2.1.

Dental Plaque And Calculus

2.1.1. Dental Plaque
Dental plaque is a soft deposit that accumulates on the teeth. Plaque can be
defined as a complex microbial community, with greater than 10 bacteria per
10

milligram and extends from the gingival margins into pockets. 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 and lipids. (Cawson, 2002)

Figure 1. a microscopic view of a smear of mature supragingival plaque. Note the presence of a variety
of different bacterial forms (cocci, rods, filaments, as well as a eukaryotic cell).

Dental plaque can be classified in several different ways. Plaque is classified

as supragingival or subgingival based on its relationship to the gingival margin.

Figure 2. Supragingival plaque is evident on the tooth above the gingival margin.

2.1.2. Dental Calculus (Tartar)

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. Calculus is hardened calcified
plaque. It is sometimes called tartar. It sticks firmly to teeth. 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. Generally, it can only be removed by a dentist or dental hygienist, with
special instruments. (Cawson, 2002)

Figure 3. The calculus on the root surface of an extracted tooth is seen in this figure. 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.

Extension and calcification of plaque leads to formation of subgingival

calculus within periodontal pockets. The deposits are thin, more widely distributed,
harder, darker and more firmly attached than supragingival calculus. Calculus appears
laminated histologically, with altered staining, probably due to breakdown products
from blood cells oozing into the pockets. Subgingival calculus helps to perpetuate
chronic periodontitis. It forms a reservoir of bacteria, helping to sustain inflammation,
and acts as a barrier to healing. (Beck J, 2000)

2.1.3. Dental Plaque can cause Halitosis and Gingivitis

First microscopic and electron microscopic research revealed the intimate
relationship between dental plaque and the gingival and periodontal tissues. Then,
epidemiological studies in many countries pointed to a close association between
tooth deposits and periodontal diseases. Finally, in 1965, the experimental gingivitis
studies demonstrated that the accumulation of plaque on healthy gingival produced
gingivitis (Loe et al. 1965).
Supragingival plaque related to healthy gingival tissues has a bacterial
composition that is different from that of plaque associated with gingivitis, which
again is different from the make-up of subgingival plaque of the progressing or
advanced periodontal lesion. Perhaps >300 different types of microorganism have
been found in well-developed human dental plaque, some of which have been
identified, and others have not been identified (Heitz et al., 2003)
Over the past few years, a new word has found its way into the discussion for
what people understand as dental bacterial plaque. The catchword is biofilm. After
periodontal research has used more that 100 years since Dr. Black first introduced the
term dental plaque to subject this material to scientific scrutiny, plaque is now
reasonably well described and widely understood. However, new aspects of the life
within the bacterial community with its structures of communication as well as the
phenomenon of quorum sensing justify this new term as an expression of our more
detailed understanding of the biofilm. (Heitz et al., 2003)
The most common cause of bad breath (Halitosis) is poor oral hygiene. The
smell comes from a build-up of germs (bacteria) within the mouth. These are in food
debris, in plaque and gum disease, or in a coating on the back of the tongue. Bacteria
that build up on a person's teeth, tongue and gums can cause plaque (the soft, white
deposit that forms on the teeth's surface), gum disease and tooth decay. The bacteria
combine with saliva to break down food particles and proteins, this releases an
unpleasant-smelling gas. Good oral hygiene will often solve the problem. That is,
regular teeth brushing, cleaning between the teeth, cleaning the tongue, and
mouthwashes. Other causes of persistent bad breath are uncommon. (NHS, 2014)

The most common cause of gingivitis is poor oral hygiene that encourages
plaque to form. Plaque is an invisible, sticky film composed mainly of bacteria.
Plaque forms on your teeth when starches and sugars in food interact with bacteria
normally found in mouth. Plaque forms when bacteria that occur naturally in the
mouth combine with saliva to form an adhesive coating over the teeth, called biofilm.
Plaque begins to form from the moment you finish brushing your teeth and, if it is left
to accumulate undisturbed for longer than two days, it can begin to cause gingivitis.
Gingivitis can occur wherever there is plaque build-up, at or below the gum line. If
plaque is allowed to accumulate for longer periods of time, it can also solidify on the
teeth in the form of calculus, also known as tartar. This often occurs around the lower
front teeth and the upper molars, where the openings of the saliva ducts are close to
the teeth. Tartar can retain even more plaque than the teeth normally would because
its surface is rougher. Tartar can also develop resulting from the mineral content in
your saliva. Tartar makes plaque more difficult to remove and creates a protective
shield for bacteria. The longer that plaque and tartar remain on teeth, the more they
irritate the gingiva, the part of gum around the base of teeth. Toxins produced by
bacteria in dental plaque irritate the gum tissue and cause infection, inflammation,
and pain. In period of time, gums become swollen and bleed easily. Tooth decay
(dental caries) also may result. (Mayo, 2002)
In most cases, initial plaque development starts in the niche created where the
gingival margin meets the tooth surface.

(a)

(b)

Figure. 4. Plaque begins to form in the gingival sulcus and other protected niches of the tooth. (a)
Destruction of collagen will occur as a direct result of microbial action through their release of toxins,
lipopolysaccharides or enzymes. (b) Bacterial plaque forms as a biofilm in the gingival sulcus shortly
after the cleansing of the tooth surface.

2.2 Halitosis
2.2.1 Definition
Halitosis is derived from

halitus (breath) and Greece Enosis (State). So a

State of halitosis bad breath. This term generally

breath originating from

State

of

refers

to a

State of

bad

metabolic systemically including the

gastrointestinal tract.Halitosis can be a physiological or pathological halitosis.

Halitosisis a physiological halitosis who is temporary and occurs when a
substance that caused the smell of Hematology to the lungs and is usually derived
from foods, such as onions and turnips and canal so come from beverages, such
as coffee, the as

well as

alcoholic

beverages. Halitosis is halitosis that physiological effectoccurs

mechanism similar

to

that

of halitosis physiological,

in a
in

this

case the

materials are hematologis to the lungs. The main causes of this State because of

the State

of disorder

that is

localor systemic

diseases such

as diabetes

mellitus, uremia, gastritis, peptic ulcers, and hepatitis.

2.2.2 Etiology
Halitosis can be caused by factors of physiological and pathological derived
from the

oral

cavity or intra oral

and systemic

factors or extra orally. Based

on surveys that have been conducted in the United States, the main causes
of halitosis most (90%) is due to factors involving the oral cavity. Needs to
be emphasis that halitosis is not a disease, but is considered a symptom of certain
systemic diseases. But that does not mean that any unpleasant smell that indicates the
presence of a particular disease.
2.2.2.1 Intraoral
In the

oral

cavity of

substrate (leftovers)

person, there

are exogenous proteinsubstrate-

and endogenous protein(deskuamasi epithelium of

the

mouth, saliva and blood proteins) which contains many amino acids containing sulfur
(S). In addition halitosis are also produced by thebacteria that normally live on
the surface

of

the

tongue andthroat that

helps in the

process

of food

digestion with splitting of protein. The species of bacteria that is present on

the oral surfacecan be sakarolitik, i.e. use of carbohydrates as an energy source.Other
species are asakarolitik or proteoliti,
acids as its

i.e.,

the use of

proteins, peptides,

main source. Most Gram-positive

amino

bacteria are gram-

negative bacteria and sakarolitik isproteolytic. according to research spearheaded

by Prof. Dr. JosephTozentich. from the University of British Columbia, Vancouver,
managed to detect that there is a volatile sulfur compounds andsmells foul as a
result cannot
production

of protein decomposition by anaerobic gram-negative bacteria in

mouth. Volatile sulfur compounds is

(VSCs) containinghydrogen

referred

to

the

as Volatile Sulfur Compounds

sulfide (H2S), Methil mercaptan (CH3SH)

and Dimethylsulfide (CH3SCH3) which is the main cause of halitosis which comes
from the oral cavity.

Condition of the mouth that can trigger the onset of bad breath is less or stopping
of flow (flow) saliva, increased anaerobic gram-negative bacteria, a growing number
of food proteins, pH of the oral cavity are more alkaline and the rising number
of dead cell sand necrotic epithelial cells in the mouth. Although the causes
of halitosis has not fully known, most of the causes are known to come from food
scraps left inside the oral cavity which are processed by the normal flora of the
mouth cavity. Some factors of the oral cavity which need special attention because it
has the role as well as a major influence on the onset of halitosis at someone such
as saliva, tongue, teeth and interdental space of ginggiva.
1.1.
Some types

Ektra oral fisiology

of

cuisine and

substance of

food

consumed daily can

also cause foul breath odor less. Fried foods contain a lot of seasoning and onionlike odor that can survive in

the

mouth for

10-12

hours. Even the smell

of it

still feels after the teeth are cleaned. This odor arising from substance such food is
absorbed by the gastrointestinal tract and excreted slowly through the lungs. This
situation has

been

demonstrated by Morris

providing a capsule containing garlic to

patients who

and Read
researched

by

and produced

the smell that last a long time on the respiratory air. Other researchers also proved
that the smell of the garlic in a short time was able to be felt on respiratory and
survive for several hours while the digestive tract such as the intestine is the separate
parts of the stomach.
1.2.

