Tratamiento Endodóntico en la dentición primaria

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By Sajeev Koshy, MBA, MDS and Robert M. Love, RIDS,PhD, FRACDS, Department of Oral Diagnostic and Surgical Sciences, School of Dentistry, University of Otago, Dunedin, New Zealand.

Address for correspondence: Associate Professor Robert M. Love, Head of Department, Department of Oral Diagnostic and Surgical Sciences, School of Dentistry, University of Otago. PO Box 647, Dunedin, New Zealand. Email: robert.love@dent.otago.ac.nz

Endodontic Treatment In The Primary Dentition Abstract A number of factors are involved in the development of pulp and periapical disease in primary and permanent teeth, with dental caries being the main factor. Although these factors are similar, the clinical management of a primary or permanent tooth with pulp or periapical disease may be quite different. This is based mainly on the differences between the two types of teeth, with primary tooth longevity, coronal structural integrity, root canal morphology, and root anatomy being impottant features to be taken into account when treatment planning. This paper reviews some aspects of primary teeth and the various treatment options for the management of pulp and periapical disease.

Introduction Despite advances in the prevention of dental caries and an increased understanding of the importance of maintaining the natural dentition. premature loss of pulpally-involvedprimary teeth remains a common problem. Such loss can lead to aesthetic. phonetic. malocclusal or functional problems that may be transient or permanent in nature (I, 2). The most common cause of pulp exposure is caries (Fig. I). but it may also occur during cavity preparation, erosion or fracture of the crown.

Figure I : Extensive cories on the occlusol surface of the decrduous lower nght second molar hos exposed the pulp with development ofpulpol ond periopicol diseose. AUSTRALIAN ENDODONTICJOURNALVOLUME 30 No. 2 AUGUST

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A tooth can remain functional without a vital pulp. The Objectives of endodontic treatment of a primary tooth with an infected pulp is to maintain the arch length, maintain the integrty and health of oral tissues. to relieve pain. and to maintain the patient's general health (3) This paper will review endodontic management of primary teeth in children and adolescents.

Tooth Morphology It is essential that the anatomy of the root canal system of a primary tooth be mentally visualised before attempting any treatment. Studies have mapped out the anatomy of the canal systems of primary teeth (4, 5)with Barker and colleagues precisely describing the root canal systems of the primary dentition (6) (see for a review). There are some characteristics that are common to all primary teeth: the crown-root ratio is greater than that of permanent teeth. the roots of primary teeth are more slender, and primary tooth roots diverge more widely to facilitate space for the permanent tooth germ (7) The roots of the primary teeth complete their formation between one and four years after tooth eruption and their physiological resorption starts soon after. In the primary dentition. the apical foramina are located near the anatomical apices of the roots and as resorption progresses the foramina move coronally as the roots are shortened (8- I I)

The Pulpo-Dentine Complex The principal functions of the pulp are the formation of dentine and participation in defence processes. The pulp contains cells, intercellular substance, collagen fibres, blood vessels and nerves. Pulps or primary teeth have been investigated (12). and their histological appearance show similarities to permanent teeth ( 13). Odontoblast cells line the periphery of the pulp space and extend their cytoplasmic processes into the dentinal tubules. The pattern of this layer is flat cells in the apical region. cuboidal cells in the middle. and columnar odontoblasts in the coronal pulp. A cell-free zone is located just below the odontoblastic layer and contains unmyelinated nerves and blood capillaries ( 14). A cell-rich zone may not be present in the primary pulp (I5); however, this may be related to occlusal attrition and formation of irritation dentine ( 12). Irritation dentine may also be referred to as irregular secondary dentine, reparative dentine or tertiary dentine ( I 6). The core of the dental pulp contains large blood vessels and nerves that are surrounded by loose connective tissue ( 12). Collagen fibres are densely packed and coronally orientated in the apical third of the 59


The severi of the pulpal reaction to dental caries in deciduous teeth is inversely related to the thickness and degree of calcification of the remaining dentine over the pulp (2 I). The caries process initially produces a chronic inflammatory reaction in the pulp, the blood vessels of the pulp dilate and scattered chronic inflammatory cells are seen subjacent to the area of the infected dentinal tubules. As the carious lesion progressestowards the pulp. bacteria and their products evoke an acute response in the pulp characterised by an infiltration of acute inflammatory cells, and the chronic pulpitis becomes acute. Continued bacterial invasion of the pulp results in pulp necrosis (I3). Primary teeth are capable of defensive reactions similar to that of permanent teeth even if the pulp is inflamed due to carious exposure (22), although the primary tooth pulp responds more severely to caries than the permanent pulp (2 I ). Treating pulps successfully relies on the prevention of recontamination by microorganisms once treatment has been completed. Recently, with improved visualisation through magnification and the use of caries detectors the operator can effectively remove the carious lesion while retaining the uninfected dentine that has been shown to remineralise in permanent teeth (32-34). The mechanism of action of the caries detector dyes is reported to be by staining denatured collagen, but demineralised enamel also stains (35). Clinical studies have shown that the use of a caries detector is more effective than the tactile and visual methods of detectingcaries in permanent teeth (36-38). No studies appear to have been published concerning the primary dentition.

such as radiography and sensibility tests are employed to reach a diagnosis and treatment plan. The clinician should elicit answers to the location, onset, character, timing, and duration of the pain and whether there are any aggravating or relieving factors, radiating featwedreferred pain, or local effects. With a child patient the dentist should be aware of the limitations imposed and be able to distinguish between provoked dentine sensitivity/hypersensitivity and pulpal pain. Dentinal pain can be stimulated by thermal, chemical or mechanical irritants that result in increased dentinal tubule fluid outflow and activation of A-delta nerve fibres in the peripheral pulp. Clinical management of the cause(s) that allow the increased fluid flow, such as caries, exposed dentine or microleakage around restorations. usually corrects the condition. Pulpitis is commonly characterised as a pain that can be spontaneous, constant. throbbing, and may be debilitating in that it may keep the patient awake at night. It is a result of activation of deep pulpal C-fibre nerves due to the inflammatory condition of the pulp and indicates irreversible pulpal inflammation. A clinician must also be aware of other conditions that could mimic dental pain. A spontaneous throbbing pain simulating a pulpitis can also be caused by food impaction associated with an inflamed dental papilla (25). A careful clinical examination should include palpation, assessment of tooth mobility, tenderness to percussion. and changes in colour. Sensibility tests are considered of minor importance in primary teeth because false positive results can be obtained (26). Responsiveness to electric pulp testing is directly related to the stage of tooth development (27). Attempts to compare the sensibili of the primary and permanent dentitions by electric pulp testing have proved inconclusive (28). Laser Doppler flowmetry has been used to assess the blood flow in primary incisor teeth affected by traumatic injuries and proved valuable (29). while pulse oximetry may be an objective, atraumatic clinical alternative to the electrical and thermal methods of assessing pulp sensibility in primary teeth (30). Radiographs are useful in visualising the presence or absence of caries with or without pulp involvement, deep restorations. periapical pathology. root resorption or pulpal changes such as calcific metamorphosis (25). The dentists should be familiar with the interpretation of radiographs in children; features include larger bone marrow spaces, superimposition of developing tooth buds and normal resorption patterns of the teeth (3 I ). Very occasionally a final diagnosis of the pulpal condition can be determined only by the response of pulp tissue to local haemorrhage control measures. Bleeding that can be readily controlled with moistened cotton pledgets is generally indicative of pulp that can repair such as in traumatic or iatrogenic pulp exposure. Difficulty in controlling haemorrhage indicates that the pulp is infected and inflamed (pulpitis) and it will not repair; in this situation. symptoms associated with C-nerve fibre activation are commonly present. Conversely, no or limited bleeding from the root canal system and the presence of tenderness to percussion, localised swelling or a draining sinus are indicators of a degenerative or nonvital infected pulp.

