AVA lecture notes 2005 - Endodontics in Practice.doc.doc
ENDODONTICS IN PRACTICEDr Rod Salter BVSc MACVSc (Veterinary Dentistry)Melbourne Veterinary Referral Centre70 Blackburn Rd Glen Waverley 3150Abstract:The pulp of the tooth is important. This introductory endodontic lecturereviews the normal anatomy and function of the pulp and how thispredisposes to “tooth death disease” when pulpal pathology occurs.Two “practitioner possible” techniques are discussed on what to do, and howto treat, the pulp of both vital or non-vital teeth.Anatomically the tooth is divided into the crown, (the portion visible abovethe gum line) the neck (the junction) and the root (the portion under thegingiva enclosed in the socket).The apex of the tooth is the tip of the root. Lateral canals provide passagebetween the central pulp cavity and periodontal tissues in locations other thanat the apex. Lateral or accessory canals are uncommon in dogs and cats. Thepulp, located within the tooth, emerges from the tooth and connects with theperiodontal ligament at the apex. The pulp is composed of soft connectivevascular and nerve tissue. It contains odontoblasts, fibroblasts, fibrocytes,collagen fibers, elastic fibers, blood vessels, and nerves. It is this tissue thatresponds most dramatically to any insult or injury to the dentition.Innumerable dentinal tubules perforate the dentin at right angles to the pulpand contain cytoplasmic extensions from the odontoblasts called Tomesfibers. The odontoblasts function to produce dentin throughout the vital life ofthe tooth, resulting in thicker dentinal walls and narrower pulp cavities as theteeth mature.In young animals, in which the apex is not yet fully developed, the pulpconnects with the surrounding periapical tissue through a wide opening. Afterthe root lengthens, the opening at the apex narrows. With increasing age andexposure to physiologic functioning, a layer of cementum gradually covers thedentin and the pulp chamber and root canal narrow.Pulp tissue consists of four layers. The odontoblastic layer covers theperiphery of the pulp chamber, with processes extending into the dentinaltubules. Weils basal layer (cell-poor layer), lies next to the odontoblastic layerin mature teeth. A cell-rich layer is located between the cell-poor layer and thefourth layer which is the central pulp. The dental pulp is a blood-rich organ.Vessels that pass through the apical foramina are distributed throughout thepulp. Most vessels are thin walled with large lumens. Pulp also containslymph vessels.Physiologically the pulps functions are formative, nutritive, sensory, anddefensive. Pulpal tissues produce dentin. As maturation occurs, additionallayers of dentin are added, with each odontoblast enclosed and remainingvital in its dentinal tubule that extends to the dentinoenamel / dentinocementaljunction. The dentinal tubules and the odontoblastic process narrow towardthe periphery of the tooth, tapering to an almost closed structure at the
enamel junction cemental wall. The cellular content of the dentinal tubules issignificant in endodontic treatment inasmuch as open dentinal tubules canlead to pulpal disease. Pulpal disease decreases dentinal deposition, whichceases entirely after pulpal death.The pulp provides nutrients to the surrounding tissues during and afterdevelopment. The sensory function of the pulp is a response to pain vianerves that enter the apical foramen.As regards pathophysiology the pulps response to injury is via inflammation.Continued severe irritation results in pulpal death because hyper vascularityand swelling in a closed space effect necrosis once arterial inflow ceases, aconsequence of excessive pressure within the pulp space.Pulpal insult can result from extension of the inflammatory process throughthe dentinal tubules, by direct dentinal insult from topical irritants, throughlocalisation of blood-borne bacteria in hyperaemic pulp, or as a result ofperiodontal disease in combination periodontic-endodontic lesions. Pulpaldamage also occurs as a result of trauma (pulpal exposure resulting fromcoronal fracture or intradental hemorrhage without pulp exposure),penetration by bacteria from such factors as caries or external resorption, oriatrogenic factors, or it can be idiopathic in origin.Pulpal disease passes from reversible hyperemia to an irreversible pulpitisand ends in suppurative pulpitis and necrosis.Periapical inflammation and abscess formation are extensions of the pulpalinflammatory response. Microorganisms present in dentin and canalsconstitute the main sources of dentin microbial irritants of the dental pulp andperiapical tissues, respectively.As a consequence of pulp exposure to the oral cavity, the pulp systemharbours bacteria and their by-products. The pulp does not have the capabilityto rid itself of these damaging bacteria as they are located within both the pulpand the dentinal tubules. At best, the defences will temporarily halt or slowtheir spread or tissue destruction. Sooner or later the bacterial infection will beextensive and will spread throughout the canal. Then bacteria and/or bacterialby-products and other irritants from necrotic tissue will diffuse from the rootcanal into the periapical tissues with resultant development of a periapicalinflammatory lesion.Severity of trauma and the degree of apical closure are important factors inthe recovery of the pulpal tissue from physical trauma. Teeth sustainingminimal trauma and teeth with immature apexes have more chance of pulpalsurvival than do teeth that have been subjected to severe trauma or teeth withclosed apexes.Secondary dentin is formed by the odontoblasts after root formation has beencompleted. The continuous deposition of dentin results in a progressivereduction in the size of the pulp chamber and root canal. The formation ofsecondary dentin is the tooths response to the stimuli of the normal agingprocess. The formation of tertiary dentin results from irritation of odontoblasticprocesses within the dentinal tubules. Tertiary dentin is produced by theodontoblasts that are directly affected by the irritation.
