GRUP FTUTOR : Prof. Dr. Mieke Sylvia MAR., drg., M.S., Sp.Ort.1. Nabiela Rahardia

021211131052

2. Firly Rakhmawati

0212111310533. Nike Kurniawati

0212111310544. Claudia Yosephine Sianipar

0212111310555. Rizky Nugraha Putra

0212111310566. Rega Maurischa A.P.

0212111310577. Setian Fitri Sayekti

0212111310588. Viviana Saputra

0212111310599. Risky Anita Oktaviani

02121113106010. Cyntia Nur Malikfa Nugraha

02121113106111. Cornelia Johana Corputty

02121113305112. Luluk Rachmawati

02121113305213. Reno Andrey Sudarmanto

02121113305314. Amelia Sinta Mahardini

021211133054

FACULTY OF DENTISTRYAIRLANGGA UNIVERSITY2014ABSTRACT

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 treatmentCONTENT

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 clinical cases in the field of dentistry1.2.2 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 nature1.3 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 2REVIEW OF LITERATURES2.1. 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, 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 Stateof bad breathoriginatingfrom a State of metabolicsystemicallyincludingthe gastrointestinal tract. Halitosiscan beaphysiologicalorpathologicalhalitosis.Halitosisis aphysiologicalhalitosiswhois temporary andoccurs when a substance thatcausedthesmell ofHematologytothe lungs and is usuallyderived fromfoods, such asonions andturnips andcanal so come frombeverages, such ascoffee,theas wellas alcoholic beverages.Halitosisishalitosisthatphysiologicaleffect occurs in mechanismsimilar to that ofhalitosisphysiological, in this casethe materialsarehematologistothe lungs.The main causes ofthisStatebecause of theState ofdisorder thatis localorsystemic diseasessuch asdiabetes mellitus,uremia, gastritis, peptic ulcers,and hepatitis.2.2.2 Etiology

Halitosiscan be causedby factorsof physiologicaland pathologicalderived fromthe oral cavityorintraoral andsystemic factorsorextraorally.Based onsurveys thathave been conducted in theUnited States,the main causes ofhalitosismost (90%)is due tofactorsinvolvingthe oral cavity. Needs to beemphasisthat halitosisis not a disease, but is considereda symptom ofcertain systemicdiseases.But that does notmeanthat any unpleasantsmell thatindicatesthe presence of aparticulardisease.2.2.2.1 Intraoral

Inthe oral cavityof a person,there areexogenousproteinsubstrate-substrate(leftovers) andendogenousprotein(deskuamasiepitheliumof the mouth,salivaand bloodproteins) whichcontainsmanyamino acidscontainingsulfur (S).In additionhalitosisare alsoproduced by thebacteria thatnormallylive on thesurface of the tongueandthroatthat helpsinthe process offood digestionwithsplittingof protein.The speciesof bacteria thatis present on theoralsurfacecan besakarolitik,i.e.useof carbohydratesas an energy source.Other speciesareasakarolitikorproteoliti, i.e., theuseof proteins,peptides, amino acidsasits mainsource.MostGram-positive bacteriaaregram-negativebacteriaandsakarolitikisproteolytic. according to researchspearheaded byProf.Dr. JosephTozentich.from the Universityof British Columbia,Vancouver, managed todetect thatthere is avolatilesulfurcompoundsandsmellsfoulas a resultcannot

production ofproteindecompositionbyanaerobicgram-negativebacteriain the mouth.Volatilesulfurcompoundsis referred to asVolatileSulfurCompounds (VSCs)containinghydrogen sulfide(H2S),Methilmercaptan(CH3SH) andDimethylsulfide (CH3SCH3) which isthe main cause ofhalitosiswhich comes fromthe oral cavity.

Condition ofthe mouththat can triggerthe onsetof bad breath isless orstopping offlow (flow)saliva,increasedanaerobicgram-negativebacteria,a growing number offoodproteins,pH ofthe oral cavityare morealkalineandthe rising number ofdead cell sandnecroticepithelial cellsin the mouth. Although the causes ofhalitosishas notfully known, most ofthe causesare known tocome fromfood scrapsleftinsidethe oral cavitywhich are processed bythe normalflora ofthe mouthcavity.Some factorsof the oral cavitywhich needspecialattentionbecause it hasthe roleas wellas a major influence onthe onset ofhalitosis at someonesuch assaliva,tongue,teethandinterdentalspace of ginggiva.1.1. Ektra oral fisiology