Diagnosis Of Pulpal Pathology

Pulp Treatment Procedures

It has been reported that there is an 80% correlation between the clinico-radiographicevaluation of a symptomatic primary tooth and the histologic findings in the pulp (23) Similarly. Stoner (24) reported that if more than 4 mm of the marginal ridge of a primary molar had been destroyed by caries there was a high likelihood of pulpal involvement. A comprehensive detailed dental and medical history, history of present complaint. clinical examination, and the use of special tests

The American Academy of Pediatric Dentistry categorises pulp treatment for primary teeth as either conservative or radical (3). Conservative pulp treatment aims to maintain pulp vitality, while radical treatment consists of pulpectomy and root-filling. Primary teeth with pulp exposures should always be treated either by pulp treatment or extraction. The indications and contraindications for retainingthe primary dentition are outlined below (39)

pulp, whereas in the middle and coronal third the fibres are thin, loosely packed and randomly spread out. The distribution of collagen fibres in primary teeth is similar to that of permnent teeth (I3). Studies relating to primary tooth innervation are few and comparisons with the permanent dentition are fewer. An in vitro study by Rodd and Boissonade involving 60 mandibular primary second molar and 60 permanent first molar teeth extracted from children when under general anaesthesia showed that in both dentition types the pulp horns were the most densely innervated areas ( 17). The nerve fibres appeared slightly more abundant and the sub-odontoblastic nerve plexus was denser in the permanent teeth than in the primary teeth. The greatest difference was noticed within the mid-coronal regions where the nerve trunks were larger than those of the primary teeth. It was concluded in this study that there was a quantitative ddference in coronal nerve distribution between the primary and permanent dentition, with the permanent dentition having a greater innervation density in all regions ( 17). In addition, dentine permeability of primary teeth is lower than permanent teeth due to smaller tubule concentrationand diameter ( 18). These factors may be the reason for the clinical observation that primary teeth are less sensitive to noxious stimuli than permanent teeth ( 19. 20).

Reaction To Dental Caries And Operative Procedures

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Indirect Pulp Capping

If the primary tooth is to be conserved rather than extracted, pulp treatment is indicated: I. When the tooth exhibits signs of pulpitis;

The American Academy of Pediatric Dentistry describes indirect pulp treatment (IPT) of a tooth as the incomplete removal of carious dentine in order to avoid a pulp tissue exposure, and then treatment of the decay process with a biocompatible material (3). The aim of the procedure is to maintain the health of the pulp by placing a dressing on a thin remaining layer of dentine to promote reparative dentine, to arrest caries. eliminate bacteria. and to promote dentine sclerosis (52). In order for successful treatment the caries must not have produced a detectable exposure and the tooth must be symptomless. The most common medicament for indirect pulp treatment is calcium hydroxide; however, it has been shown that the removal of soft carious dentine had a beneficial effect on the pulp regardless of the medicament applied (53). This effect was probably caused by removal of infected dentine. leaving only affected (demineralised but uninfected) dentine (54). Dentine bonding agents for direct and indirect pulp treatment have been suggested (55). However. Nakajima and co-workers (56) found that there was a significant loss of bond strength to human carious dentine when compared with sound dentine from extracted permanent molars. A loss of bond strength suggests a reduced sealing ability of the material. It is essential that the capping material be sealed effectwely to prevent contamination by saliva and bacteria. Clinicians differ on whether indirect pulp capping should be a single or two-stage procedure. The rationale behind the twostage technique is that viable bacteria may remain in the deeper dentine layers but become inactivated over a period of time after the cavty has been properly sealed. When reparatwe dentine has formed the tooth is re-entered for the purpose of excavating the previously-carious dentine and to confirm the formation of reparative dentine (25). Some authors have advocated performingIPT in a primary tooth (2. 26) because. with proper case selection, it has been shown to have a success rate ranging from 85-100% in deciduous teeth (57-63). In contrast, others consider the indirect pulp capping procedure to be questionable because carious dentine is often left behind (64. 65) and therefore advocate aggressive removal of carious dentine (66. 67). A recent retrospectivestudy comparing treatment of deep caries in primary molars with IPT or formocresol pulpotomy concluded that IPT success was significantly higher (68). In the study, 55 primary molar teeth with deep caries were treated by IPT using glass ionomer cement as a capping material and restored with a stainless steel crown. The success rate (based on strict clinical and radiographic findings) for the IPT group was 93%, while formocresol pulpotomy (n = 78) had a success rate of 74%. The mean follow-up period was 4.2 years. The researchers concluded that a primary tooth presenting with signs and symptoms of pain compatible with a diagnosis of reversible pulpitis could be more successfully treated by a one-step IPT than with a formocresol pulpotomy. In addition, the immediate provision of a stainless steel crown was seen to enhance the prognosis for a formocresol pulpotomy. Zinc phosphate cement was used to cement the stainless steel crowns in this study, though the superior sealing properties of modem adhesive cements (69) may offer greater benefit.

2. When the interproximal marginal ridge has been lost due to caries; 3. When there is radiographic evidence of caries extending more than half-way from the dentino-enameljunction to the pulp; or 4. When there are clinical signs of pulp necrosis.

Contraindications Primary tooth retention is contraindicated when there is: I. A medical problem ( e g damaged heart valves); 2. Extensive caries penetratingto the floor of the pulp chamber: 3. Insufficient tooth structure remaining for a coronal restoration; 4. A tooth close to exfoliation; 5. A tooth with advanced pathological tooth resorption; 6. A mixed dentition associated with crowding. where the balanced loss of a first primary molar may be justified; or 7. A patient who has previously failed to comply with dental treatment.

Conservative Treatment It was believed for many years that the toxic effects of dental materials caused pulpal inflammation (40-42). More recent evidence has shown that pulpal inflammation resulting from dental materials is mild and transient. with adverse reactions occurring due to pulpal invasion by bacteria or their toxins (43). Marginal leakage around restorationsis the most common route for bacterial invasion and pulpal degeneration under restorations. Dentine permeability influences bacterial invasion and the clinical concept of sealing the tooth/restoration interface and underlyingdentine from the oral environment is the basis of pulpal protection. Numerous materials have been recommended for sealing primary teeth such as calcium hydroxide bases and polycarboxylate cements (44). with glass ionomer cements having a proven clinical record. The use of resin bonding techniques has some support; Cannon and colleagues (46) tested the use of bonded amalgams in primary teeth and concluded that placement of adhesive amalgam is highly recommendedfor use in a paediatric dentistry. In contrast. Mahler and colleagues (45) concluded that there was no difference between bonded and unbonded amalgam restorations after one year and suggested that use of bonding agents under traditional amalgam restorations is unnecessary. The nature of the bond between resin and amalgam is not yet clear. It is believed that there is a micro-mechanicalmixing of amalgam with resin during condensation (47), but there is also a potential weakening of the mechanical properties of amalgam (48). A comparison of five resin adhesive systems to primary enamel was investigated in I I 5 extracted bovine primary incisors and it was observed that no significant dhference was obtained for bond strength with the latest generation of total-etch resin systems (49). Comparing dentine of primary and permanent teeth, it was concluded that less time was required for appropriate acid-conditioningof primary dentine surfaces (50). Modern thinking on the aetiology of pulp reactions to thermal sensitivity rejects the need for thermal protection of the pulpodentine complex (40, 5 I). Rather, as previously discussed, dentine sensitivity from cold stimuli is due to dentinal tubule fluid movement. As such. sealing of the pulpo-dentine complex from microleakage from the oral environment is the principle for limiting thermally-inducedsensitivity. AUSTRACIAN ENDODONTICJOURNAIVOLUME 30 No. 2 AUGUST 2004

