyphosphonates to inhibit mineralization
by slowing crystal growth and reducing coalescence.

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. The calculus on the root surface of an extracted
tooth is seen in Figure 2. Note the brown to black coloration of the
subgingival calculus that extends to the apex of the distobuccal root, in
contrast to the whitish color of the supragingival calculus.

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 Major Differences

TREATMENT

Scaling and polishing

DENTAL CARIES

Dental caries can be defined as the localized destruction of the tissues of

the tooth by bacterial fermentation of dietary carbohydrates. Cavities
begin as small demineralized areas below the surface of the enamel ; once
enamel has been affected, caries can progress through the dentine and
into the pulp . Demineralization of the enamel is caused by acids,
particularly lactic acid, produced from the microbial fermentation of
dietary carbohydrates. Lesion formation involves dissolution of the
enamel and the transport of the calcium and phosphate ions away into the
surrounding environment. The initial stages of caries are reversible and
remineralization can occur, particularly in the presence of fluoride. oral
bacteria converted dietary carbohydrates into acid which solubilized the
calcium phosphate of the enamel to produce a caries lesion.

The bacteria most responsible for dental cavities are the mutans
streptococci, most prominently Streptococcus mutans and Streptococcus
sobrinus, and lactobacilli. If left untreated, the disease can lead to pain,
tooth loss and infection.. Today, caries remain one of the most common
diseases throughout the world. Cariology is the study of dental caries.

What causes dental caries?

 Diet: Intake of fermentable carbohydrates, especially sucrose .
 Host: Quantity and quality of saliva, the quality of tooth, etc.
 Microflora: Infection by a specific set of cariogenic bacteria within
dental plaque.

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 Mutans Streptococci
 The most prominent species found in the oral cavity include S. mutans,
S. sanguis, S. mitoir, S. salivarius, and S. milleri.
 MS bacteria comprise the most important group of streptococci
implicated in caries etiology.

Ecology of Mutans Streptococci

 MS does not colonize the mouth of infants prior to the eruption of
teeth.
 Likewise it disappears from the mouth following extraction of all
teeth.
 Infants most likely become infected from their parents or from other
individuals with whom they have frequent contact since the organisms
are not found free-living in nature and it has only been isolated from
humans and certain animals.
 Infants whose mother’s harbor higher levels of MS in saliva become
colonized more readily than infants of mothers with low salivary S.
mutans levels.
 MS are transmitted vertically, from mother to child.
 Mother’s with high caries experience tend to have children with high
caries.
 The genetic inheritance from both the mother and father has an
influence on caries susceptibility of the child.
 MS does not colonize teeth uniformly.
 The organism may be more frequently isolated from fissures and
interproximal surfaces, those areas most frequently involved in caries,
than from buccal or lingual smooth surfaces.
 In addition, some smooth surfaces may consistently harbor detectable
concentrations of the organisms where as comparable surfaces on other
teeth in the same mouth do not.
 This suggest that MS does not spread readily from one tooth surface to
another.

Virulence determinants of the mutans streptococci

 Acidogenicity and aciduricity:

- Acidogenicity is the ability of bacteria to produce acid from fermentable

carbohydrates.

- Aciduricity is the ability of bacteria to grow and metabolize under

highly acidic conditions.

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 How cariogenic bacteria cause caries?
 Acid production (Acidogenicity) Lower the pH to below 5.5, the
critical pH, which drives the dissolution of calcium phosphate
(hydroxyapatite) of the tooth enamel.
 Inhibit the growth of beneficial bacteria.
 Further lower the pH, promote progression of the carious lesion.
 Acid tolerance (aciduricity).
 Allows the cariogenic bacteria to thrive under acidic conditions while
other beneficial bacteria are inhibited.
 This results in dominance of the plaque by cariogenic bacteria.
 The capacity of oral bacteria to tolerate acidic environment is of a
major importance to the ecology of plaque communication and is
directly related to caries pathogenesis.

SM and response to acid

 SM has constitutive acid tolerance properties:

-The aciduricity is highly attributable to an enzyme called F-ATPase.

-Extrude protons allowing the organism to maintain an adequate pH

when the external pH decreases to 4.0 and lower.

Sucrose metabolism of S. mutans

 The most important substrate for the involvement of S. mutans in the
caries process is the disaccharide sucrose.
 Sucrose not only serves as a primary energy source but it is also permit
the initiation of additional biochemical events which are responsible
for the cariogenic potential of this organism.

