pediatric tics - chap 17 - ingle

8/4/2019 Pediatric tics - Chap 17 - Ingle

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Treatment of pulpally inflamed primary and perma-nent teeth in children presents a unique challenge tothe dental clinician. Pulp diagnosis in the child isimprecise as clinical symptoms do not correlate well

with histologic pulpal status. Age and behavior cancompromise the reliability of pain as an indicator ofthe extent of pulp inflammation. Furthermore, treat-ment goals are developmentally oriented and may berelatively short term by comparison to the long-termrestorative permanence of adult endodontics.Because of this latter fact, a major focus in pediatricpulp therapy is vital pulp treatment, that capitalizeson the healing potential of the noninflamed remain-ing portions of the pulp. With instances of irre-versibly inflamed and necrotic radicular pulps, con-

ventional concepts of nonvital pulp treatment areindicated. However, they must be modified to accom-modate physiologic root resorption in primary teethand continued root development in young perma-nent teeth.

Lewis and Law succinctly stated the ultimate objec-tive of pediatric pulp therapy: The successful treat-ment of the pulpally involved tooth is to retain thattooth in a healthy condition so it may fulfill its role as auseful component of the primary and young perma-nent dentition.1 Premature loss of primary teeth fromdental caries and infection may result in the following

sequelae:

Loss of arch length Insufficient space for erupting permanent teeth Ectopic eruption and impaction of premolars Mesial tipping of molar teeth adjacent to primary

molar loss Extrusion of opposing permanent teeth Shift of the midline with a possibility of crossbite

occlusion Development of certain abnormal tongue positions

It is for this reason that maximum attempts must bemade to preserve primary teeth in a healthy state untilnormal exfoliation occurs. A major contention in con-temporary research involving vital pulp treatment is

the definition of healthy pulp statusascribed to manyof the treatment outcomes. This issue will be addressedin more detail later in this chapter.

Vital pulp therapy is based on the premise that pulptissue has the capacity to heal. In addition to the bio-logic basis for the healing capacity of the pulp, differ-ences between primary and permanent teeth exist froma morphologic and histologic standpoint. These differ-ences must be addressed by the clinician to successful-ly treat pulpally inflamed teeth in children.

PULP MORPHOLOGY

Anatomic Differences Between Primary andPermanent Teeth

Anatomic differences between the pulp chambers androot canals of primary teeth and those of young perma-nent teeth have been described2 (Figure 17-1): (1) Pulpchamber anatomy in primary teeth approximates thesurface shape of the crown more closely than in perma-nent teeth. (2) The pulps of primary teeth are propor-tionately larger and the pulp horns extend closer to theouter surfaces of the cusps than in permanent teeth. (3)

The pulp-protecting dentin thickness between the pulpchamber and the dentinoenamel junction is less than inpermanent teeth. These three factors increase the poten-tial for pulp exposure from mechanical preparation,dental caries, and trauma. (4) An increased number ofaccessory canals and foramina, as well as porosity in pul-pal floors of primary teeth, has been noted in compari-son with permanent teeth.3 This is thought to accountfor the consistent pulp necrosis response of furcationradiolucency in primary teeth versus periapical radiolu-cency in permanent teeth.46

Chapter 17

PEDIATRIC ENDODONTICS

Clifton O. Dummett Jr and Hugh M. Kopel


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A comparison of root canals in primary teeth withthose of young permanent teeth reveals the followingcharacteristics: (1) the roots of primary teeth are pro-portionately longer and more slender; (2) primary rootcanals are more ribbon-like and have multiple pulp fil-aments within their more numerous accessory canals;(3) the roots of primary molars flare outward from thecervical part of the tooth to a greater degree than per-manent teeth and continue to flare apically to accom-modate the underlying succedaneous tooth follicle; (4)the roots of primary anterior teeth are narrowermesiodistally than permanent anterior tooth roots; and(5) in contrast to permanent teeth, the roots of primaryteeth undergo physiologic root resorption. These fac-tors make complete extirpation of pulp remnants

almost impossible and increase the potential of rootperforation during canal instrumentation. As a result,the requirements of primary root canal filling materialsmust encompass germicidal action, good obturation,and resorptive capability.3