Direct Pulp Capping The aim of direct pulp capping is to maintain pulp vitality by direct placement of a matenal onto pulp (39). The basis of success is the eliminationof infection from the pulpo-dentinecomplex A number of materials may be used, however, the dressing of choice remains calcium hydroxide due to its antimicrobial properties and its long61


Fgure 2: The deciduous lower nght second mdor seen m Fg. I treoted using the formocresol pulpotomy technique. demonstrated ability to allow reparative dentine formation (70). Fairbourne et 01. (76) tested the effect of a calcium hydroxide (Dycal. Dentsply) and a zinc-oxide/eugenol (IRM, Dentsply) material on bacteria in deep carious lesions when used as a direct pulp cappng material and concluded that both materials, when placed in contact with carious dentine. caused a significant decrease in bacterial numbers in deep carious dentine. The use of dentine bonding agents for direct pulp capping has been studied and recommended by some researchers (55. 72) on the basis of their sealing abillty. Similarly. with appropriate case selection, mineral trioxide aggregate (MTA. ProRoot@,.Dentsply) has demonstrateda high degree of clinical success (77-79). Tumer et ol. (7 I ) investigated the quality of dentine bridges following direct pulp capping of primary canines. They claimed that a dentine bridge is ineffective as a barrier because of its porosity. Histologicalserial sections reveal tunnel defects through the entire bridge thickness after reparative dentine bridge formation. even though radiographically it seems acceptable (64). However, it does not seem logical to expect that reparative dentine should produce an impermeablebarrier. Rather, dentine bridge formation should be seen as a sign of pulp healing. Direct pulp capping will not succeed if the pulp is irreversibly inflamed. Matsuo and co-workers (80) reported that the degree of haemorrhage on pulpal exposure is the only statistically significant predictor of clinical success. Direct pulp capping of carious exposures in the primary dentition has a poor prognosis because internal resorption is a likely sequel (39, 73). Because of the poor success rate of pulp capping and the high success rates for formocresol pulpotomy. it is rare for a direct pulp capping procedure to be used in the treatment of primary teeth (3. 74). It is only recommendedwhen a small traumatic exposure occurs during l pulp (75). cavlty preparation of a v ~ anon-infected

Pulpotomy Pulpotomy is surgical amputation of the entire coronal portion of the pulp tissue with the aim of leaving a vltal radicular pulp (2, 39). The presence of any signs or symptoms of inflammationextending beyond the coronal pulp is a contraindication to treatment (25). Pulpotomy is the most widely accepted procedure for the treatment of primary teeth with carious or traumatic exposures (8 1-86) (Fig. 2). A review of the literature shows that the indications for performing a pulpotomy vary across and within studies (87-89). However, the accepted indications for pulpotomy are: carious pulp exposure; mechanical exposure; traumatic exposures (> 0.5 mm); the tooth being restorable; and at least half the root length remain62

ing. It is contraindicated if there is: a mucosal swelling of pulpal origin, pathologic mobility or root resorption, periapical or intraradicular radiolucency. pulp calcifications. or excessive bleeding from the amputated radicular stumps (25). A child with medical problems or who is uncooperative is included in the list of contraindications. The ideal dressing material must be bacteriocidal. promote healing of the radicular pulp, be biocompatible and not interfere with the physiological process of root resorption (25). Some studies report performing a single-step procedure. a two-step procedure. or both (87. 88. 90). The medicaments used include: full-strength Buckley's formocresol (formaldehyde I9%. tricresol 35%. and glycerine 15% by volume); 1/5 dilution of Buckley's solution (9 1-93); ferric sulfate (94-97); 2% glutaraldehyde (97- 100); calcium hydroxide ( I0 I, 102); preparations containing corticosteroids ( 103, 104); collagens ( 105- 107); freeze-dried bone ( 108); bone morphogenic protein ( I 09. I 10); and osteogenic protein ( I I I). The reported success rate varies widely from 70-98% (88. 9 1-93), Formocresol pulpotomy may induce early exfoliation of teeth (91, 112. 113) leading to functional problems and loss of maintenance of arch length. The final restoration of the tooth is also an important factor in the success of a pulpotomy procedure (102, I 14). Formocresol pulpotomies. temporised with IRM and covered with a stainless steel crown between one and six months later. were less successful (39% success rate) than teeth with immediate placement of crowns (82% success rate) (68). This indicates that IRM used as a temporary restoration seals the pulp chamber poorly and allows microleakage ( I IS). Additionally, stainless steel crowns on posterior teeth can prevent crown and root fractures ( I 16). Calcium hydroxide has been used as a dressing material for pulpotomy (I 12, I 17. I 18). and in Scandinaviancountries it is used as the dressing of choice. Some researchers believe that the use d calcium hydroxide in the primary dentition is contraindicated for pulpotomy because of unfavourable results ( I 19). In one study of calcium hydroxide pulpotomy over two years the success rate was 3 I% (73) while in another study with a one-year follow-up, it was 49% ( 120). The failures were mainly due to internal resorption and chronic pulpal inflammation. In another study of partial pulpotomy using calcium hydroxide in 93 lower mandibular molars with a one-year follow-up, the success rate was 83%. In this technique, the superficial part of the coronal pulp (where there was carious exposure) was ground away with high-speed diamond burs and flooded with sterile saline until the bleeding had stopped. Calcium hydroxide paste was gently pressed against the wound surface to ensure tissue contact and the cavv then sealed with ZnO-eugenol and amalgam ( I 18). In a study of 45 primary molars, a conventional pulpotomy procedure was carried out using mineral trioxide aggregate (MTA) or formocresol. After a follow-up pertod ranging from 6-30 months with a mean of 13 months, it was concluded that MTA showed greater clinical and radiographic success as a dressing material compared to formocresol (I2 I). Fuks and coworkers (25) achieved a success rate over 6-35 months of 93% with pulps treated with ferric sulphate and 84% with those treated with diluted formocresol. while the short-term success of 2% glutaraldehyde has been shown in several studies (92, 97. 100. I 22- I 25). Collagen gel and cyanoacrylate cements are other materials that have been suggested as alternatives for vital pulpotomy (2, 107).

F o * m o c d Toxicity There is concern that formocresol is a toxic medicament with mutagenic and carcinogenic properties ( I 26- I 3 I ). The formoAUSTRACIAN ENDODONTlCIOURNAL VOLUME 30 No. 2 AUGUST 2004