Patology Factor

Factors cause halitosis most often seen is caused due to less hygiene and health of the
oral cavity. In patients who are poor hygine tend to occur oral decay detritus that
accumulates on the sidelines of teeth by bacteria in the oral cavity. This situation will
grow worse in patients who have a tendency to form calculus quickly.

Gingivitis and periodontitis is the most common inflammatory disease occurs and
triggers the

onset

of halitosis is

caused gram-

negative fusobacterium nucleatum as veilonella, andporphyromonas gingivalis hidden

in periodontal diseased tissue and cause a gas smell. (Ravel, 2006) In addition due to
the decay

of detritus caught in paperback, this condition can

decaying saliva so

that adds

to

the severe bad

also

be quickly

breath individuals.

In

addition, the necrotic tissue is formed and the reduced blood supply causes the levels
of

oxygen in

the

area

of infection also

diminished. Thus the

bacteria will

flourish and continue to deliver substances that serve as a virulence as well as it may
cause apurulent

feses exudate out

through the

Groove of

the

gingiva.

Metabolic reaction of H2S gas and produces embossed NH2(Amino) so the elevation
of the concentration of volatile sulfur in the air in the oral cavity.
2.

Halitosis Classification

Based

on

the etiologinya factor, halitosis distinguished atasa true,halitosis (genuine) pseudohali

tosis and halitophobia. GenuineHalitosis distinguished again over
and

pathological. Physiological Halitosis is temporary

and does

maintenance, reverse halitosis pathological is halitosis is

be resolved simply

by the

maintenance

the physiological
not

require

permanent and

cannot

of

oral hygiene alone,

but require a handling and care according to the source the causes of halitosis
2.1.
Halitosis is

Halitosis Fisiology
a physiological halitosis who is

temporary

and does

not

require

maintenance. On this type of halitosis is not found of any pathological condition that
cause halitosis. An example is the morning breath, that is the smell of breath at wakeup time. This situation caused no active muscular cheeks and tongue as well as the
reduced flow

of saliva during sleep. Breath smells of

this can

be

overcome

by stimulate the flow of saliva and get rid of the rest of the food in the
mouth by chewing, brushing your teeth or gargle

2.2.

Patology Halitosis

Halitosis is a pathological halitosis permanent and cannot beresolved simply by the

maintenance of oral hygiene alone, butrequire a handling and care according to
the source the

cause

ofhalitosis. Any growth

with oral hygieneconditions are

bad is

of

the

bacteria associated

cause

of halitosis most

commonlyintraoral pathological
encountered. Tongue coating, caries and periodontal disease are the main causes
of halitosis is

related

to the

condition.Chronic

the nasal cavity and paranasal

indigestion, peptic
diseases such

sinuses, tonsils(tonsilhlith) infections,

ulcers can

as

infection in

also produceodorous gases. In

diabetes,renal

addition, systemic

failure, ketoasidosir and liver

disorders can

also cause badbreath are typical. Diabetic Ketoacidosis acetone smelling breathmenge
luartan. Air breathing in

people

damage andammonia smelling accompanied

in patients

with disorders

with kidney

by complaints

of the

bladder as cirrhosis hepatis will smell the

liver
breath of

of dysgeusi, whereas
and the

gall

arms, knownwith

the

term foetor hepaticus.

3.

Prevention and treatment of Halitosis

Halitosis treatment depends

on the

cause, it

is

important that the

dentist can

distinguish the causes of bad breath as abnormal its inside or outside of the
mouth. Generally halitosis can be reduced or eliminated altogether by keeping oral
hygiene such as brushing teeth, using dental floss, clean tongue, use mouthwash and a
healthy diet, but sometimes it takes treatment by professionals to make a referral. To
be able to cope with the halitosis effectively, thoroughly vetting is required and the
right diagnosis. Precaution and treatment on halitosis are:
3.1.
Brushing Teeth
Teeth should
be brushed twice

day. Teeth brushed

with a

soft

brush and bristle brush heads are small. Avoid the use of the brush bristles are

rough because of the rough brush bristles could lead to a recession of the
gingiva.

Brushing teeth should

use tooth

paste

containing fluorine to

prevent dental caries at once.

3.2.
Dental Floss
FLOSS the teeth (dental floss) used to clean the teeth, narrow slits that can't
be achieved with

toothbrush. This

is

done

by cutting

the

thread approx 40 cm, then played on both the right and left middle finger. The
thread is inserted into the gap between the teeth and held with the thumb in
order

to

be strong

and not

be

separated when such movements

are done sawing. These actions should be done once a day, but whenever
possible is

done twice

day. After this

stage is

allowed to clean or rinsed gargle with water.

3.3.
Tongue Cleaning
The surface of the tongue is cleaned by brushing the tongue twice a day
using a toothbrush or a special cleaning tool tongue (tongue scrapper). The
surface of the tongue brushed gently and slowly so that the tongue was
not injured. While the tongue lift ahead, place the tongue scrapper as far as
possible to

the back

pulled forward and

of

the
down

tongue, while still stand, while being

with light pressure. Use a

clean cloth/paper tissue or running water to clean the tongue scrapper. Repeat
this procedure 2-4 times until the entire surface is cleaned.
3.4.
Mouthwash
Mouthwash is used at least once a day. The most appropriatetime to
use mouthwash before

bed is because antibacterialmouthwash give

effect during sleep when the bacterial cause ofbad breath is increased. Drug
gargle containing alcohol may cause dry mouth and when usedfor a long
time may
you use non

cause oral mucosa chipped. Therefore, we

recommend

that

alcoholic mouthwash such

ascontaining sodium saccharin. Use need not be too excessive, less is more
10-15 ml is enough to wet the entire surface of the mouth. Gargleat the lack
of 1-2 minutes. Do not gargle right out of the bottle, as if touched by saliva,

the material will be contaminated, so the rest of the active ingredients in the
bottle can be damaged, as a result of no use anymore for the next usage
3.5.
Healthy Diet
A Healthy Diet is done by eating fibrous vegetables such as fresh food and
has a coarse consistency that
tongue, avoid eating foods
of water each

can

help rid dorsum

that cause odor, as

day. Recently,

well as

of

the

drinking

plenty

research in Japan

reported

that unsweetened yogurt may reduce the compound causes halitosis. This is
evidenced by a decrease in the level of the compound were found in
the hydrogen sulfide to 80% after consuming 90 grams of yogurt every day
for 6

weeks. In

addition,

results

of

research in

America shows that

the polyphenols (such as catechin and the aflavin), compounds contained in

tea can also inhibit the growth of bacteri causes of halitosis. Catechin
contained in green tea or black tea while the aflavin more dominant on black
tea. Reducing consumption

of

foods with high

free candy (non-cariogenik) especially

when the

protein. Chew sugar

mouth feels dry. Drinking

lots of water in a day. Avoid alcohol consumption, smoking, drugs that can
decrease the flow of saliva.
3.6.
Professional Treatment
When caries, periodontal disease or other mouth infections that
onset

of halitosis, special handling is

example, do
addition, the

required by

the patching, scaling or

dentist will

deprive the

cause the

professionals,

for

dental root (root planning). In

rest

of the

roots

of teeth or

roots radix when that cause the onset of halitosis

2.3. Treatment Periodontia

2.3.1 Scaling and Root Planning
Scaling is the removal of plaque, calculus, and stain from the crown and root
surfaces; both above (supragingival) and below (subgingival) the gum (gingiva). This

is as opposed to root planning, which is the definitive removal of cementum or dentin

from the root surface in attempt to smooth rough surfaces and dislodge calculus.
Without clean, smooth, hard roots, the results of curreteage may be limited because
rough roots are foci for plaque accumulation and attachment of calculus. The more
altered and damaged the root surface has been from calculus (tartar) and plaque
accumulation, the greater the need for root planning. (Cohen, 2007).
The purpose of scaling and root planning is to eliminate microorganisms,
endotoxins, and calculus to reduce inflammation, promote tissue regeneration, and
make root surfaces biologically acceptable to gingival tissues. Any tooth deposits that
can cause inflammation of the gum tissue must be eliminated. The root surface must
be made as smooth as possible. Irregularities in the root surface can accumulate
bacteria and contribute to gum inflammation. Irregularities are sites of bacteria and
plaque buildup. The bacteria and the toxins they produce in the plaque are held
against the tooth by the calculus. In this way, plaque and calculus on the teeth are risk
factors to gum disease (Darby and Walsh, 2010).
Once scaling and root planning have been completed, it is more important for
patient to practice the brushing and interdental cleaning techniques in which the
patient were instructed. If the dentists have recommended any additional oral care
products and devices, patients must use them too. Patients cooperation is vital if the
procedures are to be successful. To remain disease-free, patient will need to remain
constain in their oral self-care regimen (Darby and Walsh, 2010).
2.3.2 Dental Health Education
When periodontal treatment is complete, the long-term stability of the
periodontal tissues is achieved with a programme of supportive periodontal care. In
order to achieve this aim, the attainment of a high level of plaque control is essential
and selective re-treatment is also often necessary to remove recurring deposits of
plaque and calculus. The intervention may include reinforcement of oral hygiene
instruction with either supragingival scaling, subgingival debridement or perhaps, a
combination of two regimens (Jenkins and Heasman, 2003)
Oral Hygiene Instruction (OHI) forms a vital part of the role of the Oral Health
Educator (OHE). Research shows that effective plaque control alone is the single