Histologic Considerations

Numerous descriptions of pulp histology exist thatidentify the various cell components of pulp tissue.7,8

Consistently, the pulp is primarily connective tissueand has considerable healing potential. Features that

862 Endodontics

distinguish pulp tissue from other connective tissueinclude the presence of odontoblasts, absence of hista-mine-releasing mast cells, tissue confinement in a hardcavity with little collateral circulation, and vascularaccess limited to the root apex.7,8 Pulp healing capabil-ity is affected by endogenous factors of coronal cellu-

larity and apical vascularity. Both are increased in pri-mary and young permanent teeth.8 Pulps become morefibrous, less cellular, and less vascular with age.8

Exogenous factors affecting pulp healing include bacte-rial invasion and chemical/thermal insult. Currentresearch in pulp biology and restorative materialsstrongly substantiates the need for bacterial microleak-age control in maximizing pulp survival.9

Fox and Heeley concluded that, histologically, nostructural differences exist between primary pulp tissueand young permanent pulp tissue with the exception ofthe presence of a cap-like zone of reticular and collage-

nous fibers in the primary coronal pulp.10 However,many clinicians have noted different pulp responsesbetween primary and young permanent teeth to trau-ma, bacterial invasion, irritation, and medication.Anatomic differences may contribute to these respons-es. Primary roots have an enlarged apical foramen, incontrast to the foramen of permanent roots, which isconstricted. The resultant reduced blood supply inmature permanent teeth favors a calcific response andhealing by calcific scarring.11 This hypothesis isexemplified in older pulps, in which more calcifiednodules and ground substance are found than in youngpulps. Primary teeth, with their abundant blood sup-ply, demonstrate a more typical inflammatoryresponse than that seen in mature permanent teeth.

The exaggerated inflammatory response in primaryteeth may account for increased internal and externalroot resorption from calcium hydroxide pulpotomies.The alkalinity of calcium hydroxide can produce severepulp inflammation and subsequent metaplasia withresultant internal primary root resorption. It has beenshown that the greater the inflammation, the moresevere the resorption (Figure 17-2). Although it is sus-

pected that pulps of primary teeth have a differentfunction from those of permanent teeth, no supportingdata are available.

Some clinicians believe that primary teeth are lesssensitive to pain than permanent teeth, probablybecause of differences in the number and/or distribu-tion of neural elements. When comparing primary andpermanent teeth, Bernick found differences in the finaldistribution of pulp nerve fibers.12 In permanent teeth,these fibers terminate mainly among the odontoblastsand even beyond the predentin. In primary teeth, pulp

Figure 17-1 Comparative anatomy between primary (left) and

permanent (right) molars. Primary teeth are smaller in all dimen-

sions; their enamel cap is thinner, with less tooth structure protect-

ing the pulp. Primary pulp horns are higher, particularly mesial.

The roots of primary molars are longer and more slender, are

pinched in at the cervical part of the tooth, and flare more toward

the apex to accommodate permanent tooth buds. All of these fac-

tors tend to increase the incidence of pulp involvement from caries

or complicate canal preparation and obturation. Reproduced with

permission from Finn SB.2


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Pediatric Endodontics 863

nerve fibers pass to the odontoblastic area, where theyterminate as free nerve endings. Bernick postulatedthat if primary teeth were not so short-lived in the oralcavity, their nerve endings might terminate among theodontoblasts and in the predentin as in permanentteeth12 (Figure 17-3).

Rapp and associates concurred with Bernickshypothesis and also stated that the density of the inner-vation of the primary tooth is not as great as that of the

permanent tooth and may be the reason why primaryteeth are less sensitive to operative procedures.13 Theyagree, however, that as the primary teeth resorb, there isa degeneration of the neural elements as with otherpulp cells. Neural tissue is the first to degenerate whenroot resorption begins, just as it is the last tissue tomature when the pulp develops.