In cases of dental attrition and abrasion, the formation of tertiary dentin willusually seal off the pulp cavity. With progressive wear, the tertiary dentin maybecome clinically evident as a brown spot in the centre of the occlusalsurface. This can be differentiated from an exposed pulp chamber by probingwith a dental explorer. The brown colour is explained by the irregular nature ofthe tertiary dentine which causes it to stain easily. With severe dentalabrasion, pulp exposure may occur if tertiary dentin formation can not keeppace with the rapid wear. Dentin exposed by uncomplicated dental fractures isinitially painful because of the presence of intradentinal nerve fibers and fluidmovement through the tubules. Pain is manifested by sensitivity to heat, coldand pressure. The pain eventually disappears as sclerosis and calcification ofthe dentinal tubules occur.Complicated dental fractures cause pulp exposure. Haemorrhage occurs andan acute pulpitis ensues which is very painful. Soon thereafter, bacterialinvasion and obliteration of the blood vessels cause pulp necrosis. Bloodvessel obliteration occurs because the narrow root canal does not allow forthe swelling associated with an inflammatory reaction. At this stage thecondition is no longer painful and it can go unnoticed for a considerable periodof time. Sooner or later, however, the infection spreads through the apicaldelta and causes a periapical periodontitis, which in turn progresses to aperiapical granuloma or a periapical abscess. At this stage the condition ispainful and facial soft tissue swelling may be evident. A periapical granulomais visible on radiograph as a round radiolucent area.The pulp tissue in essence reacts to numerous various irritants like otherconnective elsewhere in the body. The dentinal tubules which continously“harbour” bacteria and necrotic material ensure the contamination iscontinuous and persistent.Pulp pathology can range from a transient inflammation (reversible pulpitis) toirreversible pulpitis, which will proceed to total necrosis. Clinically significant isthe usual absence of noticeable symptoms to the patient, regardless of theseverity or progress of inflammation. Thus, the destruction of the pulp oftenproceeds without the knowledge of the patient the owner or the vet!Injury to pulp tissue results in cellular damage and release of nonspecificmediators of inflammation, such as histamine, bradykinin, and arachidonicacid metabolites. In addition to nonspecific inflammatory preparations,reactions, immunologic responses can also initiate and perpetuate pulpaldiseases. Potential pulpal antigens include bacteria and their by-products,which directly or through dentinal tubules can initiate different types ofimmunologic reactions. The presence of potential antigens and theidentification of immunocompetent cells such as PMN leukocytes,macrophages, lymphocytes, plasma cells and mast cells as well as variousclasses of immunoglobulins indicate that mediators of immunologic reactionsalso participate in pathologic changes during pulpal pathosis.As a consequence of these releases, there is increased vascular permeability,vascular stasis, and emigration of leucocytes at the site of injury. Increasedcapillary permeability due to inflammation causes movement of fluid from thevessels into the tissue. If removal of fluid by venules does not keep up withfiltration of fluid from capillaries, an exudate forms in the pulp. The pulp is
encased in rigid walls therefore, a small increase in tissue pressure as a resultof increased capillary permeability causes passive compression and evencomplete collapse of the venules at the site of pulpal injury.Affected teeth may first present with a pink or blue tinging of the tooth. If thepulpitis is reversible, the colour may eventually diminish and the tooth willreturn to its normal appearance. If irreversible destruction has occurred, thecolour changes to a purple-gray as the pulp dies and the blood cellcomponents are degenerated.If exudate produced during irreversible pulpitis is absorbed or drains throughcaries or an exposure into the oral cavity , pulpal necrosis is delayed and theradicular pulp may remain intact for long periods. In contrast, closure orsealing off of inflamed pulps induces rapid and total pulp necrosis andperiapical pathosis. In addition to liquefaction necrosis, ischemic necrosis ofdental pulp can occur as a result of traumatic injury and disruption of bloodsupply. Depending on the severity of irritation, its duration, and host response,periapical pathology of pulpal origin can range from slight