cresol pulpotomy was first introduced in 1904 ( I 32) and was popularised by Sweet (8 I ). In recent years. the one-visa technique has become almost universally accepted. This involves a 5-minute application to the amputated radicular pulp of a formocresol solution consisting of 19% formaldehyde and 35% cresol in a glycerine base (133). or a 1:s dilution of Buckley's solution (91). followed by a lining of ZnO-eugenol containing formocresol. The aim is fixation and disinfection of the coronal part of the radicular pulp and preservation of the vltalty of the apical pulp ( I 34). Formaldehyde has been demonstrated in the vascular system following experimental formocresol pulpotomy procedures ( I 35). In this in vivo dog model. I6 pulpotomieswere performed on each of the dogs and it was found that 5% to 10% of I4C-labelled formaldehyde was absorbed systemically from the site. In vitro studies have demonstrated that formocresol diffuses out of the pulp chamber over a period of days following its placement ( I 36. 137). Formocresol in toxic levels produces cardiovascular changes, alterations of both plasma and urinary enzymes and histological changes in kidney, liver, heart and lung tissue of dogs (I 38). Block and colleagues (I39) demonstrated that formocresol can produce antigenic activity in dog pulp tissue. It has been demonstrated that formaldehyde vapour induces nasal squamous cell tumours in rats ( 140). Formaldehyde is believed to be an initiator. with slight promoter effects (I 4 I) of damage to DNA leading to neoplastic changes. Local effects of formocresol range from irritation of the periapical area in humans (I42) to toxic effectson periapical tissues in animal models ( I 43, 144). There has been no relationship demonstrated between the use of formocresol pulpotomy and changes to the permanent successor teeth ( 145). Until alternative medicaments have been evaluated and their success determined, diluted formocresol pulpotomy is the recommended treatment of inflamed primary teeth pulps ( 146) (Fig. 2). The use of I :5 dilution of proprietary Buckley's formocresol (9 I). while discontinuing the addition of formocresol to the ZnOeugenol lining, is a well-established practice (147. 148). From the available literature. it is not possible to establish a cause-and-effect relationship in humans between the use of formocresol and mutagenic change. A cautious approach to its use is. however, suggested ( 129). Non-pharmacological haemostatic techniques for pulpotomy. such as electrosurgery and laser therapy have been investigated (149). Carbon dioxide lasers have been used for pulpotomy procedures ( 150). Electrosurgical pulpotomy for primary teeth has been described ( I5 I ) as a smooth and time-efficient method. Ruemping and co-workers ( 152) compared the results of electrosurgery with formocresol pulpotomy and the results showed histologically that they were comparable. In contrast. Shulman and colleagues ( I 53) found that the electrosurgical technique caused pathologic root resorption and furcal morbidty. Problems with excessive heat generation may have produced the result. A retrospective study was conducted to determine the long-term clinical and radiographic success rates for this procedure in human primary molars with a mean operative observation time of 2.3 years. The success rate was 99.4% after excluding 32 teeth that had undergone normal exfoliation (154). However, in a dog model study comparing electrosurgical and formocresol pulpotomy techniques, it was concluded that histopathologically the formaldehyde technique was superior (I55).

Radical Treatment Pulpectomy and root canal treatment is indicated in primary teeth with a necrotic pulp or pulpitis of the radicular pulp. The roots AUSTRALIAN ENDODONTIC lOURNAL VOLUME 30 No 2 AUGUST 2004

hgure 3 A deciduous lower right second molar mth occlusal caries and no succident permonent second premolac This tooth should be considered a permonent tooth when contemplating endodontic treatment The morphology of the root canal system and root curvature must be considered when treatment plortning

should be at least two-thirds of their normal length. The goal of treatment is to retain primary teeth that would otherwise be lost. Few studies have investigated the microbial flora of infected primary teeth but a study has confirmed similarity to that of infected permanent teeth (I70). In primary teeth, the bone lesion can be found anywhere along the root or in the furcation because pulpo-periodontalcommunications are caused by the resorption of the canal wall ( I7 I ). The presence of accessory canals in abscessed primary molars has been investigated to ascertain the reason for the inter-radicularsites of abscesses, but accessory canals were found in only 29% of the diseased teeth examined (I72). This could not be considered as the sole reason for inter-radicular radiolucencies ( 173); the pathway of infection and involvement of the furcation area of non-vital primary molars is probably multifactorial. Some or all of the mechanisms may play a role, including the structural alteration and the increase in porosity of the dentine and cementum making up the pulpal floor of the teeth ( I 74. 175). As with permanent teeth, inflammationand infection of the pulp can lead to acute and chronic apical periodontitis and periapical abscess. Additionally. radicular cysts associated with primary teeth have been reported ( 176, 177). Difficulties in the preparationof the root canals, the morphology of the primary dentition (Fig. 3) and uncertainty over the effects of filling materials makes root canal treatment quite challenging. The objective of instrumentation is debridement ( 156) rather than precise shaping of the canal (I57). The paste used for root canal filling must resorb at a rate similar to the primary root ( 158. 159). The material of choice for root canal filling is ZnO-eugenol (160-162). Yacobi et 01. reported a success (as measured by asymptomatic tooth retention) rate following ZnO-eugenol obturation of 89% at 6 months and 76% at I 2 months postoperatively for anterior teeth, and 92% and 84% for the 6- and I 2-monthly reviews for posterior teeth (86). ZnO-eugenol. however. has a major disadvantage because of the diference in the rate of resorption of the ZnO-eugenol compared to the root (I63). ZnO-eugenol root-filling material can be effectively placed into a canal using a pressure syringe, Lentulo spiral, or by using an endodontic plugger ( 168). Other commonly used materials are calcium hydroxide. iodoform paste, and gutta-percha with sealer ( I58. I59. 164- 166). In contrast, iodoform pastes such as the Kri pastes are resorbed too quickly from the canal ( 158, 165, 167) while calcium hydroxide is not recommended in pulp treatment of 63


primary teeth due to the frequent occurrence of internal root resorption. Machida (159) found that a mixture of calcium hydroxide and iodoform resorbed at a rate llttle faster than the rate of resorption of primary teeth, and suggested this as an ideal rootfilling material. Rtkin ( I 58) investigated a sample of 45 non-vital primary teeth of which 20 teeth were associated with active discharge of pus from the canals and two with a draining sinus. Root canals were debrided with endodontic files and RC Prep and Miltons solution. Kri paste was used as the filling material and the teeth were restored with amalgam. After one year, all the teeth were functional with no clinical symptoms. The primary objective in endodontic treatment of abscessed primary teeth is to remove infection. A root canal treatment, rather than a pulpotomy procedure. best achieves this. Gutta-percha does not resorb and hence does not satidy the criteria for root-filling in primary teeth that are expected to undergo physiologic resorption. However, Gerlach ( 164) reported guttapercha root fillings did not interfere with root resorption while other studies have reported clinical success with gutta-percha ( 166, 169). When it is anticipated that the deciduous tooth can be retained for a number of years, for example, when there is no succident permanent tooth (Fig. 3). conventional root canal preparation and gutta-percharoot-filling is the treatment of choice.

Conclusion Primary teeth. successfully treated with an appropriate technique and material remain as functional units in the dental arch until exfoliated. However, constant research and review will help the clinician to identify better materials and modify techniques to enhance the success rates of the various procedures.

References I. Levine N, Pulver F. Torneck CD. Pulpal therapy in primary and young permanent teeth. In: Wei SHY. editors. Pediatric dentistry: total patient care. Philadelphia: Lea and Febiger; 1988. p.298-3 I I. 2. Fuks AB. Eidelman E. Pulp therapy in the primary dentition. Curr Opin Dent I99 I ; I36-63, 3. American Academy of Pediatric Dentistry. Guidelines for pulp therapy for primary and young permanent teeth: reference manual. Pediatr Dent 1999; 2 I:62-63. 4. Hess W. Zurcher E. The anatomy of the root canals of the teeth of the permanent dentition and the anatomy of the root canals of the teeth of the deciduous dentition and of the first permanent molars. London: John Bale Sons and Daniellson Ltd; 1925. 5. JorgensonKD. The deciduous dentition. Acta Odontol Scand 1956; I4(suppl):20. 6. Barker B W , Parsons KC. Williams GL, Mills PR. Anatomy of root canal. IV Deciduous teeth. Aust Dent J 1975;