Primary and permanent teeth also differ in their cel-lular responses to irritation, trauma, and medication. Ithas been shown, for example, that the incidence ofreparative dentin formation beneath carious lesions is

more extensive in primary than in permanentteeth.1417 McDonald reported that the localization ofinfection and inflammation is poorer in the primarypulp than in the pulp of permanent teeth.18

MANAGEMENT OF DEEP CARIOUS LESIONSAND PULP INFLAMMATION IN PRIMARY

AND YOUNG PERMANENT TEETH

Pulp therapy for primary and young permanent teethhas historically been subject to change and controversy.Pulp medicaments, such as zinc oxideeugenol (ZOE)cement, calcium hydroxide, and formocresol, have beenthe basis for much of this controversy. A better under-

standing of the reactions of the pulp and dentin to thesemedicaments has developed over time, primarilythrough improvements in histologic techniques.Anderson and colleagues felt that the pulp and dentinshould be considered as one organ.19 Frankl determinedthat this pulpodentinal system reaction is proportionalto the intensity and duration of the offending agents ofcaries, trauma, medicaments, or restorative materials.20

A correct diagnosis of pulp conditions in primaryteeth is important for treatment planning. McDonaldand Avery have outlined several diagnostic aids in select-

Figure 17-2 Internal resorption triggered by inflammation. A,

Advanced caries in a 5-year-old child. Note calcification (arrow) in

the first primary molar (contraindication for pulp therapy). B,

Same patient 6 months later. Marked internal resorption, forecast in

the earlier radiograph, indicates advanced degenerative changes.

Reproduced with permission from Law DB, Lewis TM, Davis JM.

An atlas of pedodontics. Philadelphia: WB Saunders; 1969.

Figure 17-3 Section of pulp from a human primary molar. Note

that the majority of nerves terminate at the pulp-odontoblastic

(PO) border. Only isolated nerve fiber penetrates the P-O border to

terminate in the zone of Weil. D = dentin; N = nerve fiber;

O = odontoblasts; Pr = predentin; PO = pulp-odontoblast border.

Reproduced with permission from Bernick S.12

A

B


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ing teeth for vital pulp therapy.3 Eidelman et al.21 andProphet and Miller22 have emphasized that no singlediagnostic means can be relied on for determining adiagnosis of pulp conditions. Rayner and Southam havestated that the inflammation response to the effects ofdentin caries in the deciduous pulp is more rapid than in

the permanent pulp.23 Yet Taylor concluded that in spiteof being inflamed and infected by the carious process,primary molars are still capable of marked defense reac-tions similar to those observed in permanent teeth.24

The goal in managing the deep carious lesion ispreservation of pulp vitality before arbitrarily institut-ing endodontic therapy. A suggested outline for deter-mining the pulpal status of cariously involved teeth inchildren involves the following:

1. Visual and tactile examination of carious dentin andassociated periodontium

2. Radiographic examination ofa. periradicular and furcation areasb. pulp canalsc. periodontal spaced. developing succedaneous teeth

3. History of spontaneous unprovoked pain4. Pain from percussion5. Pain from mastication6. Degree of mobility7. Palpation of surrounding soft tissues8. Size, appearance, and amount of hemorrhage associ-

ated with pulp exposures

Pediatric pulp therapy for primary and young per-manent teeth involves the following techniques:

1. Indirect pulp capping2. Direct pulp capping3. Coronal pulpotomy4. Pulpectomy

The first three methods are vital techniques thatinvolve conservative management of portions of

inflamed pulp tissue with the preservation of theremaining vital pulp. The pulpectomy procedure is anonvital technique and involves the complete extirpa-tion of the irreversibly inflamed and/or necrotic pulpfollowed by canal obturation with a resorbable medica-ment in primary teeth and conventional root canal fill-ing in permanent teeth.