inflammation toextensive tissue destruction. Injury to periapical tissues usually results incellular damage and release of nonspecific as well as specific immunologicmediators of inflammatory reactionsOnce the pulpal tissue becomes infected, organisms will continue to invade,seeking new nutrients. As the apical periodontal ligament is the only directlyassociated soft tissue in this situation, bacterial involvement will eventuallyextend to these tissues. The periapical tissues have good collateralcirculation, which allows the building of a defensive barrier in an attempt toconfine the pathogens and their toxins within the root canal system andperiapical tissues. In more chronic cases, this barrier generally takes the formof granulation tissue, although it may take purulent or cystic forms at the apex.However, in acute periapical disease abscess formation is more common.Chronic proliferative changes at the apex stimulate dissolution or resorption ofperiapical bone. This results in the classic periapical lucency on radiographs.Whether an acute or chronic process develops depends on the severity oftrauma, pathogenicity of the organism, degree of organism challenge, andhost resistance.Vital PulpotomyVital Pulpotomy or Partial coronal pulpectomy is indicated for freshcomplicated crown fractures with vital pulp, in both mature and immatureteeth. The procedure should be performed as soon as possible following pulpexposure. No fixed guidelines exist regarding the maximum period ofacceptable delay. The decision to proceed with a partial coronal pulpectomyrather than a total pulpectomy is usually made in the initial stage of theprocedure: if the pulp bleeds freely on probing and if the blood appearsnormal, a partial coronal pulpectomy is indicated. If haemorrhage is non-existent or minimal, a partial coronal pulpectomy is ill-advised.The pulpal tissue is excised to a depth of 8- 10 mm using a spoon excavatoror a high-speed burr. The resultant hemorrhage should be staunched withoutdamaging the pulp; this can generally be achieved by the gentle and patientapplication of sterile paper points. The calcium hydroxide dressing can beapplied as a powder, as a thick paste made by mixing the powder with sterile
saline, or as a commercially available preparation. An intermediate layerconsisting of a hard-setting cement is then used, followed by a restorative.Calcium hydroxide stimulates the formation of a dentinal bridge that coversthe remaining vital pulp. The main advantage of this technique is that thetooth remains vital and therefore maintains its original strength. In theimmature tooth, where the pulp cavity is still very wide, the tooth is not welldeveloped and the apex is not closed, secondary dentin formation and apexformation (apexogenesis) can proceed. The main disadvantage of a partialcoronal pulpectomy is that the remaining pulp may necrose and give rise tosubsequent periapical pathology. The incidence of this complication inanimals is unknown. Regular follow-up radiographic examinations aretherefore indicated.Vital pulpotomy attaches great importance to the preservation of the vitality ofthe pulp as this improves the prognosis of the tooth and this is especiallycrucial in the immature tooth (ie a patient less than 18 months old ) where aliving pulp allows for closure of the apex, continued development of the crownlength and thickening of the dentinal walls (collectively this procedure istermed apexogenesis ).The permanent teeth erupt into the mouth with often as much as 50% of rootdevelopment to occur. Root development depends on the vitality of Hertwigsepithelial root sheath and as growth continues the root lengthens and the rootcanal is narrowed by continued dentinal deposition which compresses thepulp tissue. Additional depostion of dentin and cementum then closes theapex of the tooth. Pulpal exposures of up to 2 weeks duration have beentreated in immature teeth with a fair degree of success due to the richvascularity and cellular content of the pulp.In essence in vital pulpotomy the unhealthy pulp is removed from the pulpchamber ,the remaining exposed pulp is cleansed and the fracture site isrestored with an appropriate surface restorative.Contraindications to perform a Vital Pulpotomy include pulp suppuration,radiographic evidence of periapical changes indicative of a periapicalabscess, root fracture. These describe a chronic inflammatory pulp responsewhich is non conducive to Vital Pulpotomy.A post operative Xray is taken as are follow up Xrays 6 and 12 months later -compare the treated tooth to a simultaneously taken Xray of the