Sometypes of cuisineand substanceof food consumeddailycan alsocausefoulbreathodorless.Fried foodscontaina lot of seasoningandonion-likeodorthatcansurvivein the mouthfor 10-12 hours.Eventhesmell ofit stillfeelsafter theteethare cleaned.Thisodorarising fromsubstancesuchfoodis absorbed by thegastrointestinal tractandexcretedslowlythrough the lungs.This situationhas been demonstratedbyMorris andRead by providingacapsulecontaininggarlicto patientswho researched andproduced thesmell thatlast a long timeon the respiratoryair.Other researchersalsoproved thatthe smell ofthe garlicin a short timewasable tobe feltonrespiratoryand survivefor several hourswhilethe digestive tractsuch as the intestineis theseparate parts ofthe stomach.1.2. Patology Factor

Factorscausehalitosismostoften seeniscaused due tolesshygieneand health ofthe oral cavity.In patientswho arepoorhyginetend to occuroraldecaydetritusthat accumulateson the sidelinesof teethby bacteriainthe oral cavity. This situationwill growworsein patients whohave a tendencyto formcalculusquickly.Gingivitisandperiodontitisisthe most commoninflammatory diseaseoccursand triggersthe onset ofhalitosisis causedgram-negativefusobacteriumnucleatumasveilonella,andporphyromonasgingivalishidden inperiodontaldiseasedtissue andcauseagassmell.(Ravel, 2006)In additiondue to thedecay ofdetrituscaughtinpaperback,thisconditioncan also bequickly decayingsalivaso thatadds to theseverebad breathindividuals. In addition,thenecrotictissueis formedandthereducedblood supplycauses thelevels of oxygenin the area ofinfectionalso diminished.Thusthe bacteriawill flourishandcontinue todeliver substances thatserve asavirulenceas wellasit may causeapurulent fesesexudateout throughthe Grooveof the gingiva. Metabolicreaction ofH2SgasandproducesembossedNH2(Amino)sothe elevation oftheconcentration ofvolatilesulfurin the air inthe oral cavity.2. Halitosis Classification

Based on theetiologinyafactor,halitosisdistinguishedatasatrue,halitosis(genuine)pseudohalitosisandhalitophobia.GenuineHalitosisdistinguishedagainover thephysiological and pathological.PhysiologicalHalitosisistemporary anddoes not require maintenance,reversehalitosispathologicalishalitosisis permanentand cannot beresolvedsimply bythe maintenance of oralhygienealone, butrequireahandlingand careaccording to thesourcethe causes ofhalitosis2.1. Halitosis Fisiology

Halitosisis aphysiologicalhalitosiswhois temporary anddoes not require maintenance.Onthistype ofhalitosisis not foundof any pathologicalconditionthat causehalitosis.An example is the morningbreath, that isthe smell ofbreathatwake-uptime.This situationcausednoactivemuscularcheeks andtongueas wellas the reducedflow ofsalivaduringsleep.Breathsmellsof thiscan be overcome bystimulate the flow ofsalivaand get rid ofthe rest ofthefoodin the mouthbychewing,brushing your teethor gargle2.2. Patology Halitosis

Halitosisis apathologicalhalitosispermanentand cannot beresolvedsimply bythe maintenance oforalhygienealone, butrequireahandlingand careaccording to thesourcethe cause ofhalitosis.Anygrowth of bacteriaassociated withoralhygieneconditionsare badis the cause ofhalitosismost commonlyintraoralpathological

encountered.Tonguecoating,cariesandperiodontal diseaseare the main causes ofhalitosisis related tothe condition.Chronic infectionin thenasalcavityandparanasal sinuses,tonsils(tonsilhlith)infections, indigestion,peptic ulcerscan alsoproduceodorousgases.In addition,systemic diseasessuch as diabetes,renal failure,ketoasidosirandliver disorderscan alsocausebadbreatharetypical.DiabeticKetoacidosisacetonesmellingbreathmengeluartan.Airbreathingin people withkidney damageandammoniasmellingaccompanied bycomplaints ofdysgeusi, whereas inpatients withdisorders ofthe liver andthe gall bladderascirrhosishepatiswillsmellthe breathof arms,knownwith the termfoetorhepaticus.