INDIRECT PULP CAPPING

Indirect pulp capping is defined as the application of amedicament over a thin layer of remaining carious

864 Endodontics

dentin, after deep excavation, with no exposure of thepulp. In 1961, Damele described the purpose of indi-rect pulp capping as the use ofreconstructed dentinto prevent pulp exposure.25 The treatment objective isto avoid pulp exposure and the necessity of more inva-sive measures of pulp therapy by stimulating the pulp

to generate reparative dentin beneath the cariouslesion. This results in the arrest of caries progressionand preservation of the vitality of the nonexposedpulp.26 This technique can be used as a one-sitting pro-cedure or the more classic two-sitting procedure. Thelatter involves re-entry after a 6 to 8-week interval toremove any remaining carious dentin and place thefinal restoration3,27 (Figure 17-4).

DiMaggio found, in a histologic evaluation of teethselected for indirect treatment, that 75% would havebeen pulp exposures if all of the caries had initiallybeen removed. Using clinical criteria, this same study

showed a failure rate of only1% for indirect pulp capscompared with 25% failure for direct caps.28 A histo-logic examination, however, raised these failure rates to12% and 33%, respectively. Trowbridge and Bergerstated that complete removal of softened dentin, withensuing pulp exposure, may contribute nothing ofdiagnostic value in estimating the extent of existingpulp disease.29 In fact, other studies have shown thatthe true picture of pulp disease cannot be assessed onthe basis of such diagnostic criteria as history of pain,response to temperature change, percussion, and elec-tric pulp testing.30,31

Figure 17-4 Indirect pulp-capping technique. A, Medicament,

either zinc oxideeugenol cement, calcium hydroxide, or both,

against remaining caries. B, Lasting temporary restoration.

Following repair, both materials are removed along with softened

caries, and final restorations are placed.


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Historical Review

The concept of indirect pulp capping was firstdescribed by Pierre Fauchard as reported by JohnTomes in the mid-18th century, who recommendedthat all caries should not be removed in deep, sensitivecavities for fear of exposing the nerve and making the

cure worse than the disease.32 John Tomes, in his mid-19th century textbook, stated, It is better that a layerof discolored dentin should be allowed to remain forthe protection of the pulp rather than run the risk ofsacrificing the tooth.32 Although neither of these den-tal pioneers referred to any specific medication for thesoftened dentin, they recognized the healing capacityof the pulp.

In 1891, W. D. Miller discussed various antisep-tics that should be used for sterilizing dentin.34 Incontrast to these early reports advocating conservativemanagement of deep lesions, G. V. Black felt that in the

interest of scientific dental practice, no decayed or soft-ened material should be left in a cavity preparation,whether or not the pulp was exposed.35

Rationale

Indirect pulp capping is based on the knowledge thatdecalcification of the dentin precedes bacterial invasionwithin the dentin.3638 This technique is predicated onremoving the outer layers of the carious dentin, thatcontain the majority of the microorganisms, reducingthe continued demineralization of the deeper dentinlayers from bacterial toxins, and sealing the lesion toallow the pulp to generate reparative dentin. Fusayamaand colleagues demonstrated that in acute caries,dentin discoloration occurred far in advance of themicroorganisms, and as much as 2 mm of softened ordiscolored dentin was not infected.38 In a later study,Fusayama found that carious dentin actually consists oftwo distinct layers having different ultramicroscopicand chemical structures.39 The outer carious layer isirreversibly denatured, infected, and incapable of beingremineralized and should be removed. The inner cari-ous layer is reversibly denatured, not infected, and

capable of being remineralized and should be pre-served. The two layers can be differentiated clinically bya solution of basic fuchsin.39

Whitehead and colleagues compared deep excava-tions in primary and permanent teeth.40 After all soft-ened dentin had been removed from the cavityfloor,they found that 51.5% of the permanent teeth werefree from all signs of organisms, and a further 34%had only 1 to 20 infected dentinal tubules in any onesection.40 Primary teeth, however, showed a muchhigher percentage of bacteria in the cavityfloor after

all softened dentin was removed. These results werefurther supported by Shovelton, who found thatalthough the deepest demineralized layers of dentinwere generally free from infection, the possibility of afew dentinal tubules containing organisms did exist,especially in primary teeth.41 This finding was sup-

ported by Seltzer and Bender.42

Thus, complete clini-cal removal of carious dentin does not necessarilyensure that all infected tubules have been eradicated.Conversely, the presence of softened dentin does notnecessarily indicate infection.