contralateraltooth - vitality is determined by comparing these films to the postoperativefilms looking for increased dentinal wall thickness and apical closure. Similarlythe treatment’s effectiveness can be assessed by evaluating the thickness ofthe dentinal bridge. Radiographic signs of treatment failure include internallysis and periapical bone lysis - either of these signs are indications forpulpectomy.In summary Vital pulpotomy requires sterile preparation of both the tooth andthe instruments. Vital pulpotomy allows normal physiological development ofimmature teeth and with their thicker walls these fully developed teeth are lessbrittle than nonvital teeth that have experienced arrested internaldevelopment. Vital pulpotomy is less traumatic and expensive than surgicalextraction of teeth with solid alveolar attachment. Vital pulpotomy is a
technique readily suited to general practitioners who would regularly seecandidates for this procedure.Pulpectomy / Root canal therapyAlthough the objective of endodontic therapy is the management andtreatment of the injured pulp, attention must be given to the tissuessurrounding the pulp, and periapical tissues.Root canal therapy has many advantages over extraction. The best reason isthat the tooth is saved rather than resorting to "toothenasia". Standard rootcanal therapy is less traumatic for the patient and more aesthetically pleasingto the owner than surgical extraction, and the cost of root canal therapy issimilar to that of surgical extraction.The objectives of Endodontic Therapy are to relieve pain, remove infection,prevent further infection, restore and maintain function, and avoidcomplications associated with extraction..“In the treatment of any disease, a cure can only be affected if the cause isremoved. Since endodontic diseases originate from an infected or affectedpulp, it is axiomatic that the root canal must be thoroughly and carefullydebrided and obturated." Dr. I Wolch, 1975.There are three major goals of veterinary endodontic therapy that should beattained for reasonable assurance of success. 1. Initially the entire contents ofthe pulp chamber and canal should be removed with endodontic files andirrigation 2. Using endodontic files, the canals should be cleaned andenlarged so as to give the canal a slight funnel shape, and 3. The apex (orapices) of the treated tooth should be sealed and the canal packed with anendodontic filling material, and the coronal end sealed against further invasionof organisms. This then constitutes “The Endodontic Triad."The preparation phase means proper coronal access. Before the endodonticsystem can be dressed, any unsupported or fractured tooth structure shouldbe removed to provide a clear view of the remaining sound tooth structure.This phase is concerned with the debridement of the root canal system andshaping of the root canal in preparation to receive a specific type of filling.Sterilization involves irrigation of the root canal to disinfect the canal andremove pulp tissue remnants and dentin debris, and the installation ofintracanal medication for staged treatment. Obturation is the development of afluid-tight three dimensional seal at the apical foramen and total obliteration ofthe root canal. This is to eliminate the avenues of leakage from the oral cavityor periradicular tissues into the root canal system.Preparation: Coronal Access. This should be well planned to gain straight lineaccess to the root canal. Preoperative radiographs should always be taken toassess the shape and location of the canals, root pathology, and periapicalpathology. Coronal access is made with a variety or burs including #lor #2round bur, or a #330 pear bur. Initial penetration through the enamel shouldbe perpendicular to the enamel, and then angled toward the apex once intothe dentin.Access sites: Canine teeth: Fracture location can play a role, but usually2-4mm coronal to the gingival margin. Check depth and angle with aradiograph. Incisor teeth: through the fracture site, on the facial surface, or on