most import method of preventing periodontal disease. In practical OHI sessions, the
OHE must be able to: (Felton et al., 2014)
1. Motivate patients to improve plaque control
2. Explain and demonstrate disclosing
3. Give practical instruction on interdental cleaning
4. Advise on the most suitable toothbrush for their use
5. Demonstrate suitable tooth brushing techniques
6. Discuss the advantages and disadvantages of various toothpastes
The objective of plaque control is the periodic removal of the accumulated
plaque at interval which is sufficiently frequent to prevent pathologic events arising
from recurrent plaque formation. Genereally, the patients need two thorough
brushings a day. However, the thoroughness of tooth cleaning is more important than
the specific method of tooth brushing and the frequency (Marya, 2011).
An efficient toothbrushing technique only cleans approximately 65% of the
tooth surface, leaving vulnerable interdental col area untouched. Where there is no
loss of interdental papillae, dental floss will be required to remove interdental plaque.
Where there has been interdental attachment loss, with loss of interdental papillae or
the underlying bone, a curved interdental brush works best to reach subgingivally and
into the interdental col or pocke (Noble, 2012).
2.3.3 Mouthrinse
Mouthrinses constitute a simple and commonly used delivery system for
antimicrobial agents. Schaeken et al. (1996) has showed the efficacity of mouthrinses
containing 0.4% zinc sulphate and 0.15% triclosan on plaque accumulation,
development of gingivitis, and formation of calculus in a 28-week clinical test. In an
effort to promote good oral health, the use of mouthrinses to penetrate and disrupt the
biofilm as an adjunct to mechanical methods of biofilm management has been
studied. Other studies have also reveals the efficacy of delmopinol, pyrophosphates,
zinc suplhate with triclosan, and essential oil/ZnCl2 mouthrinses in the control of
calculus formation (Dumitrescu, 2010).
The ingredients in most of the mouthwashes/rinses include the use of alcohol.
Alcohol mouthwashes/rinses have been accused of increasing the risk of oral cancer.
Although alcohol is used primarily to keep other antibacterial ingredients dissolved, it
may have some antibacterial properties itself (Gutkowski, 2012)

2.4

Caries
Dental caries also known as tooth decay or a cavity, is an infection, bacterial in

origin, that causes demineralization and destruction of the hard tissues of the teeth
(enamel, dentin and cementum). It is a result of the production of acid by bacterial
fermentation of food debris accumulated on the tooth surface. If demineralization
exceeds saliva and other remineralization factors such as from calcium and
fluoridated toothpastes, these once hard tissues progressively break down, producing
dental caries (cavities or carious lesions, that is, holes in the teeth). Today, caries
remains one of the most common diseases throughout the world. Cariology is the
study of dental caries.
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.
2.4.1 Signs and Symptoms
A person experiencing caries may not be aware of the disease. (Health
Promotion Board, 2006) The earliest sign of a new carious lesion is the appearance
of a chalky white spot on the surface of the tooth, indicating an area of
demineralization of enamel. This is referred to as a white spot lesion, an incipient
carious lesion or a "microcavity". (Richie S. King, 2011) As the lesion continues to
demineralize, it can turn brown but will eventually turn into a cavitation ("cavity").
Before the cavity forms, the process is reversible, but once a cavity forms, the lost
tooth structure cannot be regenerated. A lesion that appears dark brown and shiny
suggests dental caries were once present but the demineralization process has
stopped, leaving a stain. Active decay is lighter in color and dull in appearance.
(Clarke Johnson, 2007)

As the enamel and dentin are destroyed, the cavity becomes more noticeable.
The affected areas of the tooth change color and become soft to the touch. Once the
decay passes through enamel, the dentinal tubules, which have passages to the nerve
of the tooth, become exposed, resulting in pain that can be transient, temporarily
worsening with exposure to heat, cold, or sweet foods and drinks. A tooth weakened
by extensive internal decay can sometimes suddenly fracture under normal chewing
forces. When the decay has progressed enough to allow the bacteria to overwhelm the
pulp tissue in the center of the tooth a toothache can result and the pain will become
more constant. Death of the pulp tissue and infection are common consequences. The
tooth will no longer be sensitive to hot or cold, but can be very tender to pressure.
Dental caries can also cause bad breath and foul tastes.[5] In highly progressed
cases, infection can spread from the tooth to the surrounding soft tissues.
Complications such as cavernous sinus thrombosis and Ludwig angina can be lifethreatening. (Richard W Hartmann, 2008)
2.4.2 Cause
There are four main criteria required for caries formation: a tooth surface
(enamel or dentin), caries-causing bacteria, fermentable carbohydrates (such as
sucrose), and time. (Southam JC, Soames JV, 1993) However, it is also known that
these four criteria are not always enough to cause the disease and a sheltered
environment promoting development of a cariogenic biofilm is required. The caries
process does not have an inevitable outcome, and different individuals will be
susceptible to different degrees depending on the shape of their teeth, oral hygiene
habits, and the buffering capacity of their saliva. Dental caries can occur on any
surface of a tooth that is exposed to the oral cavity, but not the structures that are
retained within the bone. (Smith B et al, 1990)
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. 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. (Rogers AH, 2008)

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 and autoimmune disorders, such as Sjgren's syndrome, that may destroy
the salivary glands, there also exists therapies such as saliva substitutes and
remineralization products. These patients may be 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).
All caries occur from bacterial acid demineralization that exceeds saliva and
fluoride remineralization, and acid demineralization occurs where bacterial plaque is
left on teeth. Because most plaque-retentive areas are between teeth and inside pits
and fissures on chewing surfaces where brushing is difficult, over 80% of cavities
occur inside pits and fissures. Areas that are easily cleansed with a toothbrush, such
as the front and back surfaces (facial and lingual), develop fewer cavities.
Some foods have an acidic pH of 5.5 or lower which can result in
demineralisation in the absence of bacteria. This is known as erosion, rather than
caries, because the acid is not bacterial in origin. Attack by acid from systemic
complications such as bulimia and stomach difficulties as well as vomiting can cause
tooth erosion.
2.4.2.1 Teeth
There are certain diseases and disorders affecting teeth that may leave an
individual at a greater risk for cavities. Amelogenesis imperfecta, which occurs
between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does
not fully form or forms in insufficient amounts and can fall off a tooth. In both cases,
teeth may be left more vulnerable to decay because the enamel is not able to protect
the tooth. (Neville, B.W. et al, 2002)
In most people, disorders or diseases affecting teeth are not the primary cause
of dental caries. Approximately 96% of tooth enamel is composed of minerals. These

minerals, especially hydroxyapatite, will become soluble when exposed to acidic

environments. Enamel begins to demineralize at a pH of 5.5. (Dawes C, 2003) Dentin
and cementum are more susceptible to caries than enamel because they have lower
mineral content. (Mellberg JR, 1986) Thus, when root surfaces of teeth are exposed
from gingival recession or periodontal disease, caries can develop more readily. Even
in a healthy oral environment, however, the tooth is susceptible to dental caries.
The evidence for linking malocclusion and/or crowding to the dental caries is
weak. (Borzabadi-Farahani, A et al, 2011) However, the anatomy of teeth may affect
the likelihood of caries formation. Where the deep developmental grooves of teeth are
more numerous and exaggerated, pit and fissure caries are more likely to develop (see
next section). Also, caries are more likely to develop when food is trapped between
teeth. (Sherif Mohamed et al, 2012)
2.4.2.2 Bacteria
The mouth contains a wide variety of oral bacteria, but only a few specific
species of bacteria are believed to cause dental caries: Streptococcus mutans and
Lactobacilli among them. These organisms can produce high levels of lactic acid
following fermentation of dietary sugars, and are resistant to the adverse effects of
low pH, properties essential for cariogenic bacteria. As the cementum of root surfaces
is more easily demineralized than enamel surfaces, a wider variety of bacteria can
cause root caries including Lactobacillus acidophilus, Actinomyces spp., Nocardia
spp., and Streptococcus mutans. Bacteria collect around the teeth and gums in a
sticky, creamy-coloured mass called plaque, which serves as a biofilm. Some sites
collect plaque more commonly than others, for example sites with a low rate of
salivary flow (molar fissures). Grooves on the occlusal surfaces of molar and
premolar teeth provide microscopic retention sites for plaque bacteria, as do the
interproximal sites. Plaque may also collect above or below the gingiva where it is
referred to as supra- or sub-gingival plaque, respectively. (Rogers AH, 2008)
These bacterial strains, most notably S. mutans can be inherited by a child from
a caretaker's kiss or through feeding premasticated food. (Douglass, JM, 2008)