I I. Kulild JC. Peters DD. Incidence and configuration of canal systems in the mesiobuccal root of maxillary first and second molars. J Endod 1990; I6:3 I I - 17. 12. Fox AG. Heeley JD. Histological study of pulps of human primary teeth. Arch Oral Biol 1980; 25: 103- 10. 13. Seltzer 5. Bender IB. The Dental Pulp. Biologic Considerations in Dental Procedures. 3rd ed. Philadelphia: Lippincott; 1984. 14. Torneck CD. Dentin-Pulp complex. In: Ten Cate AR. editor. Oral histology, development, structure and function. St Louis: CV Mosby; 1985. I 5. Provenza DV Fundamentalsof oral histology and embryology. Philadelphia: Lippincott; 1972. p. I 5 1-67, 16. Wennberg A. Mjor IA, Heidi 5. Rate of formation of regular and irregular secondary dentine in monkey teeth. Oral Surg Oral Med Oral Pathol 1982; 54:232-37. 17. Rodd HD. Boissonade FM. Innervation of human tooth pulp in relation to caries and dentition type. J Dent Res 2001;

80:389-93. 18. Malferrari S. Finger WJ,Garcia-Godoy F. Resin bond strength of Gluma 2000 to primary dentine. Int J Paediatr Dent 1995; 5173-80. 19. Rapp R. Avery JK. Strachan DS. The distribution of nerves in human primary teeth. Anat Rec 1967; I 59:89- 103. 20. Egan CA. Bishop MA, Hector MI? An immunohistochemical study of the pulpal nerve supply in primary human teeth: evidence for the innervation of deciduous dentine. J Anat 1996; 188~623-3I . 2 I. Rayner JA. Southam JC. Pulp changes in deciduous teeth associated with deep carious dentine. J Dent 1979; 7:39-42. 22. Taylor BR. Berman DS. JohnsonNW. The response of pulp and dentine to dental caries in primary molars. J Int Assoc Dent Child I97 I ; 2:3-9. 23. Schroder U. Agreement between clinical and histologic findings in chronic coronal pulpitis. Scand J Dent Res 1977;

86~273-78. 24. Stoner JE. Dental caries in deciduous molars. Br Dent J 1967; 123: 130-34. 25. Fuks AB. Pulp therapy for the primary and young dentitions. Pediatr Dent 2000; 4457 1-96. 26. McDonald RE, Avery DR. Treatment of deep caries, vital pulp exposure, and pulpless teeth. In: McDonald RE. Avery DR. editors. Dentistry for the child and adolescent, 5th ed. St Louis: Mosby; 1994. 27. Klein H. Pulp responses to an electric pulp stimulator in the developing permanent anterior dentition. J Dent Child 1978;

45: 199-202. 28. JohnsenDC. Harshbarger J. Nash DA. Vitalometer testing of primary and permanent canine teeth. Pediatr Dent 1979; 1~27-30. 29. Fratkin RD. Kenny DJ.Johnston DH. Evaluation of a laser

20: I01-06, 7. Finn SB. Morphology of the primary teeth. In: Finn SB. editor. Clinical Pedodontics. Philadelphia: Saunders; I973. p.45-70. 8. Kaffe 1. Kaufman A. Llttner MM. Lazarson A. Radiographic

30.

study of the root canal system of mandibular anterior teeth. Int Endod J 1985; I8:253-59. 9. van Beek GC. Dental Morphology: an illustrated guide. Bristol: JohnWright and Sons Ltd; 1983. 10. Hibbard ED, Ireland RL. Morphology of the root canals of the primary teeth. J Dent Child 1957; 24:250-57.

32.

64

31.

33.

doppler flowmeter to assess blood flow in human primary incisor teeth. Pediatr Dent 1999; 2 153-56. Goho C. Pulse oximetry evaluation of vitalty in primary and immature permanent teeth. Pediatr Dent 1999; 2 I : I 25-27. Belanger GK. Pulp therapy for the primary dentition. In: Pinkham JP et 01.. editors. Pediatric dentistry: infancy through adolescence. Philadelphia: WB Saunders; 1988. p.257-67. Katao S. Fusayama T. Recalcification of artificially decalcified dog dentin in vitro. J Dent Res 1970; 49: I06 1-67, Frank RM. Vegel JC. Ultrastructure of the human odontoblastic process and its mineralisation during dentinal caries. Caries Res 1980; I9:367-80. AUSTRALlAN ENDODONTICJOURNAL VOLUME 30 No. 2 AUGUST 2004


34. van de kjke JW. Use of dyes in cariology. Int Dent J I99 I 41:l 11-16, 35. Kuboki Y, Lin CF. Fusayama T. Mechanism of differentiated staining in carious dentine. J Dent Res 1983; 62:7 13- 15. 36. Anderson MH. Charbeneau GT. A comparison of digGI anc optical criteria for detecting carious dentine. J Prosthet Dent 1985; 531643-46. 37. Joyston-Bechal5, Kidd EAM, Allan R. Smith MM. Use of caries detector dye in cavlty preparation in VIVO. Caries Res 1989; 23: 109. 38. Franco SJ. Kelsey WP Caries removal with and without a disclosing solution of basic fuchsin. Oper Dent I99 I ; 6~46-49. 39. Llewelyn DR. UK national guidelines in paediatric dentistry. Int J Paediatr Dent 2000; IO:248-52. 40. Brannstrom M. Communication between the oral cavty and the dental pulp associated with restorative treatment. Oper Dent 1984; 957-68. 4 I. Stanley HR. Pulpal responses to ionomer cements -. biological characteristics. J Am Dent Assoc 1990; I20:25-29. 42. Stanley HR. Pamejer CH. Sequential death of exposed pulps with 'total etch'bnding treatments [abstract]. J Dent Res 1997: 76(special issue):305. 43. Cox CF. Keall CL. Keall HI. Ostro E. Bergenholtz G. Biocompatability of surface-sealed dental materials against exposed pulps. J Prosthet Dent 1987: 57: 1-8. 44. Pashley DL. Clinical consideration of microleakage. J Endod 1990; 16170-77. 45. Mahler DB. Engle JH. Simms LE, Terkla LG. One-year clinical evaluation of bonded amalgam restorations. J Am Dent Assoc 1996; I 27:345-49. 46. Cannon ML. Tylka JA, Sandrick J. Three-year clinical study of adhesive and conventional amalgam restorations [abstract]. J Dent Res 1999; 78(special issue):230. 47. Swift EJ. Perdig30 J. Heyman HO. Bonding to enamel and dentin: a brief history and state of the art. Quintessence Int 1995; 26:95. 48. Charlton DG. Murchison DF. Moore BK. Incorporation of adhesive liners in amalgam: effect on compressive strength and creep. Am J Dent I99 I ; 4: 184. 49. Hosoya Y, Tominago A. A comparison of five adhesive systems to primary enamel. Pediatr Dent 1999; 2 I :46-5 I. 50. Nor JE. Feigal RJ, DennisonJB. Edwards CA. Dentin bonding: SEM comparison of the dentin surface in primary and permanent teeth. Pediatr Dent 1997; 19: 246-57. 51. Stanley HR. Human response to restorative procedures. Gainesville. Florida: Storter; I98 I. p.9,38.42.43.46.49.72. 52. Shovelton DS. The maintenance of pulp v~llty.Br Dent J I972; I33:95- I0 I, 53. Langeland K. Langeland LK. Indirect capping and the treatment of deep carious lesions. Int Dent J 1968; 181326-80. 54. Massler M. Preventive endodontics: vital pulp therapy. Dent Clin North Am 1967; I I:663-73. 55. Kanca J. Replacement of a fractured incisor fragment over pulpal exposure: a case report. Quintessence Int 1993; 24:8 1-84, 56. Nakajima M, Sano H. Burrow MF. Takatsu T, Yoshiyama M. Ciucchi B. Pashley DH. Bonding to caries affected dentin [abstract]. J Dent Res 1995; 74(special issue):36. 57. Dimaggio JJ, Haws RR. Continued evaluation of direct and indirect pulp capping [abstract]. J Dent Res 1963; 4 I :38.