A number of investigators have provided evidencethat the pulp can readily cope with minute contami-nation. Reeves and Stanley43 and Shovelton44 showedthat when the carious lesion proximity to the pulp wasgreater than 0.8 mm (including reparative dentinwhen present), no significant disturbance occurredwithin the pulp of permanent teeth. Rayner and

Southam, in studying carious primary teeth, found themean depth of pulp inflammatory changes from bac-terial dentin penetration to be 0.6 mm in proximity tothe pulp, with some changes occurring within a1.8 mm pulp proximity.23 Massler considered thatpulp reactions under deep carious lesions result frombacterial toxins rather than the bacteria themselves.45

Massler and Pawlak used the terms affected andinfected to describe pulp reaction to deep cariousattack.46 This histologic study showed that the affect-ed pulp, beneath a deep carious lesion with a thinlayer of dentin between the pulp and the bacterialfront, was often inflamed and painful but containedno demonstrable bacteria. However, when significantnumbers of bacteria were found within the infectedpulp, a microscopic exposure in the carious dentin wasseen. Canby and Bernier concluded that the deeperlayers of carious dentin tend to impede the bacterialinvasion of the pulp because of the acid nature of theaffected dentin.47

The results of these studies indicate the presence ofthree dentinal layers in a carious lesion: (1) a necrotic,soft, brown dentin outer layer, teeming with bacteria

and not painful to remove; (2) a firmer, discoloreddentin layer with fewer bacteria but painful to remove,suggesting the presence of viable odontoblastic exten-sions from the pulp; and (3) a hard, discolored dentindeep layer with a minimal amount of bacterial invasionthat is painful to instrumentation.

Response to Treatment

Sayegh found three distinct types of new dentin inresponse to indirect pulp capping: (1) cellular fibrillardentin at 2 months post-treatment, (2) presence of


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globular dentin during the first 3 months, and (3)tubular dentin in a more uniformly mineralized pat-tern.17 In this study of 30 primary and permanentteeth, Sayegh concluded that new dentin forms fastestin teeth with the thinnest dentin remaining after cavitypreparation. He also found that the longer treatment

times enhanced dentin formation.17

Diagnosis of the type of caries influences the treat-ment planning for indirect pulp capping. In the activelesion, most of the caries-related organisms are found inthe outer layers of decay, whereas the deeper decalcifiedlayers are fairly free of bacteria. In the arrested lesion, thesurface layers are not always contaminated, especiallywhere the surface is hard and leathery. The deepest lay-ers are quite sclerotic and free of microorganisms.48

Deep carious dentin is even more resistant to decompo-sition by acids and proteolysis than is normal dentin.This was especially true in arrested caries.49,50

Procedures for Indirect Pulp Capping

Case selection based on clinical and radiographic assess-ment to substantiate the health of the pulp is critical forsuccess. Only those teeth free from irreversible signsand symptoms should be considered for indirect pulpcapping. The following measures should be employedfor those teeth appropriate for this technique.