Lactobacillus
 Lactobacillus are strong acid producers and are among the most
aciduric and acidogenic bacteria. .
 Lactobacillus may not be involved in caries initiation but rather may
become secondary invaders, which contribute to the progression of
already existing lesions.
 This was supported by the observation that lactobacilli are not
detectable in plaque covering incipient lesions in smooth tooth
surfaces.

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 Filamentous bacteria
 Several types of filamentous organisms will initiate root caries in
experimental animals.
 Actinomyces and rothia species have been found in dental plaque and
root caries.
 Actinomyces viscosus is an acidogenic bacterial and is often among the
predominant flora of plaque covering root surfaces.

Gram negative cocci

 Veillonella: this organism has anti carious activity because it utilizes
the lactic acid and converts it to propionic and other weak acids.

Tooth decay disease is caused by specific types of

bacteria that produce acid in the presence of
fermentable carbohydrates such as sucrose,
fructose, and glucose. The mineral content of teeth
is sensitive to increases in acidity from the
production of lactic acid. To be specific, a tooth
(which is primarily mineral in content) is in a
constant state of back-and-forth demineralization
and remineralization between the tooth and
surrounding saliva. For people with little saliva,
especially due to radiation therapies that may
destroy the salivary glands, there also exists remineralization gel. These
patients are particularly susceptible to dental caries. When the pH at the
surface of the tooth drops below 5.5, demineralization proceeds faster
than remineralization (meaning that there is a net loss of mineral structure
on the tooth's surface). Most foods are in this acidic range and without
remineralization, this results in the ensuing decay. Depending on the
extent of tooth destruction, various treatments can be used to restore teeth
to proper form, function, and aesthetics, but there is no known method to
regenerate large amounts of tooth structure. Instead, dental health
organizations advocate preventive and prophylactic measures, such as
regular oral hygiene and dietary modifications, to avoid dental caries.

S. mutans, S. sanguis, and S. mitis are, besides Actinomyces viscosus and

A. naeslundii, responsible for dental caries . These streptococci can attach
to the proteins covering the tooth enamel, where they then convert
sucrose into extracellular polysaccharides (mutan, dextran, levan). These
sticky substances, in which the original bacterial layer along with

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secondary bacterial colonizers are embedded, form dental plaque. The
final metabolites of the numerous plaque bacteria are organic acids that
breach the enamel, allowing the different caries bacteria to begin
destroying the dentin.

bacteria are responsible for both dental caries and periodontal diseases.
Extension of these diseases commonly causes infection in the adjacent
tissues, notably the pulp, periapical area and oro-facial soft tissues. More
rarely, infection may become established in the bone of the jaw to cause
osteomyelitis.

MAJOR FACTORS OF DENTAL CARIES.

1. Role of bacteria
2. Role of plaque:
3. Role of saliva:
4. Role of carbohydrates

MINOR FACTORS:
 Enamel composition
 Morphology of the tooth
 Position of the tooth
 Diet
 Immunity .

CLASSIFICATION
Dental caries can be classified
with respect to the site of the
lesion (Fig. 32.1):
 pit or fissure caries (seen
in molars, premolars and
the lingual surface of
maxillary incisors)
 smooth-surface caries
(seen mainly on
approximal tooth surfaces
just below the contact
point)
 root surface caries (seen
on cementum or dentine
when the root is exposed
to the oral environment)
 recurrent caries (associated with an existing restoration).

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 Rampant caries can occur in particular subgroup of people who are
especially prone to decay, such as xerostomic patients (who have a
markedly reduced salivary flow rate due to radiation treatment for head
and neck cancer), those with Sj ِgren’s syndrome, or as a side-effect of
medication.
‘Nursing-bottle’ caries is the extensive and rapid decay of the maxillary
anterior teeth associated with the prolonged and frequent feeding of
young infants with bottles or pacifiers containing formulas with a high
concentration of fermentable carbohydrate. Plaque bacteria receive an
almost continuous provision of substrates from which they can make acid.

CARIES PREVENTION
 Fissure sealants
 Fluoride (may also have some anti-glycolytic effects).
 Antimicrobial agents (these agents can be applied in toothpastes,
mouthrinses and varnishes. Some also inhibit glycolysis).
 Sugar substitutes (prevent acid production, but xylitol may selectively
inhibit Strep. mutans)

Treatment:-Treatment can help prevent tooth damage from leading to

cavities.

Treatment may involve:

a-Fillings b-Crowns c- Root canals

References:-
1-Oral microbiology .5th edition.

2-Essentials of Microbiology for Dental Students. 2006 ,2nd Edition.

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