Fermentable carbohydrates
Bacteria in a person's mouth convert glucose, fructose, and most commonly
sucrose (table sugar) into acids such as lactic acid through a glycolytic process called
fermentation. If left in contact with the tooth, these acids may cause demineralization,
which is the dissolution of its mineral content. The process is dynamic, however, as
remineralization can also occur if the acid is neutralized by saliva or mouthwash.
Fluoride toothpaste or dental varnish may aid remineralization. If demineralization
continues over time, enough mineral content may be lost so that the soft organic
material left behind disintegrates, forming a cavity or hole. The impact such sugars
have on the progress of dental caries is called cariogenicity. Sucrose, although a
bound glucose and fructose unit, is in fact more cariogenic than a mixture of equal
parts of glucose and fructose. This is due to the bacteria utilising the energy in the
saccharide bond between the glucose and fructose subunits. S.mutans adheres to the
biofilm on the tooth by converting sucrose into an extremely adhesive substance
called dextran polysaccharide by the enzyme dextransucranase. (Silverstone LM,
1983)
2.4.2.3 Exposure
The frequency of which teeth are exposed to cariogenic (acidic) environments
affects the likelihood of caries development. After meals or snacks, the bacteria in the
mouth metabolize sugar, resulting in an acidic by-product that decreases pH. As time
progresses, the pH returns to normal due to the buffering capacity of saliva and the
dissolved mineral content of tooth surfaces. During every exposure to the acidic
environment, portions of the inorganic mineral content at the surface of teeth
dissolves and can remain dissolved for two hours. Since teeth are vulnerable during
these acidic periods, the development of dental caries relies heavily on the frequency
of acid exposure. The carious process can begin within days of a tooth's erupting into
the mouth if the diet is sufficiently rich in suitable carbohydrates. Evidence suggests
that the introduction of fluoride treatments have slowed the process. (Summit, James
B. et al, 2001) Proximal caries take an average of four years to pass through enamel
in permanent teeth. Because the cementum enveloping the root surface is not nearly

as durable as the enamel encasing the crown, root caries tends to progress much more
rapidly than decay on other surfaces. The progression and loss of mineralization on
the root surface is 2.5 times faster than caries in enamel. In very severe cases where
oral hygiene is very poor and where the diet is very rich in fermentable
carbohydrates, caries may cause cavities within months of tooth eruption. This can
occur, for example, when children continuously drink sugary drinks from baby bottles
(see later discussion).
2.4.2.4 Other factors
Reduced salivary flow rate is associated with increased caries since the
buffering capability of saliva is not present to counterbalance the acidic environment
created by certain foods. As a result, medical conditions that reduce the amount of
saliva produced by salivary glands, in particular the submandibular gland and parotid
gland, are likely to dry mouth and thus to widespread tooth decay. Examples include
Sjgren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis.[28]
Medications, such as antihistamines and antidepressants, can also impair salivary
flow. Stimulants, most notoriously methylamphetamine ("meth mouth"), also occlude
the flow of saliva to an extreme degree. Tetrahydrocannabinol, the active chemical
substance in cannabis, also causes a nearly complete occlusion of salivation, known
in colloquial terms as "cotton mouth". Moreover, 63% of the most commonly
prescribed medications in the United States list dry mouth as a known side-effect. [28]
Radiation therapy of the head and neck may also damage the cells in salivary glands,
somewhat increasing the likelihood of caries formation. (Neville, B.W. et al, 2002)
The use of tobacco may also increase the risk for caries formation. Some brands
of smokeless tobacco contain high sugar content, increasing susceptibility to caries.
(Neville, B.W. et al, 2002) Tobacco use is a significant risk factor for periodontal
disease, which can cause the gingiva to recede. (Anonim, 2007) As the gingiva loses
attachment to the teeth due to gingival recession, the root surface becomes more
visible in the mouth. If this occurs, root caries is a concern since the cementum
covering the roots of teeth is more easily demineralized by acids than enamel. [33]
Currently, there is not enough evidence to support a causal relationship between

smoking and coronal caries, but evidence does suggest a relationship between
smoking and root-surface caries. (Banting, D.W, 2006)
Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all
atoms with electrical charge and ionic radius similar to bivalent calcium, such as
cadmium, mimic the calcium ion and therefore exposure may promote tooth decay.
(Arora M et al, 2008)
Poverty is also a significant social determinant for oral health. [44] Dental caries
have been linked with lower socio-economic status and can be considered a disease of
poverty. (DYE, B, 2010)
Forms are available for risk assessment for caries when treating dental cases;
this system using the evidence-based Caries Management by Risk Assessment
(CAMBRA). It is still unknown if the identification of high-risk individuals can lead
to more effective long-term patient management that prevents caries initiation and
arrests or reverses the progression of lesions. (Tellez, M., 2012)
2.4.3 Classification
Caries can be classified by location, etiology, rate of progression, and affected
hard tissues.[64] These forms of classification can be used to characterize a particular
case of tooth decay in order to more accurately represent the condition to others and
also indicate the severity of tooth destruction. In some instances, caries are described
in other ways that might indicate the cause. G.V. Black classification:
1. Class I - pit and fissure caries (anterior or posterior teeth)
2. Class II - approximal surfaces of posterior teeth
3. Class III - approximal surfaces of anterior teeth without incisal edge
involvement
4. Class IV - approximal surfaces of anterior teeth with incisal edge involvement
5. Class V - gingival/cervical surfaces on the lingual or facial aspect (anterior or
posterior)
6. Class VI - incisal edge of anterior teeth or cusp heights of posterior teeth

According to the depth of the hole, caries can be grouped into:

1. Caries insipiens
Insipiens caries is caries that occurs on the surface of the tooth enamel.
Usually in these cases no pain tooth enamel appears only in black or brown
stains.
2. Superficial caries
This is the caries has reached the inside of the tooth enamel. Sometimes a
tooth ache.
3. Caries media
Caries Caries is a media that has reached the dentin (dental bone) or the midsection between the surface of the tooth and the pulp. At this stage, the tooth
will be sore when exposed to cold stimuli, sour and sweet foods.
4. Caries profunda
It is close to or even caries reaches the pulp, causing inflammation of the pulp.
At this stage, the patient will usually feel pain when eating, and even the pain
of a sudden without any stimulation.
2.5

Irreversible Pulpitis
An irreversible pulpitis may be acute, subacute, or chronic. It may be

partial or total. The pulp may be infected or sterile. Clinically the acutely
inflamed pulp is thought to be symptomatic, the chronically inflamed pulp
asymptomatic. Clinically the extent of pulp inflammation, partial or total, cannot
be determined. Based on present knowledge, irreversible pulpitis in any of its
many forms requires endodontic therapy. Dynamic changes in the pulp are
always

occurring. The change

from

quiescent

chronicity

to

symptomatic

acuteness may develop over a period of years or in a matter of hours. With

pulp inflammation there is an exudate. If the exudate can be vented to relieve the
pain that accompanies edema, the tooth may remain quiescent. Conversely, if the
exudate that is being continuously formed remains within the hard confines of
the root canal, pain will probably occur. (Cohen S & Burns, 1994)

2.5.1 Symptomatic irreversible pulpitis

One

type

of irreversible

pulpitis

is

characterized

by

spontaneous

intermittent or continuous paroxysms of pain. "Spontaneous" in this context

means

that

no stimulus

is evident.

Sudden

temperature

changes

induce

prolonged episodes of pain. There may be a prolonged (i.e., remaining after the
stimulus is removed) painful response to cold that can be relieved by heat.
There may also be a prolonged painful response to heat that can be relieved by cold.
There may even be a prolonged painful response to both heat and cold
stimulation. Continuous spontaneous pain may be excited merely by a change in
posture (e.g., when the patient lies down or bends over). Commonly, patients
recognize this empirically and may spend the night sleeping fitfully in an
upright position. Pain from symptomatic irreversible pulpitis tends to be moderate to
severe, depending on the severity of inflammation. It may be sharp or dull,
localized or referred (e.g., referred from mandibular molars toward the ear or
up to the temporal area), intermittent or constant. Radiographs alone are of
little assistance in diagnosing a symptomatic irreversible pulpitis. They are
helpful in detecting suspect teeth (i.e., those with deep caries or extensive
restorations). In the advanced stages of an irreversible pulpitis the inflammatory
process may lead to development of a slight thickening in the periodontal
ligament. (Cohen S & Burns, 1994)
A symptomatic irreversible pulpitis can be diagnosed by a thorough dental
history, visual examination, radiographs, and thermal tests. The electric pulp test
is of questionable value in accurately diagnosing the disease. An untreated
symptomatic irreversible pulpitis may persist or abate if a vent is established for the
inflammatory exudate (e.g., the removal of food packed into a deep carious pulp
exposure to provide a vent for the inflammatory exudate). The inflammation of
an irreversible pulpitis may become so severe as to cause ultimate necrosis. In
the transition from pulpitis to necrosis the typical symptoms of irreversible

pulpitis are altered according to the extent of the necrosis. (Cohen S & Burns,
1994)
2.5.2 Asymptomatic irreversible pulpitis
Another type of irreversible pulpitis is asymptomatic because
inflammatory

exudates

are

quickly

vented.

