GRUP F

TUTOR : Prof.

Dr. Mieke Sylvia MAR., drg., M.S., Sp.Ort.

1. Nabiela Rahardia
2. Firly Rakhmawati
3. Nike Kurniawati
4. Claudia Yosephine Sianipar
5. Rizky Nugraha Putra
6. Rega Maurischa A.P.
7. Setian Fitri Sayekti
8. Viviana Saputra
9. Risky Anita Oktaviani
10. Cyntia Nur Malikfa Nugraha
11. Cornelia Johana Corputty
12. Luluk Rachmawati
13. Reno Andrey Sudarmanto
14. Amelia Sinta Mahardini

FACULTY OF DENTISTRY
AIRLANGGA UNIVERSITY
2014

ABSTRACT

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A 40-years-old woman with maxillary right molar teeth caries and two right maxillary
premolar teeth had been removed. Patients admitted feel spontaneous pain at the side of tooth
caries that has occurred since a week ago. Patients want the doctor made the fixed dentures in
the jaw tooth loss. The purpose of our discussion is to determine the diagnosis and the correct
handling of the case. Our hypothesis is this woman affected by irreversible pulpitis due to
caries had reached the pulp tissue is characterized by spontaneous pain. The treatment to be
taken is the first need to eliminate the spontaneous pain. It also provided a topical application
to remove stomatitis. Then give the root canal planning. It was only made fixed dentures as
requested patient. Condition of the fixed dentures is loose oral hygiene of the patient must be
in good condition, no ulcer, caries, and periodontal disease in the teeth, this is done to avoid
any traumatic or things that are not desirable at the time of fixed dentures has worn off
patients. Keep in mind that there are patients given rehabilitation and maintenance is once
every 6 months.
Keyword: irreversible pulpitis, fixed dentures, root canal treatment

CONTENT

CHAPTER 1
INTRODUCTION

1.1 Background
Health is the most important part in human life, this include physically and spiritually
health. Health that needs to be considered beside the general health is oral health, because
oral health can affect overall health. Optimal oral health can be achieved by a treatment
with an expert like a dentist.
A dentist should have specialized knowledge and skills in dealing with problems that
are related to dental health. Complex treatment of dental health is very important. As a
dentist should be aware that patients with state of the teeth and mouth problems are
complex should be treated with caution and appropriate. A dentist have to know that
patients with complex oral and mouth problem should be treated carefully.
In this case, a woman patient aged 40 years who works as a secretary of the company
came to the RSGM-P FKG Unair ask for a fixed dentures on the upper right side. On that
side there are cavities and throbbing pain in patient which happen spontaneously since 1
week ago. The patient also complained of bad breath and stomatitis on the inside of the
cheek (near the cavities). It is known that patient has a bad oral hygiene and it was found
that radiographic widening of the apical periodontal ligament.
After knowing the case and the information, we can analyze and determine the
appropriate therapy in these patients.
Analysis and therapy plan should also involve several aspects, such as the
identification of oral soft tissue abnormalities, determine the diagnosis and treatment plan
regarding periodontal disorders, understand the identification, etiology, and diagnosis and
treatment plans in case of tooths crown damage and pulp tissue abnormalities, capable of
handling cases in oral surgery clinic, capable of planning orthodontic treatment to support
other treatments, knowing and understanding the condition of patients who require
extended care in the field of Prosthodontics, determining the appropriate kind of
radiographic to support the diagnosis and treatment planning and post-treatment
evaluation, and capable to determine the kinds of drugs that can be used in case of
emergency.
1.2 Purpose
1.2.1 Spesific Purpose
Students are able to understand the step based on priority conditions for treatment of
1.2.2

clinical cases in the field of dentistry

General Purpose
- To identify the oral soft tissue abnormalities
- Determining the diagnosis and treatment plan involving periodontal disorders
- Understand the diagnostic tests and dental care plan for children

- Understanding the identification, etiology and diagnosis as well as the kinds of

treatment plans in case of damage to the crown of the tooth and the pulp tissue
disorders
- Conducting clinical case management in oral surgery
- Plan orthodontic treatment to support other disciplines appropriate cases
- Knowing the conditions of patients who require immediate care or advanced
carefield Prosthodontics
- Determining the kind of radiographic which can be used to support the diagnosis
and treatment planning as well as post-treatment evaluation
- Determining the kind of drug that can be used in case of an emergency nature
1.3 Problem
A 40 years female patient, came to the RSGM-P FKG Unair to ask for a fixed dentures on
the upper right side. On that side there are cavities and throbbing pain in patient which
happen spontaneously since 1 week ago. The patient also complained of bad breath and
stomatitis on the inside of the cheek (near the cavities).
1.4 Benefits
Capable to identify the etiology, diagnosis, and treatment plan in the case and is expected
to be useful for the students when it became a dentist someday.