the lingual or palatal surface. Mandibular teeth: Mesial root: through themesio-occlusal pit on the lingual side, and the distal root on the occlusalsurface. Maxillary 4th premolar teeth: Mesial roots: transcoronal approach,about ½ way from the gingival margin to the cusp on the buccal aspect of thecrown, the distal root, about 1 mm distal to the buccal groove on the buccalaspect of the crown. The palatal root can be accessed separately if necessary, or is accessible via the transcoronal approach. Be careful to avoid furcationperforation. A furcation is the site where 2 roots separate from the crown.Prevention of perforation of this area demands that you follow the principles ofaccess preparation, have a through knowledge of tooth anatomy and the useof radiographs.Continue preparation by locating the canals with a pathfinder or small sizeendodontic file. The goal is to leave as much tooth structure as possible whileremoving enough to allow easy instrumentation. Cleaning and shaping thecanal involves the use of a variety of instruments including barbed broaches,Hedstrom files, K-type files, K-type reamers, Gates-Glidden drills, and Peesoreamers.Barbed broaches are used for pulp extirpation. Fully rotate with the canal toengage the pulp tissue. Never force or allow broach to bind against the walls,and dont use in small canals. Hedstrom files have an excellent cutting effect,and cuts only in one direction- retraction. The file resembles a wood screw. Ifused with rotation, the flutes are locked in the dentin, and are easily fracturedif turned or twisted. A K-reamer has half as many twists as a K-file. Both ofthese cut by being tightly inserted into the canal, twisted clockwise ¼ turn,and withdrawn. The cut is made during retraction of the reamer, andpenetration and retraction with the file.General file principles: Use 1 to 3 times and then replace. Larger files can beused longer. Inspect the files for unraveling, twists, and bends. DISCARD IFDEFECTIVE!Gates Glidden Drills and Peeso Reamers are engine driven instruments usedon a slow speed contra angle handpiece. They are used to prepare thecoronal portion of the root canal. Gates Glidden drills tend to separate nearthe shank.Many instrument aids are available. Talk to the supplier and find what worksbest for you. Chelating agents lubricate the file, soften the dentin and removethe smear layer. The smear layer is a combination of organic and inorganicdebris crushed into a fine paste along the walls of the pulp cavity. The smearlayer is created by instrumentation. The disadvantages of removing the smearlayer are that it may help occlude the apex and lateral canals, and may helpseal the dentinal tubules. The advantages of removing the smear layer areimproved removal of bacteria, and may improve the canal sealer interlock.Root canal irrigants should be used frequently during the process ofinstrumentation. Sodium hypochlorite (bleach) is an antimicrobial that helpsdissolve organic debris. Be sure to protect the oral tissue when irrigating withthis product. Hydrogen peroxide can be used in conjunction with bleach. It hasa good effervescent action, and some antimicrobial properties.Throughout the debriding or filing process, the root canal must berecapitulated. A smaller diameter file is intermittently inserted to the measured
apical length and the small bits of debris that are packed into the apex areremoved to insure total canal debridement. This confirms the patency of thecanal, dislodges dentin chips and debris. Instrumentation and recapitulationcontinues until clean shavings emerge on the file and the desired canal shapeis achieved.The goal is a continuously tapered preparation of the root canal. There aretwo basic approaches. I. Step-back technique: Preparation is begun at theapex working back up the canal coronally with larger and larger instruments.2. Step (crown) -down technique: Preparation begins coronally and isadvanced apically using smaller and smaller instruments. 3. Hybridapproaches.With the Step-back technique, establish the working length with a small fileand endostop. Confirm the working length radiographically. Prepare the apicalportion of the canal first with recapitulation using progressively larger files.The step back is done in 1 mm. increments. The Gates Glidden drills are usedfor coronal and midroot preparations.With the Step-down technique (crown-down technique) -Prepare properaccess and locate the canal. The working length is not established first. Thecoronal 2/3 of the canal is enlarged first using files and Gates Glidden burs.The apical portion if prepared last. This minimizes binding of files in thecoronal 1/3 of the canal.The goals of either technique is an apex that is clean with "natures" shapebasically unchanged, a body shape that is smooth, continuous flowing, andtapered, and the canal is free of pulp remnants and debris.When satisfied with the shape of the canal, irrigate again with bleach andwater, then dry with paper points. These are available in 25 and 55 mmlengths, with the 25mm at the same sizes as files, and 55mm, in extra fine,fine, medium and coarse.If persistent hemorrhage is encountered when drying