Indications. The decision to undertake the indi-rect pulp capping procedure should be based on thefollowing findings:

1. Historya. Mild discomfort from chemical and thermal

stimulib. Absence of spontaneous pain

2. Clinical examinationa. Large carious lesionb. Absence of lymphadenopathyc. Normal appearance of adjacent gingivad. Normal color of tooth

3. Radiographic examinationa. Large carious lesion in close proximity to the pulp

b. Normal lamina durac. Normal periodontal ligament spaced. No interradicular or periapical radiolucency

Contraindications. Findings that contraindicatethis procedure are listed below:

1. Historya. Sharp, penetrating pain that persists after

withdrawing stimulusb. Prolonged spontaneous pain, particularly at night

866 Endodontics

2. Clinical examinationa. Excessive tooth mobilityb. Parulis in the gingiva approximating the roots of

the toothc. Tooth discolorationd. Nonresponsiveness to pulp testing techniques

3. Radiographic examinationa. Large carious lesion with apparent pulp exposureb. Interrupted or broken lamina durac. Widened periodontal ligament spaced. Radiolucency at the root apices or furcation areas

If the indications are appropriate for indirect pulpcapping, such treatment may be performed as a two-appointment or a one-appointment procedure.

Two-Appointment Technique (First Sitting).

1. Administer local anesthesia and isolate with arubber dam.

2. Establish cavity outline with a high-speed hand-piece.

3. Remove the majority of soft, necrotic, infecteddentin with a large round bur in a slow-speed hand-piecewithout exposing the pulp.

4. Remove peripheral carious dentin with sharp spoonexcavators. Irrigate the cavity and dry with cottonpellets.

5. Cover the remaining affected dentin with a hard-set-ting calcium hydroxide dressing.

6. Fill or base the remainder of the cavity with a rein-forced ZOE cement (IRM Dentsply-Caulk; Milford.)or a glass-ionomer cement to achieve a good seal.

7. Do not disturb this sealed cavity for 6 to 8 weeks. Itmay be necessary to use amalgam, composite resin,or a stainless steel crown as a final restoration tomaintain this seal.

Two-Appointment Technique (Second Sitting, 6 to8 Weeks Later). If the tooth has been asymptomatic,the surrounding soft tissues are free from swelling, andthe temporaryfilling is intact, the second step can be

performed:

1. Bitewing radiographs of the treated tooth should beassessed for the presence of reparative dentin.

2. Again use local anesthesia and rubber dam isolation.3. Carefully remove all temporary filling material,

especially the calcium hydroxide dressing over thedeep portions of the cavityfloor.

4. The remaining affected carious dentin shouldappear dehydrated and flaky and should be easilyremoved. The area around the potential exposure


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should appear whitish and may be soft; this is pre-dentin. Do not disturb!

5. The cavity preparation should be irrigated and gen-tly dried.

6. Cover the entire floor with a hard-setting calciumhydroxide dressing.

7. A base should be placed with a reinforced ZOE orglass ionomer cement, and the tooth should receivea final restoration.

One-Appointment Technique. The value ofre-entry and re-excavation has been questioned bysome clinicians when viewed in light of numerousstudies reporting success rates of indirect pulp cappingwith calcium hydroxide ranging from 73 to 98% (Table17-1). On this basis, the need to uncover the residualdentin to remove dehydrated dentin and view the scle-rotic changes has been questioned. The second entry

subjects the pulp to potential risk of exposure owing tooverzealous re-excavation.7

Leung et al.51 and Fairbourn and colleagues52 havebeen able to show a significant decrease of bacteria indeep carious lesions after being covered with calciumhydroxide (Dycal, Dentsply-Caulk; Milford.) or a modi-fied ZOE (IRM) for periods ranging from 1 to 15months. These investigators suggested that re-entry to

remove the residual minimal carious dentin after cap-ping with calcium hydroxide may not be necessary if thefinal restoration maintains a seal and the tooth is asymp-tomatic.

After cavity preparation, if all carious dentin wasremoved except the portion that would expose the pulp,

re-entry might be unnecessary.7

Conversely, if the clini-cian had to leave considerably more carious dentinowing to patient symptoms, re-entry would be advisedto confirm reparative dentin and pulp exposure status. Ifa pulp exposure occurs during re-entry, a more invasivevital pulp therapy technique such as direct pulp cappingor pulpotomy would be indicated. Tooth selection forone-appointment indirect pulp capping must be basedon clinical judgment and experience with many cases inaddition to the previously mentioned criteria.