the

An asymptomatic irreversible

pulpitis may develop by the conversion of a symptomatic irreversible pulpitis

into a quiescent state, or it may develop initially from a low-grade pulp
irritant. It is easily identified by a thorough dental history along with
radiographic and visual examination. An asymptomatic irreversible pulpitis may
develop from any type of injury, but it is usually caused by a large carious
exposure or by previous traumatic injury that resulted in a painless pulp
exposure of long duration. (Cohen S & Burns, 1994)
a. Hyperplastic pulpitis.
One type of asymptomatic

irreversible

pulpitis

is

reddish

cauliflower-like overgrowth of pulp tissue through and around a carious

exposure. The proliferative nature of this type of pulp is attributed to a
low-grade chronic irritation and to the generous vascularity of the pulp that
is characteristically found in young people. Occasionally there is some
mild, transient pain during mastication. If the apices are mature, complete
endodontic therapy should be provided
b. Internal resorption.
Another type of asymptomatic irreversible pulpitis is internal resorption.
This is characterized by the presence of chronic inflammatory cells in
granulation tissue and is asymptomatic (before it perforates the root).
Internal resorption is most commonly diagnosed by radiographs showing
internal expansion of the pulp with evident dentinal destruction. In
advanced cases of internal resorption in the crown, a pink spot may be
seen through the enamel. The treatment of internal resorption is immediate
endodontic therapy; to postpone treatment may lead to an untrcatable
perforation of the root, resulting in possible loss of the tooth.

c. Canal calcification.
The physical adversity of restorative procedures, periodontal therapy,
attrition, abrasion, trauma, and probably some additional idiopathic factors
can cause an otherwise normal pulp to metamorphose into an irreversible
pulpitis, manifested by deposition of abnormally large amounts of reparative
dentin throughout the canal system. (Fors & Berg, 1986)
The condition is usually first recognized radiographically. Discrete areas of
localized pulp necrosis resulting from small infarctions (e.g., caused by
deep scaling that interrupts the blood supply into a lateral canal) often
initiate

localized

calcification

as

a defense

reaction.

This

abnormal

calcification occurs in and around pulp vascular channels. The teeth are
asymptomatic but may show a slight change in crown color. Several distinct
types of calcification (denticles, pulp stones), initiated by a multitude of
factors, can occur within the pulp
d. Necrosis
Necrosis, death of the pulp, may result from an untreated irreversible
pulpitis or may occur immediately after a traumatic injury that disrupts the
blood supply to the pulp. Whether the necrotic remnants of the pulp arc
liquefied or coagulated, the pulp is still quite dead. Regardless of the type of
necrosis, the endodontic treatment is the same. Within hours an inflamed
pulp may degenerate to a necrotic state. Pulp necrosis can be partial or
total. The partial type may exhibit some of the symptoms of an
irreversible

pulpitis.

Total

necrosis,

before

it

clinically

affects

the

periodontal ligament, is usually asymptomatic. There is no response to

thermal or electric tests. Occasionally with anterior teeth the crown will darken.
Untreated

necrosis

may

spread

beyond

the

apical

foramen, causing

inflammation of the periodontal ligament; this results in thickening of the

periodontal ligament, which may be quite sensitive to percussion.
2.5.3 Radiographic

In irreversible pulpitis, the pulp is still vital but is severely inflamed. As the
pulp is encased within the rigid dentine, the inflammation that would easily subside in
other parts of the body leads to necrosis of the pulp because the edema compromises
the circulation of the blood supply. At this stage, the pulp would not respond to
conservative treatment and pulp necrosis and infection will develop. All teeth with
periapical lesions do have infected pulp (Ghom, 2008).
Periodontal Space Widening
Periodontal space is the soft tissue that lies between the tooth and its bony
socket. It continues around the entire tooth and is a continuation of the connective
tissue associated with the gingivodental fibres. Accumulation of inflammatory
exudates in the connective tissue of the periodontal ligament space. The pathological
reason for this widening are infection, trauma, orthodontic treatment, or tooth
extrusion (Ghom, 2008).
The non-pathologic reasons for widening of periodontal ligament space are
terminal stage of root formation, wide marrow space superimposed on a tooth apex
on a radiolucent anatomy such as nasal fossa, maxillary sinus, mental foramen or
submandibular fossa (Ghom, 2008).

Figure 5. Different type of change seen in periapical tissue (Ghom, 2008)

Figure 6. Periodontal Ligament (PDL) space widening in acute apical periodontitis (Ghom, 2008)

Radiographic Appearance of Dental Caries

Carious lesions are detected intraorally on the occlusal surfaces on posterior
teeth and interproximally on anterior teeth by the clinical examination techniques of
exploring and transillumination. Interproximal carious lesions between the posterior
teeth are not large enough to cause color changes at the marginal ridges are best
detected by bitewing radiographs and in some cases by properly paralleled periapical
radiographs. Facial and lingual caries can also be detected radiographically, but again,
loss of tooth structure must be sufficient to make the lession apparent (Bricker,
Langlais, and Miller, 2002).
Carious Lesion Detection
Dental caries often occurs bilaterally. Caries as a decay process does not
preferentially attack a molar on one side only. The process is not that specific. If
one discovers a cavity on one tooth in an arch, its counter-part on the opposite side
should be checked, or if. Once caries has been noticed on one proximal surface, it is
wise to check to adjacent surface for decay (Bricker, Langlais, and Miller, 2002) .

Figure 7. A to D, Several patterns of interproximal caries, E, Early interproximal carious lesions on the
lower second bicuspid and first molar (arrows) (Bricker, Langlais, and Miller, 2002).

2.5.4

Treatment

2.5.4.1 Root Canal Treatment

The object of root canal treatment is to maintain a functional tooth with
ahealthy periodontontal ligament in the dentition following pulp pathology and its
sequelae. Following the decisions that the pulp is non-vital and the tooth should be

conserved if possible, the crucial factors are that the root(s) must be amenable to root
filling and that the tooth should be restorable afterwards. The treatment plan shoul
include a provisional decision on the restoration type.
The technical objectives of root canal treatment are to:
-

Remove all accessible infected and contaminated tissue

Disinfect infected tissue that cannot be removed
Shape the canal to an appropriate form to receive the chosen filling material
Obturate the whole canal to block and seal the dead space to prevent
reccurrence of infecton

To remove all infected tissue, which includes both pulp and dentine, the full length of
the root canal must be prepared to the apical constriction. The root filling material
must be chosen before the preparation is started, so that the preparation is shaped
accordingly. For example, an apical master cone system wil requuire precise
preparation of the apical region of the root, whilst a fluid injectable system might be
able to penetrate areas that simply have had infected tissue removed (jacobsen. 2008).
Once access and initial drainage have been achieved, a rubber dam should be
applied to the tooth to complete the operation. Before any further instrumentation is
carried out, the pulp chamber should be thoroughly irrigated with a solution of
sodium hypochlorite to remove as much superficial organic and inorganic debris as
possible. This in itself may bring considerable pain relief and will make subsequent
instrumentation easier. Having debrided the canals to the best possible extent with
frequent changes of irrigant, the canals should be dried with paper points and a dry
sterile cotton wool pledget placed in the pulp chamber to prevent ingress of the
temporary dressing. The access cavity is then sealed to prevent re-infection of the
canals from the oral cavity. If complete debridement was not possible the patient must
be recalled within 48 hours. At this time it will usually be possible to complete
instrumentation and place a calcium hydroxide dressing in the canals (Carrotte,
2004).
The temptation to leave the tooth open to drain must be resisted at all costs.
The microbial flora of the canal will be changed, making treatment more difficult and
lowering the long-term prognosis. Furthermore, this treatment contravenes the prime

objective of treatment: to disinfect the root canal. If the clinician does not have
sufficient time to carry out adequate treatment when opening the tooth, good clinical
practice would suggest re-appointing the patient to the end of the treatment session
when time is available (Carrotte, 2004).
Antibiotics are only required when there is systemic spread of the infection,
the patient is unwell and has a raised temperature. Antibiotics are not an alternative to
appropriate cleaning and disinfection of the root canal. There is a serious tendency to
over prescription of antibiotics in situations where they are not indicated. If, however,
there is a clinical reason for their use, amoxycillin is usually the agent of choice,
prescribing 250 mg three times a day until the infection is under control and root
canal therapy initiated. Metronidazole is a useful alternative where the penicillins are
contra-indicated (Carrotte, 2004).
Root canal treatment with total pulp removal (pulpectomy) is the treatment of
choice with irreversible pulpitis. In emergency situations and when apexogenesis is
being attempted, partial pulp removal (pulpotomy) may be indicated. Intracanal
medications are not beneficial for pain control but may be used to prevent bacterial
contamination of the residual pulp. If a patient refuses root canal treatment (or it is
impractical), permanent pulpotomy is an option and preferable to extraction.
However, the long term success rate has not been shown to be comparable to that root
canal treatment. (Torabinejad et al. 2014)
Acute Irreversible pulpitis management:
1.
2.
3.
4.
5.
6.
7.