3. Prevention and treatment ofHalitosisHalitosistreatmentdepends onthe cause,it is importantthatthe dentistcan distinguishthe causesof bad breathasabnormal its inside oroutside ofthe mouth.Generallyhalitosiscan bereduced oreliminatedaltogetherby keepingoral hygienesuch asbrushing teeth, usingdental floss, cleantongue,usemouthwashanda healthy diet,butsometimesit takestreatmentbyprofessionals to makea referral.To be abletocope with thehalitosiseffectively, thoroughlyvettingis requiredandthe rightdiagnosis.Precaution and treatmentonhalitosis are:

3.1. Brushing TeethTeethshould bebrushedtwice a day.Teethbrushed witha soft brushandbristlebrush headsare small.Avoid theuse ofthe brush bristlesare roughbecause ofthe roughbrushbristlescould lead toa recessionof the gingiva. Brushingteethshould usetooth paste containingfluorineto preventdental cariesat once.3.2. Dental Floss

FLOSSthe teeth(dentalfloss)used to cleantheteeth, narrowslits that can't beachievedwith a toothbrush.This is done bycutting the threadapprox40cm,thenplayedon boththe right and left middle finger.The threadis insertedinto the gapbetween the teethand heldwiththe thumbin order to bestrong andnot be separatedwhensuchmovements aredonesawing.These actions should bedone oncea day,butwhenever possibleis donetwice a day.Afterthis stageis allowedtocleanorrinsedgarglewith water.3.3. Tongue Cleaning

The surfaceof the tongueis cleanedbybrushingthe tonguetwice a day usinga toothbrushora specialcleaningtooltongue (tongue scrapper).The surfaceof the tonguebrushedgently andslowlyso thatthe tonguewas notinjured.Whilethe tonguelift ahead, place thetonguescrapperas far as possibleto theback of the tongue,whilestillstand,whilebeing pulledforwardand down withlightpressure.Usea cleancloth/papertissueorrunning water to clean thetonguescrapper.Repeat this procedure2-4times untilthe entire surfaceis cleaned.3.4. Mouthwash

Mouthwashis usedat leastonce a day.The most appropriatetimeto usemouthwashbefore bedisbecauseantibacterialmouthwashgive effectduringsleepwhen thebacterialcause ofbad breathis increased.Drug

garglecontainingalcoholmay causedry mouthandwhen usedfor a long timemay causeoralmucosachipped.Therefore,we recommend that youusenon alcoholicmouthwashsuch ascontainingsodiumsaccharin.Useneed not betooexcessive,less is more 10-15mlis enoughto wetthe entire surface ofthe mouth.Gargleatthe lack of1-2 minutes.Do notgargleright out of thebottle, asiftouched bysaliva, the materialwill becontaminated, sothe rest oftheactive ingredientsin the bottlecanbedamaged,as a resultof no useanymoreforthe nextusage

3.5. Healthy Diet

A Healthy Dietis doneby eatingfibrousvegetablessuch asfresh foodand hasacoarseconsistencythat can helpriddorsum of the tongue,avoideatingfoods thatcauseodor,as wellas drinking plenty ofwatereach day.Recently, researchinJapan reported thatunsweetenedyogurtmay reduce thecompound causeshalitosis.This is evidencedby adecrease inthe level ofthe compoundwere found in thehydrogen sulfideto 80%after consuming90grams ofyogurtevery day for6 weeks.In addition, results of researchin Americashowsthat thepolyphenols(such ascatechinandthe aflavin), compoundscontainedin teacan also inhibit the growth ofbactericauses ofhalitosis.Catechin containedin green teaorblack teawhile the aflavinmore dominantonblack tea.Reducingconsumption of foodswithhigh protein.Chewsugar freecandy(non-cariogenik)especially whenthe mouthfeelsdry.Drinking lots of waterin a day.Avoid alcohol consumption,smoking, drugsthat can decreasethe flow ofsaliva.3.6. Professional Treatment

Whencaries,periodontal diseaseorothermouthinfectionsthat causethe onset ofhalitosis,specialhandlingis requiredby professionals, for example,do thepatching,scalingor dentalroot(rootplanning).In addition,the dentistwill deprivethe rest ofthe roots ofteethor rootsradixwhenthat causethe onset ofhalitosis2.3. 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, 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 TeethThere 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 BacteriaThe 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, 1983).2.4.2.3 ExposureThe 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 factorsReduced 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 long-term 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 insipiensInsipiens 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 cariesThis is the caries has reached the inside of the tooth enamel. Sometimes a tooth ache.

3. Caries mediaCaries 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 profundaIt 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

2.5.4.1Root 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 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.

2.6.4Differential 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:

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.2.7.2Indications 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 splinted2.7.4 Advantages and Disadvantages

The advantage of the use of denture bridges are as follows.

1. Because it is attached to the natural teeth are not easily dislodged or swallowed.

2. Perceived as the teeth of a patient.

3. Do not have clamps that can cause wear on the enamel surface, because each time removed and installed again in the mouth.