AUSTRALIAN ENDODONTICJOURNALVOLUME 30 No. 2 AUGUST 2CO4

58. Hawes RR, Dimaggio JJ. Sayegh F. Evaluation of direct and indirect pulp capping [abstract]. J Dent Res 1964; 43:808. 59. Aponte AJ, Hartsook JT, Crowley MC. Indirect pulp capping success verified. J Dent Child 1966; 33: 164-66. 60. Kerkhove BC Jr, Herman SC. Klein Al. McDonald RE. A clinical and television densitometric evaluation of the indirect pulp capping technique. Dent Child 1967; 34: 192-20 I . 61. Nordstrom DO. Wei SH. Johnson R. Use of stannous fluoride for indirect pulp capping. J Am Dent Assoc 1974; 88:997- 1003. 62. Sawusch RH. Direct and indirect pulp capping with two new products. J Am Dent Assoc 1982; IO4:459-62. 63. Nirsch RF. Avery DR. Evaluation of a new pulp-capping agent in indirect pulp therapy. ASDC J Dent Child 1983; 50:25-30. 64. Langeland K. Tissue changes in the dental pulp: an experimental histologic study. Odontol Tidskr 1957; 63:239-385. 65. Leinfelder KF. Changing restorativetraditions: the use of bases and liners. J Am Dent Assoc 1994; I2565-67. 66. Mathewson RJ. Primosch RE. Pulp treatment. In: Mathewson RJ, Primosch RE, editors. Fundamentals of pediatric dentistry, 3rd ed. Chicago: Quintessence; 1995. p.257-80. 67. Razi RS. Pulp therapy in the primary dentition. N Y State Dent J 1999; 65: 18-22, 68. FarNS. Coll JA. Kuwabara A, Shelton FI Success rates of formocresol pulpotomy and indirect pulp therapy in the treatment of deep dentinal caries in primary teeth. Pediatr Dent 2000; 22:278-86. 69. Shiflet K. White SN. Microleakage of cements for stainless steel crowns. Pediatr Dent I997 19:262-66. 70. Ozlov M. Massler M. Histologic effects of various drugs on amputated pulps of rat molars. Oral Surg Oral Med Oral Path01 1960: 13~455-69. 7 I. Tumer C, Courts FJ, Stanley HR. A histological comparison of direct pulp capping agents in primary canines. ASDC J Dent Child 1987; 54:423-28. 72. Kashiwada T Takagi M. New restoration and direct pulp capping systems using adhesive composite resin. Bull Tokyo Med Dent Univ I99 I; 38:45-52. 73. Via WE Evaluation of deciduous molars treated by pulpotomy and calcium hydroxide. J Am Dent Assoc 1955; 50:34-43. 74. Allen KR. Endodontic treatment of primary teeth. Aust Dent J 1979; 24:347-5 I. 75. Goodman JR. Endodontic treatment for children. Br Dent J 1985; I 58:363-5 I. 76. Fairbourne DR, Charbenau GT Loesche WJ. Effect of improved Dycal and IRM on bacteria in deep carious lesions. J Am Dent Assoc 1980; I00:547-52. 77. JunnDJ,McMillan F! Backland LK. Torabinejad M. Quantitative assessment of dentin bridge formation following pulp capping with mineral trioxide aggregate (MTA). J Endod 1998: 24:278. 78. Torabinejad M. Chivian N. Clinical applications of mineral trioxide aggregate. J Endod 1999; 25: 197-205. 79. Schmtt D. Lee J. Bogen G. Multifaceted use of ProRootTM MTA root canal repair material. Am Acad Pediatr Dent 200 I; 23~326-30. 80. Matsuo T Nakanishi T, Shimizu H. Ebisu S. A clinical study of direct pulp capping applied to cariously-exposed pulps. J End& 1996; 2 2 5 5 1-56, 81. Sweet CA. Treatment of vital primary teeth with pulpal involvement. Therapeutic pulpotomy.J Colorado Dent Assoc 1955; 33: 10- 14. 65


82. Schroder U. A 2-year follow-up of primary molars, pulpotomised with a gentle technique and capped with calcium hydroxide. Scand J Dent Res 1978; 86:273-78. 83. Wright FAC. Wdmer RP Pulpal therapy in primary molar teeth: a retrospective study. J Pedod 1979; 3: 195-206. 84. Davis MJ. Myers R, Switkes MD. Glutaraldehyde: an alternative to formocresolfor vital pulp therapy. ASDC J Dent Child 1982; 49: 176-80. 85. Avram DC. Pulver F: Pulpotomy medicaments for vital primary teeth. Surveys to determine use and attitudes in pediatric dental practice and in dental schools troughout the world. ASDC J Dent Child 1989; 56:426-34. 86. Yacobi R. Kenny DJ.JuddPL. JohnstonDH. Evolving primary pulp therapy techniques. J Am Dent Assoc I99 I; I22:83-85. 87. Redig DF. A comparison and evaluation of two formocresol pulpotomytechniques utilising 'Buckley's' formocresol. J Dent Child 1968; 3522-30. 88. Rolling I. Thylstrup A. A 3-year clinical follow-up study of pulpotomised primary molars treated with the formocresol technique. Scand J Dental Res 1975; 83:47-53. 89. Willard RM. Radiographic changes following formocresol pulpotomy in primary molars. ASDC J Dent Child 1976; 43:4 14- I5. 90. Boeve C. Dermaut L. Formocresol pulpotomy in primary molars: a long-term radiographic evaluation. ASDC J Dent Child 1982; 49: I9 1-96, 91. Morawa Al? Straffon LH. Han SS. Corpron RE. Clinical evaluation of pulpotomies using dilute formocresol. ASDC J Dent Child 1975; 42:360-63. 92. Fuks AB,Bimstein E. Clinical evaluation of diluted formocresol pulpotomies in primary teeth of school children. Pediatr Dent

1981: 31321-24. 93. Fuks AB. Holan G. Davis JM. Eidelman E. Ferric sulfate versus dilute formocresol in pulptomised primary molars: long-term follow-up. Pediatr Dent 1997; I9:327-30. 94. Landau MJ.Johnsen DC. Pulpal response to ferric sulfate in monkeys [abstract]. J Dent Res 1988; 67:2 I 5. 95. Fei AL. Udin RD. JohnsonR. A clinical study of ferric sulfate as a pulpotomy agent in primary teeth. Pediatr Dent 1991;

13~327-32. 96. Davis J. Furtado L. Ferric sulfate a possible new medicament

97.

98.

99.

100.

for pulpotomies in the primary dentition: the first year results from a 4-year study in Fortaleza, Brazil. Proceedings of the I 3th Congress of International Association of Dentistry for Children, Kyoto, Japan. Programme and abstracts, I99 I . Garcia-Godoy F. Ranly DM. Clinical evaluation of pulpotomies with ZnOE as the vehicle of glutaraldehyde. Pediatr Dent 1987; 9: 144-46. Lloyd MJ. Seale NS. Wilson CFG. The effects of various concentrations and lengths of application of glutaraldehyde on monkey pulp tissue. Pediatr Dent 1988; 10: I I5-20. Fuks AB.Cleaton-Jonesf! Michaeli Y Bimstein E. Long-term pulp response to glutaraldehyde in pulptomised monkey teeth [abstract]. J Dent Res 1989; 68:660. Fuks AB. Bimstein E. Guelmann M. Klein H. Assessment of a 2% buffered glutaraldehyde solution in pulpotomised primary teeth of school children. ASDC J Dent Child 1990;

57:37 1-75. 101. Fadavi S. Anderson AW, Punwani IC. Freeze-dried bone in pulpotomy procedures in monkeys. J Pedod 1989: I 3: 108-22.