CHAPTER 2
REVIEW OF LITERATURES

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 milligram and extends
10

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,

instruments (Cawson, 2002).

with

special

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, 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 refers to a State of bad breath originating from a
State

of

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 effect

mechanism similar

to

that

of halitosis physiological,

in

occurs
this

in
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 a person, there are exogenous proteinsubstrate-substrate (leftovers)
and endogenous protein(deskuamasi epithelium of
which contains many amino

the

mouth, saliva and

acids containing sulfur

(S). In

blood proteins)

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, i.e., the use of proteins, peptides, amino
acids as its

main source. Most Gram-positive

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

referred

to

the

as Volatile Sulfur Compounds

(VSCs) containinghydrogen 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

also cause foul breath odor less. Fried

foods contain a

food
lot

of

consumed daily can

seasoning and onion-

like 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 and Read by providing a capsule containing garlic to patients who
researched 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.
1.1.

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
the decay

and cause a gas smell. (Ravel,

2006) In

of detritus caught in paperback, this condition can

decaying saliva so

that adds

to

the severe bad

addition due

also

to

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

feses exudate out

that serve

through the

as a virulence as
Groove of

the

of H2S gas and produces embossed NH2(Amino) so the

well as it

may

cause apurulent

gingiva.

Metabolic reaction

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) pseudohalitosis an

d halitophobia. GenuineHalitosis distinguished again over
pathological. Physiological Halitosis is temporary
maintenance, reverse halitosis pathological is halitosis is

the physiological
and does

not

permanent and

and
require
cannot

be resolved simply by the maintenance of oral hygiene alone, but require a handling and
care according to the source the causes of halitosis

1.2.

Halitosis Fisiology

Halitosis is

a physiological halitosis who is

maintenance. On this type

temporary

and does

not

require

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
1.3.
Halitosis is

Patology Halitosis
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 of bacteria associated with oral hygieneconditions are bad is
the 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 infection in the nasal cavity and paranasal
sinuses, tonsils(tonsilhlith) infections,
also produceodorous gases. In

indigestion, peptic

addition, systemic

diseases such

failure, ketoasidosir and liver

ulcers can
as

diabetes,renal
disorders can

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

people

with kidney

damage andammonia smelling accompanied

by complaints of dysgeusi, whereas in patients with disorders of the liver and the gall
bladder as cirrhosis hepatis will smell the

breath of

arms, knownwith

the

term foetor hepaticus.

2.

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
using dental

or eliminated altogether by
floss,

keeping oral

hygiene such

clean tongue, use mouthwash and a

takes treatment by professionals

to

make a

healthy

referral. To

be

as brushing

teeth,

diet, but sometimes it

able to cope

with

the halitosis effectively, thoroughly vetting is required and the right diagnosis. Precaution and
treatment on halitosis are:
2.1.

Brushing Teeth

Teeth should be brushed twice a 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.
2.2.
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 a day. After this
stage is allowed to clean or rinsed gargle with water.
2.3.
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 of the
tongue, while still stand, while being
with light pressure. Use a

pulled forward and

clean cloth/paper tissue or running

down

water

to

clean

the tongue scrapper. Repeat this procedure 2-4 times until the entire surface is
cleaned.
2.4.
Mouthwash
Mouthwash is
used at

least once

use mouthwash before

day. The

most

appropriatetime to

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
cause oral mucosa chipped. Therefore, we
alcoholic mouthwash such

recommend

that

you use non

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
2.5.
Healthy Diet

A Healthy

Diet is

done by

eating fibrous vegetables such

as fresh

food and

has a coarse consistency that can help rid dorsum of the tongue, avoid eating foods
that cause odor, as
research in Japan

well as
reported

drinking

plenty

of water each

that unsweetened yogurt may

day. Recently,

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

when the

protein. Chew sugar

mouth feels dry. Drinking

lots

free candy (non-cariogenik) especially

of

water in

day. Avoid

consumption, smoking, drugs that can decrease the flow of saliva.

2.6.
Professional Treatment
When caries, periodontal disease or other mouth infections that
of halitosis, special handling is
the patching, scaling or

required by

professionals,

dental root (root planning). In

cause the
for

addition, the

alcohol

onset

example, do
dentist will

deprive the 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/ZnCl 2 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 life-threatening (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, 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. 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, 2003). Dentin and cementum are more
susceptible to caries than enamel because they have lower mineral content (Mellberg, 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 subgingival 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, 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. 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. 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. 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, 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, 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 longterm patient management that prevents caries initiation and arrests or reverses the progression
of lesions (Tellez, 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 mid-section
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 the inflammatory
exudates are quickly vented. 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 a 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 reinfection 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 reappointing 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. Profound anesthesia of affected tooth
2. Application of the rubber damn
3. Preparation of the access cavity
4. Extirpation of the pulp from the chamber
5. Thorough irrigation and debridement of the pulp chamber
6. Determination of the working length
7. 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 and 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
side

of

or

more

retainers

the

pontic.

Differential

are
movement

placed
of

on
abutments

either
can

result

in

bond

failure.

This

design

of

bridge

is

indicated

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

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

1945)

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

to

the

(Thompson, A.T.,

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 .