the canals, there is vitalpulp tissue remaining, hemorrhage from the periapical tissues, or rootresorption present. If this happens, consider 2-stage therapy. Dry the canal,place calcium hydroxide intracanal medication (paste filler, K-file or injection)as a temporary filling, and complete the procedure 3-4 weeks later.The goal of obturation is a 3 dimensional fill and a tight seal. The ability toachieve this is highly dependent on the quality of the canal preparation.Failure to fully obdurate and seal the canal will lead to endodontic failure. Youare ready for obturation when the canal is clean and shaped to an optimalsize and is dry .Two basic obturation techniques are vertical and lateralcompaction.Root canal sealers fill the space gutta percha is unable to fill. The idealcharacteristics are: tacky when mixed to provide good adhesion to the canalwall, radioopaque, will not shrink upon setting, not stain, bacteriostatic, setsslowly, tissue tolerant, and soluble in common solvents. Most root canalsealers are eugenol based (zinc oxide-eugenol); non-eugenol based such asepoxy resins and glass ionomers, and therapeutic sealers such as calciumhydroxide. Most of these come as a powder and liquid spatulated together tothicken consistency and are then introduced into the prepared root canal. The
canal may be filled by utilizing a Lentulo spiral filler on a reduction gear contraangle, or by using endodontic files or gutta percha points to place the cementinto the canal.Gutta percha is the most commonly used material to obturate root canals.They come in various lengths, with the standard sized corresponding to filesizes, or conventional, that are more tapered and pointed. Spreaders andpluggers are used to compact gutta percha into the prepared root canal.Spreaders have pointed tips, and pluggers have flat tips. Many types andsizes of spreaders and pluggers are available.A minimum of 4 films are taken during a procedure. I. Preoperative 2. Workinglength 3. Master cone placement and 4. Final obturation.The master cone is selected based on the final apical file used. The cone isgrasped with cotton pliers at a position that approximates the working length.It should fit to working length or shorter (.5mm), contact the walls in the apicalportion and demonstrate slight resistance to removal. The fit is confirmedradiographically.Prepare the sealer and place into the canal. Seat the master cone. Excesssealer will extrude out the access point. Proceed with either lateral or verticalcompaction.With lateral compaction, the spreader is inserted, allowed to remain 1 minuteas gutta percha is compacted laterally and somewhat apically. The spreaderis removed using rotation and coronal gutta percha is removed. The depth ofpenetration is measured using an endostop on the spreader. Auxiliary pointsthat seat to penetration depth are chosen. That point is dipped in sealer andinserted into the canal. The spreader is returned to the canal to laterallycompact again. Secondary vertical compaction also occurs. The process iscontinued until the canal is fully obturated and a radiograph is taken to confirmthe fill.With vertical compaction, the master cone is seated in the canal. Use heatedpluggers to soften and prefit cold pluggers to condense the gutta percha.Heated instruments are penetrated into the gutta percha, left 2-3 seconds toallow heat transfer, and removed. Large pluggers are used to compact thegutta percha. Heated instruments are again inserted to selectively removecoronal gutta percha. Mid-size pluggers are used to compact the guttapercha. The process is repeated with a smaller plugger until the apical guttapercha mass is compacted.There is no statistical difference in filling efficiency between lateral vs. verticalcompaction. Vertical compaction does fill accessory canals with a significantlygreater incidence.Remove the gutta percha from the access preparation, clean excess sealerfrom the walls. Place an intermediate layer to prevent contact of thecomposite with any remaining sealer. Acid etch the dentin and enamel, placebonding agent, place composite and light cure, and smooth the composite.Place a final layer of unfilled resin or composite sealant and cure. Coronalleakage through improperly placed restorations can result in endodonticfailure.
Final radiographs should be taken after the restorative is placed. Follow-upradiographs should be taken at 1 and 3 years if there was no periapicallucency present, and initially at 6 to 9 months if periapical lucency waspresent. Additional film intervals are based on the results of the first follow-upfilms.