66

102. Gruythuysen RJ, Weerheijm KL. Calcium hydroxide pulpotomy with a light-cured cavty-sealing material after two years. ASDC J Dent Child 1997; 64:25 1-53, 103. Paterson RC. Corticosteroids and the exposed pulp. Br Dent J 1976; 140:174-77. 104. Seow WK. Thong YH. Evaluation of the novel antiinflammatory agent tetrandrine as a pulpotomy medicament in canine model. Pediatr Dent 1993; I 5260-66. 105. Bimstein E, Shoshan S. Enhanced healing of tooth-pulp wounds in the dog by enriched collagen solution as a capping agent. Arch Oral Biol I98 I : 26:97- I0 I . 106. Fuks AB, Michaeli Y. Sofer-Saks B, Shoshan 5. Enriched collagen solution as a pulp dressing in pulpotomised primary teeth in monkeys. Pediatr Dent 1984; 6:243-47. 107. Fuks AB. Cleaton-Jones F! Michaeli Y. Bimstein E. Pulp response to collagen and glutaraldehyde in pulpotomised primary teeth of baboons. Pediatr Dent I99 I ; 13: 142-50. 108. Fadavi S. Anderson AW. A comparison of the pulpal response to freeze-dried bone, calcium hydroxide and zinc oxideeugenol in primary teeth in two cynomolgus monkeys. Pediatr Dent 1996; 1852-56. 109. Nakashima M. The induction of reparative dentine in the amputated dental pulp of the dog by recombinant bone morphogenitic proteins (BMP)-2 and 4. Arch Oral Biol I990

35493-97. I 10. Nakashima M. The induction of dentine formation on canine amputated dental pulp of the dog by bone morphogenitic proteins. J Dent Res 1994; 73: I 5 15-22. I I I . Rutherford RB. Wahle J, Tucker M. Roger D. Charette M. Induction of reparative dentine formation in monkeys by recombinant human osteogenic protein- I . Arch Oral Biol

1993; 38157 1-76, I 12. Hobson P Pulp treatment of deciduous teeth part 2 - Clinical investigation. Br Dent J 1970; I 28:275-82. 113. Haralabakis NB. Yiagtzis SC, Toutountzakis NM. Premature or delayed exfoliation of deciduous teeth and root resorption and formation. Angle Orthod 1994; 64: I 5 1-57. 114. Messer LB. Lerering NJ.The durability of primary molar restorations: 11. Observations and predictions of success of stainless steel crowns. Pediatr Dent 1988; I0:8 1-85. I IS. Barthel CR, Strobach A. Briedigkeit H. Gobel UB, Roulet JF. Leakage in roots coronally sealed with different temporary fillings. J Endod 1999; 2573 1-34, 116. Duggal MS. Curzon MEJ. Restoration of the broken down primary molar I. Pulpectomy technique. Dent Update 1989;

I6:26-28. I 17. Schroder U. Granath LE. Early reaction of intact human teeth to calcium hydroxide following experimental pulpotomy and its significance to the development of hard tissue barrier. Odontol Revy I97 I ; 22:379-95. 118. Schroder U. Szpringer-Nodzak M. Janicha J. Wacinska M. Budny J. Mlosek K. A one-year follow-up of partial pulpotomy and calcium hydroxide capping in primary molars. Endod Dent Traumatol 1987; 6:304-06. I 19. Doyle WA, McDonald RE, Mitchell DF: Formocresol versus calcium hydroxide in pulpotomy. J Dent Child 1962; 29:86-97. 120. Law DB. An evaluation of vital pulpotomy technique. J Dent 1956; 23:40. I2 I . Eidelman E, Holan G. Fuks AB. Mineral trioxide aggregate vs. formocresol in pulptomised primary molars: a preliminary report. Am Acad Pediatr Dent 200 I ; 23: I 5- 18.

AUSTRALIAN ENDODONTICJOURNALVOLUME 30 No 2 AUGUST 2004


122. Ranly DM. Lazzari EF! A biochemical study of two bi-functional reagents as alternatives to formocresol. J Dent Res 1983; 62: 1054-57. 123. Tagger E. Tagger M. Pulpal and periapical reactions to glutaraldehyde and paraformaldehyde pulpotomy dressing in monkeys. J Endod 1984; IO:364-7 I . 124. Garcia-Godoy F. A 42-month clinical evaluation of glutaraldehyde pulpotomies in primary teeth. J Pedod 1986;

10: 148-55. 125. Fuks AB. Bimstein E. Glutaraldehyde pulpotomies in primary teeth of school children: 42-month results [abstract]. J Dent Res I99 I ; 70:473. 126. Lewis BB. Chestner SB. Formaldehyde in dentistry: a review of mutagenic and carcinogenic potential. J Am Dent Assoc I98 I; I03:429-34. 127. Ranly DM. Formocresol toxicty: current knowledge. Acta Odontol Pediatr 1984; 593-98. 128. Sipes R. Binkley CJ. The use of formocresol in dentistry: a review of the literature. Quintessence Int 1986; I7:4 I 5- 17. 129. Judd PL. Kenny DJ.Formocresol concerns. A review. J Can Dent Assoc 1987; 540 1-04, 130. Brstavik D. Hongslo JK. Mutagenicity of endodontic sealers. Biomaterials 1985; 6: 129-32. 131. Orr DL. Paresthesia of the trigeminal nerve secondary to endodontic manipulation with N2. Headache 1985; 25:334-36. 132. Buckley JF! The chemistry of pulp decomposiion with a rational treatment for this condition and its sequelae. Am Dent J 1904; 3:764-7 I. 133. Teplltsky PE, Grieman R. History of formocresol pulpotomy. J Can Dent Assoc 1984; 50:629-34. 134. Ketley CR. Goodman JR. Formocresol toxicty: is there a suitable alternative for pulpotomy of primary molars? Int J Paediatr Dent I99 I; 2:67-72. 135. Pashley EL. Myers DR. Pashley DH. Whiiord GM. Systemic distribution of I 4C-formaldehyde from formocresol treated pulpotomy sites. J Dent Res 1980; 59:602-07. 136. Dankert J. Gravenmade EJ. Wemes JC. Diffusion of formocresol and glutaraldehyde through dentin and cementum. J Endod 1976; 2:42-46. 137. Lekka M, Hume WR. Wolinsky LE. Comparison between formaldehyde and glutaraldehyde diffusion through the root tissues of pulpotomy-treatedteeth. J Pedod 1984; 8: 185-90. 138. Myers DR. Pashley DH. Whiord GM. Sobel RE, McKinney RL! The acute toxicity of high doses of systemically administered formocresol in dogs. Pediatr Dent I98 I; 3:37-4 I. 139. Block RM. Lewis RD, Sheats JB, Fawley J. Cell-mediated immune response to dog pulp tissue altered by formocresol within the root canal. J Endod 1977; 3:424-30. 140. Swenberg JA. Kerns WD, Mltchell RJ, Gralla EJ. Pavkov KL. Induction of sqwmous cell carcinomas of the rat nasal cavty by inhalation exposure to formaldehyde vapour. Cancer Res

1980; 403398-402. I 4 I . Squire RA. Cameron LL. An analysis of potential carcinogenic risk from formaldehyde. Regul Toxicol Pharmacol 1984; 4: 107-29. 142. Wemes JC. Jansen HWB. Purdell-Lewis D. Boering G. Histologic evaluation of the effect of formocresol and glutaraldehyde on the periapical tissues after endodontic treatment. Oral Surg 1982; 54:329-32. 143. Simon M. van Mullem J. Lamers AC. Periapical tissue reaction in monkeys to endodontic treatment using formocresol as a disinfectant. J Endod 1979; 5239-4 I. AUSTRALIAN ENDODONTICJOURNALVOLUME 30 No 2 AUGUST 2OCN