Evaluation of Therapy. A histologic evaluation ofpulp reactions to indirect pulp capping has been report-

ed in a varying number of samples. Law and Lewisreported irritational dentin formation, an active odonto-blastic layer, an intact zone of Weil, and a slightly hyper-active pulp with the presence of some inflammatorycells.53 Held-Wydler demonstrated irritational dentin in40 of 41 young molars in which the carious dentin wascovered with ZOE cement.54 The pulp tissue was eithercompletely normal or mildly inflamed over a period of

Table 17-1 Studies on Indirect Pulp Capping in Primary and Young Permanent Teeth

Study Agent Cases Observation Period % of Success

Sowden, 1956 Ca(OH)2

4,000 Up to 7 y Very high

Law and Lewis, 1961 Ca(OH)2

38 Up to 2 y 73.6

Hawes and DiMaggio, 1964 Ca(OH)2

475 Up to 4 y 97

Kerkhove et al., 1964 Ca(OH)2

41 12 mo 95

ZOE 35 12 mo 95

Held-Wydler, 1964 Ca(OH)2

41 35630 d 88

King et al., 1965 Ca(OH)2

21 25206 d 62

ZOE 22 88

Aponte, 1966 Ca(OH)2 30 646 mo 93Jordan and Suzuki, 1971 Ca(OH)

2243 1012 wk 98

Nordstrom et al., 1974 Ca(OH)2

64 94 d 84

SnFl 90

Magnusson, 1977 Ca(OH)2

55 85

Sawusch, 1982 Ca(OH)2

184 1315 mo 97

Nirschl and Avery, 1983 Ca(OH)2

38 6 mo 94

Coll, 1988 Ca(OH)2

26 2058 mo 92.3

Ca(OH)2

= calcium hydroxide; ZOE = zinc oxideeugenol; SnFI = stannous fluoride.


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34 to 630 days. In the histologic sections, four layerscould be demonstrated (Figure 17-5): (1) carious decal-cified dentin, (2) rhythmic layers of irregular reparativedentin, (3) regular tubular dentin, and (4) normal pulpwith a slight increase in fibrous elements.

Clinical studies have shown no significant differ-

ences in the ultimate success of this technique regard-less of whether calcium hydroxide or ZOE cement isused over residual carious dentin.5557 However,Torstenson et al. demonstrated slight to moderateinflammation when ZOE was used in deep unlinedcavities that were less than 0.5 mm to the pulp itself.58

Nordstrom and colleagues reported that cariousdentin, wiped with a 10% solution of stannous fluoridefor 5 minutes and covered with ZOE, can be remineral-ized.59 It was further stated that no particular differ-ence was found in failure rates of teeth treated with cal-cium hydroxide and those treated with stannous fluo-

ride. As so many others have also concluded, the resultsfor primary and young permanent teeth do not differsignificantly(see Table 17-1).

King and associates,60 as well as Aponte et al.61 andParikh et al.,62 determined that the residual layer ofcarious dentin, left in the indirect pulp-capping tech-nique, can be sterilized with either ZOE cement or cal-cium hydroxide. However, it cannot be presumed thatall of the remaining infected or affected dentin

868 Endodontics

becomes remineralized. In contrast to ZOE, residualdentin will increase in mineral content when in contactwith calcium hydroxide.63,64

Sawusch evaluated calcium hydroxide liners forindirect pulp capping in primary and young perma-nent teeth. After periods ranging from 13 to 21 months,

he concluded that Dycal was a highly effective agent.65

Nirschl and Avery reported greater than 90% successrates for both Dycal and LIFE (SybronEndo/KerrCorp.; Orange, Calif.) calcium hydroxide preparationswhen used as bases in both primary and permanentteeth for indirect pulp-capping therapy.66

Coll et al., in an evaluation of several modes of pulptherapy in primary incisors, stated that the success ratesof indirect pulp cappings in primary incisors did notdiffer from comparable molar rates.67 They showed a92.3% success rate for treated incisors after a mean fol-low-up time of 42 months.

