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 1010 bacteria per

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 (Lo¨e 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 effectoccurs in a

mechanism similar to that of halitosis physiological, 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 a person, there are exogenous proteinsubstrate-

substrate (leftovers) 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, 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 the

mouth. Volatile sulfur compounds is referred to 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. Ektra oral fisiology

Some types of cuisine and substance of food consumed daily can

also cause foul breath odor less. Fried foods contain a lot of 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. 

1.2. 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 also be quickly

decaying saliva so that adds to the severe bad 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 the physiological

and pathological. Physiological Halitosis is temporary and does not require

maintenance, reverse halitosis pathological is halitosis is permanent and 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

2.1. Halitosis Fisiology

Halitosis is 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 wake-

up 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 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,

indigestion, peptic ulcers can also produceodorous gases. In addition, systemic

diseases such as diabetes,renal failure, ketoasidosir and liver disorders can

also cause badbreath are typical. Diabetic Ketoacidosis acetone smelling breathmenge

luartan. 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.

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 it’s 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 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.

3.2. Dental Floss

FLOSS the teeth (dental floss) used to clean the teeth, narrow slits that can't

be achieved with a 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.

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 of the tongue, while still stand, while being

pulled forward and down 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 cause oral mucosa chipped. Therefore, we recommend that

you use non 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 can help rid dorsum of the

tongue, avoid eating foods that cause odor, as well as drinking plenty

of water each day. Recently, 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 protein. Chew sugar

free candy (non-cariogenik) especially when the 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 cause the

onset of halitosis, special handling is required by professionals, for

example, do the patching, scaling or  dental root (root planning). In

addition, the 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/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 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 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 Sjögren'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

Sjögren'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 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 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. 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 6–10 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 10–12 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, Riga–Fede 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

o Use of a soft mouth guard

o Use of sedative mouth rinses

o Consumption of a soft, bland diet

o Use of warm sodium chloride rinses

o 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)

o 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 tetanggaà 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 denture’s or bridges :

1. Fixed – Fixed or Rigid bridge

One or more retainers are placed on either

side of the pontic. Differential movement of abutments 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 a 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 DentureAs 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 Ante’s 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 . 

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