144. Bamett F, Duran C, Haselgren G, Tronstad L. Tissue response to anodyne medicaments. Oral Surg 1984; 58:605-09. 145. Rolling I. Poulsen S. Formocresol pulpotomy of primary tedh and occurrence of enamel defects on the permanent successors. Acta Odontol Scand 1978; 36:243-47. 146. lngle JI, Bakland LK. editors. Endodontics. Philadelphia: Lea and Febiger; 1994. p.854. 147. Ranly DM. Montgomery EG. Pope HO. The loss of 3Hformaldehyde from zinc oxide-eugenol cement: an in vitro study. J Dent Child 1975; 42:48-52. 148. Beaver HA, Kopel HM. Sabes WR. The effect of zinc oxideeugenol cement on a formocresolised pulp. J Dent Child

1966: 33:38 1-96, 149. Udin RD. The formocresol pulpotomy revisied: looking at alternatives. J Calif Dent Assoc I99 I ; I9:27-34. 150. Shoji 5. Nakamura M, Horiuchi H. Histopathological changes in dental pulps irradiated by CO, laser: a preliminary report on laser pulpotomy. J Endod 1985; I I:379-84.

151. Andermann I. Indications for use of electrosurgery in pedodontics. Symposium on Electrosurgery. Dent Clin North Am 1982; 26:7 I 1-28, 152. Ruemping DR. Morton TH, Anderson MW. Electrosurgical pulpotomy in primates - a comparison with formocresol pulpotomy. Pediatr Dent 1983; 5: 14- 18. 153. Shulman ER. Mclver FTI, Burkes EJ. Comparison of electrosurgery and formocresol as pulpotomy techniques in monkey primary teeth. Pediatr Dent 1987; 9: 189-94. 154. Mack RB. Dean JA.Electrosurgical pulpotomy: a retrospective human study. J Dent Child 1993; 60: 107- 14. 155. Oztas N. Ulusu T. Oygur T. Cokpekin F. Comparison of electrosurgery and formocresol as pulpotomy techniques in dog primary teeth. J Clin Pediatr Dent 1994; I8:285-89. 156. Tagger E. Sarnat H. Root canal therapy of infected primary teeth. Acta Odontol Pediatr 1984; 563-66. I 57. Goerig AC, Camp JH.Root canal treatment in primary teeth: a review. Pediatr Dent 1983; 533-37. 158. Rifkin AJ. A simple effective, safe technique for root canal treatment of abscessed primary teeth. J Dent Child 1980; 47:435-4 I. 159. Machida Y Root canal therapy in deciduous teeth. J Japan Dent Assoc 1983; 36:796-802. 160. Nicholis E. Root canal treatment of primary teeth. In: Grossman LI, editor. Transactions of the Third International Conference on Endodontics. Philadelphia: University of Pennsylvania, School of Dentistry; 1964. I 6 I . Erausquin J. Muruzabal M. Root canal filling with zinc oxideeugenol cement in rat molars. Oral Surg 1967; 29548. 162. Aylard SR. Johnson R. Assessment of filling techniques for primary teeth. Pediatr Dent 1987; 9: 195-98. 163. Allen RK. Endodontic treatment of primary teeth. Aust Dent J 1979; 24:347-5 I . 164. Gerlach E. Root canal therapeutics in deciduous teeth. Dent

SUN 1932; 8:68-74. 165. Barker B W , Lockett BC. Endodontic experiments with resorbable paste. Aust Dent J I97 I ; I6:364-73. 166. Ogihara K. Goto M, Kosugi K. A clinical evaluation of root canal therapy for infected primary teeth. Japanese J Pedod 1978; I6:447-56. 167. Rifkin 4. Techniques and materials used in endodontics for primary teeth. SADJ 1982; 37:379-8 I . 168. Dandashi MB, Nazif MM. Zullo T. Elliott MA. Schneider LG, Czonstkowsky M. An in vitro comparison of three endodontic

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techniques for primary incisors. Pediatr Dent 1993;

I5:254-56. 169. lshikawa F. Sibui N. lshikawa R et a/. Possible root canal filling materials for an infected deciduous root canal treatment. JapaneseJ Pedod 1979; I7:94- 109. 170. Sat0 T Hoshimo E. Uematsu H. Noda T. Predominant obligate anaerobes in necrotic pulps of human deciduous teeth. Microbiol Ecol Health Disease 1993; 6:269-75. I 7 I. Myers DR. Durham LC. Hanes CM. Barenie JT. McKinney RV Histopathologyof radiolucent furcation lesions associated with pulpotomy-treatedprimary molars. Paediatr Dent I988;

I0:29 1-94, 172. Winter GB. Abscess formation in connection with deciduous molar teeth. Arch Oral Biol 1962; 7:373-79. 173. Moss SJ. Addelson H. Goldsmith ED. Histologic study of pulpal floor of deciduous molars. J Am Dent Assoc 1965; 701372-79.

174. Ooe T Gohdo 5. The development of human inter-radicular dentine as revealed by tetracycline-labelling. Arch Oral Biol 1964: 291257-62. 175. Bendek 5. Correa C. Donado J. Estudio en microscopa electronica de barido del piso de la camera pulpar en molares deciduous. ogta, Colombia: Universidad Odontologica.

1993; p.33-37. 76. Lustman J. Shear M. Radicular cysts arising from deciduous teeth. Review of the literature and report of 23 cases. Int J Oral Surg 1985; 14: I 53-6 I. 77. Savage NW. Adkins KF. Weit AV; Grundy GE. An histological study of cystic lesions following pulp therapy in deciduous teeth. J Oral Pathol 1986; 15209- I2.

From The Journals A Cleaning Protocol For Rotary Nickel-Titanium Endodontic Instruments Parashos f! Linsuwanont f! Messer HH. Aust Dent J 2004; 4912 1-27, This study aimed to develop a clinically-practical cleaning protocol for nickel-titanium endodontic files prior to sterilization. The experiments involved three phases of mechanical and chemical removal of root canal debris including the use of sponges soaked with chlorhexidine to remove gross debris, pre-soakingand ultrasonication. After all the cleaning sequences. there were no instances

of macroscopically visible debris. Microscopically, new files displayed both stained and unstained debris, and several experimental cleaning regimens produced files that were free of stained debris. Combining elements of the most effective cleaning sequences resulted in a cleaning protocol that predictably produced clean files. These results do not support the recommendation for the single use of endodontic files based on an inability to clean files between uses. A protocol with application to all endodontic files is presented.

Geographical Differences In Bacteria Detected In Endodontic Infections Using Polymerase Chain Reaction Baumgartner JC. Siqueira JF Jr.Xia T, Rocas IN. J Endod 2004;

30: I 4 I- 144. The purpose of this study was to use polymerase chain reaction (PCR) to detect the presence of several species of bacteria from samples of abscesses collected from Portland, Oregon or Ro de Janeiro. Brazil. Microbial samples from abscesses of endodontic

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origin were collected from patients in both cities. PCRs with species-specific oligonucleotide primers for the 165 ribosomal RNA gene were used for detection of bacteria after DNA extraction from each clinical sample. There was a statistically significant dderence in detection of the bacteria between the two geographical areas. The results suggested that differences in bacteria detected or cultured in studies could be affectedby geographical location.

AUSTRALIAN ENDODONTIC JOURNALVOLUME 30 No 2 AUGUST ZOOS


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