4. Can have the effect of dental splint that protects against stress.

5. Spread pressure function so beneficial to the entire tooth supporting tissues.

2.7.5 Stages of Preparation

Making denture bridge consists of several parts, as follows. (Prajitno, H.R, 1994)

1. Preparation

Preparation is an act pengerindaan or grinding the teeth for the purpose of providing a place for restorative materials artificial crown or fixed partial denture. 2. Printing

Before the printing is done, the state of teeth and surrounding soft tissue needs to be checked, whether all in good health and free of inflammation. There are a wide variety of printed materials, such as hydrocolloids, rubber base, polysulfide rubber base, silicon rubber base, and polyeter rubber base.

3. Preparation of the die / working model

Die is a positive reproduction of the prepared tooth and are made of cast stone or metal or hard plastic. According to the relationship with the working model of the die is divided into solitair die and removable die.4. Pattern Making Candles

Which is defined by the pattern of wax or wax-pattern is: a model of a retainer or restorations are made of wax which is then reproduced into metal or akrilik.5. Pontic

Pontic is part of a bridge denture that replaces missing natural teeth and serve to restore chewing function and speech, aesthetic comfort (comfort), as well as maintaining the relationship between the teeth tetangga prevent migration / relationship with the opponent teeth a extrusion

2.7.6 Cementing bridge

Cementing the bridge means a bridge with cement to attach the abutment in the mouth. Abutment preparation before cementing should do its best to prevent a change in the occlusal relationship and the gingiva, which may also be due to the hydraulic pressure that interferes with the pulp. It should be avoided by the operator.

Cement is used to affix the bridge is zinc phosphate cement, cement silikofosfat, EBA alumina cement, polycarboxylate cement, and composite resin cement. Selection is made by biologic properties, biophysics, and the effect on the aesthetic.

2.7.7 Types of Bridge Denture

There are 6 type of fixed partial dentures or bridges :

1. Fixed Fixed or Rigid bridge

One or more retainers are placed on eitherside of the pontic. Differential movement of abutments canresult in bond failure. This design of bridge is indicated whereexcursive 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 bridgeA 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-movable3. 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 endand 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 theresin-bonded retainer to simplify maintenance when de-bond occurs. (Thompson, A.T., 1945)

Hybrid bridge (Barclay, C.W and Walmsley, A.D. 1998)The hybrid application was for the virgin tooth at one end of the space and the heavily restored tooth at the other end. Many variations were described but all had a poor success rate. 32% failure rate in 48 months. 2.7.8 The failure of Usage Denture

As for the use of some form of failure of the bridge denture that can be found include: (Tylman SD., 1970)

1. Intrusion supporting teeth, which changes the position of the supporting teeth, away from the occlusal plane.

2. Dental caries supporters, generally due to restoration rtetainer periphery is too panjan, less long or incomplete and open. For others, the damage to the crown retainer bahna loose, embrasure is too narrow, the choice of the wrong type of retainer, and a temporary crown is merusajk or, encourage gingival too long.

3. Periodontitis support networks

4. The connector is broken.

5. People complain that there are no bad feelings. Things that can cause this disorder is premature contacts or improper occlusion, occlusion field is too broad and or accumulation of food residue between the pontic and the retainer, excessive pressure on the gingiva. Diseased cervical area, thermal shock because the patient has not been accustomed to.

6. Retainer or off of a bridge abutment. Sometimes the whole bridge can be cemented off after the cause of the release is known restoration and removed. If not all of the retainer off the bridge removed by means of bridges destroyed and re-created a new one, if anything, and conditions allow

7. Bridge lost support, may be interrupted because of the bridge, occlusal surface area, embrasure form, shape retainer, less abutment, trauma to the periodontium and printing techniques.

8. There is a change in the pulp can be caused by way of preparation, preparation yan g is not protected with a temporary crown, hidden caries, stimulation of cement as well as the occurrence of perforation.

9. The broken bridge. Can be caused by exposure to shoulder or shoulder is bad, wrong casting techniques and material fatigue.

10. Loss of a layer of aesthetic

11. Other causes that led to the bridge is not working

The efforts that can be done to prevent such failures may be the selection of the number and distribution of the supporting teeth, soft coatings applications, the use of stress-absorbing element and the use of non-rigid connectors. The difference in the movement of teeth and implants can cause various forms of malfunctions dukungazn bridge denture teeth and implants. Businesses that are most important to consider in preventing various forms of such failure is to prevent excessive pressure on the denture supporting bridge that arise due to differences in the movement.2.7.9 Antes Law

The root surface area of the abutment teeth had to equal or the surpass that of the teeth bieng replaced with pontics.Procedure :Full veneer retainer is required on the abutment which must exhibit excellent bone support . To prevent rotaion of the pontic and abutment a rest may be add to the neighboring abutment . There should be no occlusal contact on the pontic in centric orlateral excursions.The pontic should be kept as small as possible to minimize the leverage effect and it should process maximum occlusogiingival height to ensure a rigid prosthesis .