Profound anesthesia of affected tooth

Application of the rubber damn
Preparation of the access cavity
Extirpation of the pulp from the chamber
Thorough irrigation and debridement of the pulp chamber
Determination of the working length
Total extirpation of the pulp followed by cleaning and shaping of the root

canal
8. Thorough irrigation of the root canal system
9. Drying of the root canal with sterile absorbent points
10. Placement of a dry cotton pellet or pellet moistened with CMCP, formocresol
or eugenol in the pulp chamber and sealing it with the temporary restoration

11. Relief of the occlusion

12. Appropriate analgesics therapy and antibiotics, if needed. (Nisha and Amit,
2014)

2.6 Traumatic Ulcer

2.6.1 Definition and etiology
Traumatic ulcers can be due to physical (mechanical, thermal, electrical) or
chemical trauma. Traumatic ulcers are common oral lesions, and can be caused by a
sharp or broken tooth, rough fillings, orthodontic, dental instruments, biting, denture
irritation, sharp foreign bodies, numb lips or tongue being bitten after a local
anaesthetic injection, etc. (Anne Field and Lesley Longman, 2003)
Trauma, minor aphthous ulcers, drugs, and infections are responsible for most
acute, self limiting oral ulcers. Traumatic injury to the oral mucosa may be caused by
a sharp tooth margin, an overextended denture flange, or cheek biting Chemical and
thermal trauma can also cause oral ulceration. Traumatic ulceration may mask or
mimic more serious causes. The cause of trauma should be identified and removed
with follow up to ensure healing. (M.U Ahmed and M.N.Uddin, 2010)
2.6.2 Clinical features
They are clinically diverse, but usually appear as a single, painful ulcer with a
smooth red or whitish-yellow surface and a thin erythematous halo. They are usually
soft on palpation, and heal without scarring within 610 days, spontaneously or after
removal of the cause. However, chronic traumatic ulcers may clinically mimic a
carcinoma. The tongue, lip, and buccal mucosa are the sites of predilection. The
diagnosis is based on the history and clinical features. However, if an ulcer persists
over 1012 days a biopsy must be taken to rule out cancer. (Anne Field and Lesley
Longman, 2003)
Minor aphthous ulcers are painful, discrete, and round, measuring less than 1
cm in diameter with a greyish base and a red halo. As many as six may occur at a
time on multiple oral mucosal sites. The cause is unknown in most patients, although
predisposing factors such as familial tendency, local trauma, and stress are often

cited. Such ulcers most commonly involve non keratinised oral mucosa. They
typically heal Spontaneously within 10 days, although more severe forms may
persist, and recurrence is common. The majority of patients presenting with aphthous
ulcers do not have an associated underlying systemic disease, but aphthous-like ulcers
may occur in association with systemic disease such as inflammatory bowel disease,
or use of medication such as non-steroidal anti-inflammatory drugs. (M.U Ahmed and
M.N.Uddin, 2010)
2.6.3 Laboratory tests
Histopathological examination.
2.6.4 Differential diagnosis
Squamous-cell carcinoma and other malignancies, eosinophilic ulcer,
aphthous ulcer, RigaFede disease, syphilis, tuberculosis, systemic mycoses.
(Laskaris, 2006)
2.6.5 Treatment
. The treatment of ulcerated lesions varies depending upon size, duration, and
location. (M.U Ahmed and M.N.Uddin, 2010)

With ulcerations induced by mechanical trauma or thermal burns from food,

remove the obvious cause. These lesions typically resolve within 10-14 days.

Ulcerations associated with chemical injuries will resolve. The best treatment
for chemical injuries is preventing exposure to the caustic materials.

With electrical burns, verify status and administer the vaccine if necessary.
Patients with oral electrical burns are usually treated at burn centers.

Antibiotics, usually penicillin, may be administered to prevent secondary

infection, especially if the lesions are severe and deeply seated. Most
traumatic ulcers resolve without the need for antibiotic treatment.

Treatment modalities for minor ulcerations include the following:

o

Removal of the irritants or cause

Use of a soft mouth guard

Use of sedative mouth rinses

Consumption of a soft, bland diet

Use of warm sodium chloride rinses

Application of topical corticosteroids

Removal of traumatic factors. Topical steroids may be used for a short
time like kenalog (Anne Field and Lesley Longman, 2003)

Application of topical anesthetics

2.7 Fixed Partial Dentures (Bridge)

Fixed partial dentures (FPDs) are "dental prostheses that are luted, screwed, or
mechanically attached or otherwise securely retained to natural teeth, tooth roots,
and/or dental implant abutments." During the past decades, many types of FPDs or
"bridges" have been used to replace missing teeth. With the introduction and
widespread use of osseointegrated implants, many missing teeth are now being
replaced in this manner rather than with FPDs. Dental bridges can, of course, still be
used successfully, and this article will briefly review the many methods of bridge
construction and relate them to their applicability and current acceptance of the
practicing dentist and the treated patient. These will include: cast-gold, stress-broken
bridges; resin-bonded, etched retainers; porcelain-fused-to-metal (PFM) bridges; and
all-ceramic bridges, including zirconia. (Anonim, 2005)
2.7.1 The purpose Usage
The usability use of denture bridges among others: (Smith,Bernard G N dan
Howe, Leslie C, 2007)
a. improve the appearance
In patients with loss of teeth, especially anterior teeth, of course emotion
considered.
b. ability to chew
Many patients can not eat properly because of missing teeth.
c. occlusal stability
Occlusal stability can be lost due to missing teeth. Loss of teeth can cause the
surrounding teeth extrusion, migration and destabilize the patient's occlusion.

d. Improving pronunciation
Loss of upper incisors can disrupt a person's pronunciation.
e. As periodontal splinting
Tooth loss can cause adjacent teeth shake, so denture bridges can function as well
as splinting.
2.7.2 Indications and Contraindications
Indications manufacture of denture bridges are as follows.
1. Loss of one or more teeth original
2. The bite in (deep bite)
3. abutments require restoration
4. abnormal diastema, the magnitude of the prosthesis is less than normal room
5. abutments require mitigation in the form of stabilization or splint
6. There is a diastema post-treatment.
Contraindications for roducing denture bridges are:
- OH ill-maintained
- Physical handicap
- On high caries index
- Cross-bite, malposition, progeny
- Migration or extrusion that severe
2.7.3 Denture Components
Denture bridge consists of several components, which is as follows.
1. Retainer
2. Connectors
3. pontic
4. Buffer (abutment)

Figure 8. Denture Components.

Figure 9. Fixed Partial Dentures or Bridge

1. Retainer
It is part of the denture bridge denture that connects with abutment.
2. pontic
Is part of a bridge denture that replaces missing natural tooth
3. Connector (Connector)
Is part of an artificial tooth pontic bridge connecting the retainer, pontic with
pontic or retainer with the retainer so that unites these parts to be able to function
as a load distributor splinting and chew.
4. Buffer (abutments)
In accordance with the number, location and function are known term:
1. Single abutment only use one abutment
2. Double abutments when using two abutment
3. Multiple abutment when using more than two abutment
4. Terminal abutment

5. Intermediate / pier abutment

6. splinted abutment
7. Double splinted
2.7.4 Advantages and Disadvantages
The advantage of the use of denture bridges are as follows.
1. Because it is attached to the natural teeth are not easily dislodged or swallowed.
2. Perceived as the teeth of a patient.
3. Do not have clamps that can cause wear on the enamel surface, because each time
removed and installed again in the mouth.
4. Can have the effect of dental splint that protects against stress.
5. Spread pressure function so beneficial to the entire tooth supporting tissues.
2.7.5 Stages of Preparation
Making denture bridge consists of several parts, as follows. (Prajitno, H.R, 1994)
1. Preparation
Preparation is an act pengerindaan or grinding the teeth for the purpose of
providing a place for restorative materials artificial crown or fixed partial denture.
2. Printing
Before the printing is done, the state of teeth and surrounding soft tissue needs to
be checked, whether all in good health and free of inflammation. There are a wide
variety of printed materials, such as hydrocolloids, rubber base, polysulfide rubber
base, silicon rubber base, and polyeter rubber base.
3. Preparation of the die / working model
Die is a positive reproduction of the prepared tooth and are made of cast stone or
metal or hard plastic. According to the relationship with the working model of the die
is divided into solitair die and removable die.
4. Pattern Making Candles
Which is defined by the pattern of wax or wax-pattern is: a model of a retainer or
restorations are made of wax which is then reproduced into metal or akrilik.
5. Pontic
Pontic is part of a bridge denture that replaces missing natural teeth and serve to
restore chewing function and speech, aesthetic comfort (comfort), as well as
maintaining the relationship between the teeth tetangga prevent migration /
relationship with the opponent teeth a extrusion

2.7.6 Cementing bridge

Cementing the bridge means a bridge with cement to attach the abutment in the
mouth. Abutment preparation before cementing should do its best to prevent a change
in the occlusal relationship and the gingiva, which may also be due to the hydraulic
pressure that interferes with the pulp. It should be avoided by the operator.
Cement is used to affix the bridge is zinc phosphate cement, cement silikofosfat,
EBA alumina cement, polycarboxylate cement, and composite resin cement.
Selection is made by biologic properties, biophysics, and the effect on the aesthetic.
2.7.7 Types of Bridge Denture
There are 6 type of fixed partial dentures or bridges :
1. Fixed Fixed or Rigid bridge
One

or

more

retainers

side

of

the

pontic.

Differential

result

in

bond

failure.

This

design

are

placed

movement
of

bridge

of
is

on
abutments
indicated

either
can
where

excursive movements on pontics cannot be avoided. (Wright WE, 1986)

Fixed bridges are applied by either placing crowns on the abutment teeth or by
bonding the artificial teeth directly to the abutment teeth. Removable bridges are
attached to the teeth with metal clasps or by precision attachments. (Wright WE,
1986)
If you're missing one or more teeth, you may be aware of their importance to
your appearance and dental health. Your teeth work together for many daily functions
from eating to speaking. With missing teeth, it's difficult to do these things. Missing
teeth can and should be replaced. Fixed bridges or implants are a great way to restore
your dental health and appearance. (Wright WE, 1986)

Fixed Fixed or Rigid bridge

A bridge (fixed partial denture) is a device, which fills the gap where teeth are
absent. Fixed bridges are bonded into place and can only be removed by a dental
professional. Removable bridges, as the name implies, can be taken out and cleaned.
Fixed bridges offer more stability than their removable counterparts. (Wright WE,
1986)
2. Fixed Free or Stress-broken bridge
Design is in two parts, keyed together by anon-rigid attachment. Connector
which may be either ready or laboratory-made, permits movement of the two parts
relative to each other in vertical direction mainly. Provides stress breaking action.
Should be used in short spans and where opposing proximal walls of abutment cant
be prepared parallel
The stress-breaking device should always be placed in the normal distal contours
of the anterior abutment, whilst the pontic should always be attached to the posterior
abutment. The long axis of the posterior teeth usually incline slightly in a mesial
direction so that vertically applied occlusal forces produce further mesial movement.
If the female part of the connector is placed on the distal side of the anterior
abutment, mesial movement seats the male portion more completely into the female
portion. This leads to increased stabil

Fixed-movable

3. Cantilever bridge
Cantilever Bridge Denture is a denture prosthesis which is only supported on one
side by one or more abutment teeth (buffer).

Anterior Cantilever Bridge. (Barclay, C.W and Walmsley, A.D. 1998)

Posterior Cantilever Bridge. (Barclay, C.W and Walmsley, A.D. 1998)

Cantilever Bridge. (Barclay, C.W and Walmsley, A.D. 1998)

4. Spring Cantilever bridge

The spring bridge may be defined as a bridge where the pontic is not adjacent to
the abutement tooth or teeth, but is connected to a retainer by a long flexible arm so
that the force of mastication is partly absorbed by the periodontal membrane of the
abutment teeth, and partly by the mucosa in contact with the tissue area of the pontic.
This definition described a bridge design which differs markedly from classical
bridge designs, and indeed contravenes some of the rules for successful prostheses of
the usual designs in the following ways : (Thompson, A.T., 1945)
1. There is more than minimum contact between the pontic and the underlying tissue.
2. Design is not rigid, and the pontic moved during mastication
3. The design is not within the line of the arch, and forces with a relatively long
leverage arm are applied to the abutment tooth.
4. The periodontal membrane of the abutment teeth is not the only tissue to resist the
forces of mastication.

Spring Cantilever bridge (Barclay, C.W and Walmsley, A.D. 1998)

5. Maryland or Resin retained bridge
Denture is used to replace missing teeth where the tooth is located on the front
and on the neighboring teeth are still healthy or not there is a large fillings. Teeth that
are replaced are made of porcelain and metal wings that can be pasted on the back of
the teeth so as not to be seen from the front. (Thompson, A.T., 1945)

Conventional Marryland-upper arch. (Barclay, C.W and Walmsley, A.D. 1998)

6. Hybrid bridge with Conventional retainer at one end and a resin retained
retainer at the other end
A

combination

of

conventional

retainer

at

one

end

and a resin-bonded retainer at the other end of the pontic. Indicated where one of the
abutments is minimally restored,and a resin-bonded retainer is used at this site to
conserve tooth tissue. The male part of the joint is often attached to the

resin-bonded retainer to simplify maintenance when de-bond occurs. (Thompson,

A.T., 1945)

Hybrid bridge (Barclay, C.W and Walmsley, A.D. 1998)

The hybrid application was for the virgin tooth at one end of the space and the
heavily restored tooth at the other end. Many variations were described but all had a
poor success rate. 32% failure rate in 48 months.
2.7.8 The failure of Usage Denture
As for the use of some form of failure of the bridge denture that can be found
include: (Tylman SD., 1970)
1. Intrusion supporting teeth, which changes the position of the supporting teeth,
away from the occlusal plane.
2. Dental caries supporters, generally due to restoration rtetainer periphery is too
panjan, less long or incomplete and open. For others, the damage to the crown
retainer bahna loose, embrasure is too narrow, the choice of the wrong type of
retainer, and a temporary crown is merusajk or, encourage gingival too long.
3. Periodontitis support networks
4. The connector is broken.
5. People complain that there are no bad feelings. Things that can cause this disorder
is premature contacts or improper occlusion, occlusion field is too broad and or
accumulation of food residue between the pontic and the retainer, excessive

pressure on the gingiva. Diseased cervical area, thermal shock because the patient
has not been accustomed to.
6. Retainer or off of a bridge abutment. Sometimes the whole bridge can be cemented
off after the cause of the release is known restoration and removed. If not all of the
retainer off the bridge removed by means of bridges destroyed and re-created a
new one, if anything, and conditions allow
7. Bridge lost support, may be interrupted because of the bridge, occlusal surface
area, embrasure form, shape retainer, less abutment, trauma to the periodontium
and printing techniques.
8. There is a change in the pulp can be caused by way of preparation, preparation yan
g is not protected with a temporary crown, hidden caries, stimulation of cement as
well as the occurrence of perforation.
9. The broken bridge. Can be caused by exposure to shoulder or shoulder is bad,
wrong casting techniques and material fatigue.
10. Loss of a layer of aesthetic
11. Other causes that led to the bridge is not working
The efforts that can be done to prevent such failures may be the selection of the
number and distribution of the supporting teeth, soft coatings applications, the use of
stress-absorbing element and the use of non-rigid connectors. The difference in the
movement of teeth and implants can cause various forms of malfunctions dukungazn
bridge denture teeth and implants. Businesses that are most important to consider in
preventing various forms of such failure is to prevent excessive pressure on the
denture supporting bridge that arise due to differences in the movement.
2.7.9 Antes Law
The root surface area of the abutment teeth had to equal or the surpass that of the
teeth bieng replaced with pontics.
Procedure :
Full veneer retainer is required on the abutment which must exhibit excellent
bone support . To prevent rotaion of the pontic and abutment a rest may be add to
the neighboring abutment . There should be no occlusal contact on the pontic in
centric orlateral excursions. The pontic should be kept as small as possible to

minimize the leverage effect and it should process maximum occlusogiingival height
to ensure a rigid prosthesis .

References
Loe, H., Theilade, E. & Jensen, S. B. (1965) Experimental gingivitis in man. Journal
of Periodontology 36, 177187.
Heitz-Mayfield, L. J., Schatzle, M., Loe, H., Burgin, W., A nerud ., Boysen, H. &
Lang, N. P. (2003) Clinical course of chronic periodontitis. II. Incidence,
characteristics and time of occurrence of the initial periodontal lesion.
Journal of Clinical Periodontology 30, 902908.
Cawson RA, Odell EW, and Porter S. 2002. Cawson's Essentials of Oral Pathology
and Oral Medicine. 7th ed. Spain: Churcill Livingstone. pp. 68-78.
Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. 2000. Periodontal disease
and cardiovascular disease. Journal of Periodontology 67(10 Suppl):1123-37.
Mayo Clinic, 2002. Diseases and Conditions Gingivitis. Available on:
http://www.mayoclinic.org . Accessed on 16th October, 2014.
NHS, 2014. Bad Breath (Halitosis). Available on: http://www.nhs.uk . Accessed on
16th October, 2014.
Cohen ES. 2007. Atlas of Cosmetic and Reconstructive Periodontal Surgery Third
Edition. Shelton: Peoples Medical Publishing House. p. 29
Darby ML, Walsh MM. 2010. Dental Hygiene: Theory and Practice. St. Louis:
Saunders Elsevier. p. 311

Jenkins B, Heasman P. 2003. The prevention and control of periodontal disease in

Prevention of Oral Disease (Eds. Murray JJ, Nunn JH, Steele JG). Fourth Edition. Oxford:
Oxford University Press. p. 140
Marya CM. 2011. A Textbook of Public Health Dentistry. New Delhi: Jaypee Brothers
Medical Publishers (Ltd). p. 418
Noble S. 2012. Clinical Textbook of Dental Hygiene and Therapy. London: WileyBlackwell.
Felton S, Felton A, Chapman A. 2014. Basic Guide Oral Health Education and
Promotion. West Sussex: John Wiley & Sons. p. 182-183
Dumitrescu AL. 2010. Etiology and Pathogenesis of Periodontal Disease. Berlin:
Springer-Verlag Berlin Heidelberg. p. 30
Gutkowski S. 2012. Mechanical plaque removal in Comprehensive Preventive
Dentistry. (Ed. Limeback H). Iowa: Wiley-Blackwell. p. 138

Cohen S and Burns RC. 1994. Pathways of The Pulp. 6th ed.

Publisher: Mosby, Incorporate

Fors UGH, and Berg JO: Endodontic treatment of root canals obstructed

by foreign objects, Int Endod J 19:2, 1986.

Ghom. 2008. Textbook of oral radiology. New Delhi. Elsevier
Bricker SL, Langlais RP, and Miller CS. 2002. Oral diagnosis and oral

medicine. Ontario. BC Decker Inc

Carrotte, P. 2004. Endodontics: Part 3 Treatment of Endodontic Emergencies.

British Dental Journal 197, 299-305 (2004). Doi:10.1038/sj.bdj.4811641.

Jacobsen, Peter. 2008. Restorative Dentistry: An Integrated Approach.

Blacwell Publishing Ltd. p:115

Nisha and Amit. 2014. Textbook of Endodontics. India: Jaypee Brothers

Medical Publishers. p: 338

Torabinejad et al. 2014. Endodontics Principles and Practice. 4th ed. Elsevier
Health Science.
o Health Promotion Board: Dental Caries, affiliated with the
Singapore government. Page accessed August 14, 2006.
o Richie S. King (November 28, 2011). "A Closer Look at Teeth
May Mean More Fillings". The New York Times. Retrieved
November 30, 2011. "An incipient carious lesion is the initial
stage of structural damage to the enamel, usually caused by a
bacterial infection that produces tooth-dissolving acid."
o Johnson, Clarke. "Biology of the Human Dentition." Page
accessed July 18, 2007.

o
o

Hartmann, Richard W. Ludwig's Angina in Children, hosted on

the American Academy of Family Physicians website. Page
accessed May 25, 2008.
Southam JC, Soames JV (1993). "2. Dental Caries". Oral
pathology (2nd ed.). Oxford: Oxford Univ. Press. ISBN 0-19262214-5.
Smith B, Pickard HM, Kidd EAM (1990). "1. Why restore
teeth?". Pickard's manual of operative dentistry (6th ed.). Oxford
[Oxfordshire]: Oxford University Press. ISBN 0-19-261808-3.
Rogers AH (editor). (2008). Molecular Oral Microbiology. Caister
Academic Press. ISBN 978-1-904455-24-0.
Neville, B.W., Douglas Damm, Carl Allen, Jerry Bouquot. "Oral
& Maxillofacial Pathology." 2nd edition, 2002, p. 94. ISBN 07216-9003-3.
Dawes C (December 2003). "What is the critical pH and why
does a tooth dissolve in acid?". J Can Dent Assoc 69 (11): 722
4. PMID 14653937.
Mellberg JR (1986). "Demineralization and remineralization of
root surface caries". Gerodontology 5 (1): 2531.
doi:10.1111/j.1741-2358.1986.tb00380.x. PMID 3549537.
Borzabadi-Farahani, A; Eslamipour, F; Asgari, I (2011).
"Association between orthodontic treatment need and caries
experience". Acta Odontol Scand 69 (1): 211.
doi:10.3109/00016357.2010.516732. PMID 20923258.
Sherif Mohamed, Al-Sakiti, Ahmed Awadh, Mostafa, Yehya
Ahmed. Dental crowding as a caries risk factor: A systematic
reviewHafez, Hend Salah, Shaarawy, American Journal of
Orthodontics & Dentofacial Orthopedics. 2012;142(4):443-50
Douglass, JM; Li, Y; Tinanoff, N. (SepOct 2008), Association of
mutans streptococci between caregivers and their children.,
Pediatric Dentistry 30 (5): 37587
Silverstone LM (May 1983). "Remineralization and enamel
caries: new concepts". Dent Update 10 (4): 26173.
PMID 6578983.
Summit, James B., J. William Robbins, and Richard S.
Schwartz. "Fundamentals of Operative Dentistry: A
Contemporary Approach." 2nd edition. Carol Stream, Illinois,
Quintessence Publishing Co, Inc, 2001, p. 75. ISBN 0-86715382-2.
Neville, B.W., Douglas Damm, Carl Allen, Jerry Bouquot. "Oral
& Maxillofacial Pathology." 2nd edition, 2002, p. 347. ISBN 07216-9003-3.

Anonim. Tobacco Use Increases the Risk of Gum Disease,

hosted on the American Academy of Periodontology. Page
accessed January 9, 2007.
o Banting, D.W. "The Diagnosis of Root Caries." Presentation to
the National Institute of Health Consensus Development
Conference on Diagnosis and Management of Dental Caries
Throughout Life, in pdf format, hosted on the National Institute
of Dental and Craniofacial Research, p. 19. Page accessed
August 15, 2006.
o Arora M, Weuve J, Schwartz J, Wright RO (2008). "Association
of environmental cadmium exposure with pediatric dental
caries". Environ Health Perspect. 116 (6): 821825.
doi:10.1289/ehp.10947. PMC 2430240. PMID 18560540.
DYE, B. (2010). Trends in Oral Health by Poverty Status as Measured
by Healthy People 2010 Objectives. Public Health Reports, 125(6),
817.
Tellez, M., Gomez, J., Pretty, I., Ellwood, R., Ismail, A.Evidence on
existing caries risk assessment systems: are they predictive of future
caries? Community Dent Oral Epidemiol. 2012
o

(7. Thompson, A. R. The spring bridge. Brit. D.J,. 80 :3. 1945. Page 18-19)
(6. Wright WE. Success with the cantilever fixed partial denture. J Prosthet
Dent. 1986;55(5):537-539. )
M.U Ahmed and M.N.Uddin .2010. Vol 1 (2). Bangladesh Journal of Plastic Surgery
Anonim. Glossary of prosthodontic terms. J Prosthet Dent. 2005;94(1);10-92.

Laskaris. 2nd ed. 2006. Pocket Atlas of Oral Disease. Newyork

Anne Field and Lesley Longman. 5th ed. 2003. Tyldesleys Oral Medicine. Oxford
University press
1. Barclay,

C.W;

Walmsley,

A.D.

1998.

Fixed

and

Removable

Prosthodontics.Birmingham: Churcill Livingstone, hal 115.

2. Smith,Bernard G N;Howe, Leslie C. 2007. Planning and Making Crown and
Bridges, 4th ed. New York: Informa Healthcare.
3. Prajitno, H.R. 1994. Ilmu Geligi Tiruan Jembatan: Pengetahuan Dasar dan
Rancangan Pembuatan. Jakarta : EGC.
4. Tylman SD. Construction of Pontics For Fixed Partial Dentures: Indications,
Types, and Materials. In Theory and Practice of Crown and Fixed Partial
Prosthodontics. 6th ed. Saint Louis: CV Mosby 1970: 26, 165, 650-81.

5. 1 Sharda AJ, Shetty S. A comparative study of oral health

knowledge, attitude and behaviour of non-medical, paramedical and medical students in Udaipur city, Rajasthan,
India. International Journal of Dental Hygiene 2010; 8: 1019.
6. 2. Sam HSS. Prospek Oral Medicine dalam Upaya
Peningkatan Kesehatan
7.
8. Masyarakat Indonesia. Jurnal PDGI 1992; 41: 11-6.
9.
10. 3.

Liu LJ, Xiao W, He QB, Jiang WW. Generic and oral

quality of life is affected by oral mucosal diseases. BMC

Oral Health 2012; 12: 1-6.
11. 4.

Kumar S, Kriplani D, Vrinda S, Tadakamadla J,

Tibdewal H, Duraiswamy P, et al. Oral Health Attitudes

and Behaviour as Predisposing Factor for Dental Caries
Experience

Among

Health

Professional

and

Other

Professional College Students of India. Oral Health Prev

Dent 2010; 8: 195202.
12. 5.

Aubuchon SM. Development and validation of an

instrument

to

assess

knowledge,

beliefs,

college

and

students

behaviors.

oral

Tesis.

health

Alabama:

Department of Health Sciences in the Graduate School of

The University of Alabama, 2010: 2-5.
13. 6.

Ambika L, Keluskar V, Hugar S, Patil S. Prevalence of oral

mucosal lesions and variations in Indian public school

children. Braz J Oral Sci 2011; 10: 288-93.