The medicament choice for indirect pulp capping canbe based on the clinical history of the carious tooth inquestion. Some investigators recommend ZOE becauseof its sealing and obtundant properties, which reducepulp symptoms. Others recommend calcium hydroxidebecause of its ability to stimulate a more rapid formationof reparative dentin. Stanley believes that it makes nodifference which is used because neither is in direct con-tact with pulp tissue, and increased dentin thickness wasobserved to occur beneath deep lesions treated with bothagents.57 However, in case of an undetected microscopicpulp exposure during caries excavation, calcium hydrox-ide will better stimulate a dentinal bridge.57,68 Primoschet al. noted that the majority of US pediatric dentistryundergraduate programs used calcium hydroxide as theprincipal indirect pulp capping medicament in theirteaching protocols.69

Lado and Stanley demonstrated that light-cured cal-cium hydroxide compounds were equally effective ininhibiting growth of organisms commonly found atthe base of cavity preparations.70

A minimum indirect pulp post-treatment time peri-od of 6 to 8 weeks should be allowed to produce ade-

quate remineralization of the cavity floor.7,17,71

Thisdesirable outcome is essentially dependent on themaintenance of a patent seal against microleakage bythe temporary and final restorations. In this regard, thenewer resin-reinforced glass ionomer cements anddentin bonding agents should be considered.

DIRECT PULP CAPPING

Direct pulp capping involves the placement of a bio-compatible agent on healthy pulp tissue that has beeninadvertently exposed from caries excavation or trau-

Figure 17-5 Photomicrograph of four layers of healing under

indirect pulp capping of a permanent molar of a 1412-year-old

child. Zinc oxideeugenol cement capping after excavation of the

necrotic dentin layer only. No pain 480 days later when extracted. 1

= carious decalcified dentin; 2 = rhythmic layers of irregular irrita-

tional dentin; 3 = regular tubular dentin; 4 = normal pulp with

slight increase in fibrous elements. Reproduced with permission

from Held-Wydler E.54


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matic injury72 (Figure 17-6). The treatment objective isto seal the pulp against bacterial leakage, encourage thepulp to wall off the exposure site by initiating a dentinbridge, and maintain the vitality of the underlying pulptissue regions (Figure 17-7).

Case Selection

Success with direct pulp capping is dependent on thecoronal and radicular pulp being healthy and free frombacterial invasion.73,74 The clinician must rely on thephysical appearance of the exposed pulp tissue, radi-ographic assessment, and diagnostic tests to determine

pulpal status.Indications. Tooth selection for direct pulp cap-

ping involves the same vital pulp therapy considerationsmentioned previously, to rule out signs of irreversiblepulp inflammation and degeneration. The classic indi-cation for direct pulp capping has been for pinpointmechanical exposures that are surrounded with sounddentin.3,7,2124 The exposed pulp tissue should be brightred in color and have a slight hemorrhage that is easilycontrolled with dry cotton pellets applied with minimalpressure. Frigoletto noted that small exposures and agood blood supply have the best healing potential.75

Although imprecise, the term pinpoint conveys theconcept of smallness to the exposed tissue, whichshould have the lowest possibility of bacterial access. Anempirical guideline has been to limit the technique toexposure diameters of less than 1 mm. Stanley has

Figure 17-6 Direct pulp-capping technique. A, Capping material

covers pulp exposure and the floor of the cavity. B, Protective base

of zinc oxideeugenol cement. C, Amalgam restoration.

Figure 17-7 Effect of calcium hydroxide and time on the healing of the capped pulp. A, Twenty-four hours after application of calcium

hydroxide. B, After 2 or 3 weeks. C, After 4 or 5 weeks. D, After 8 weeks. Reproduced with permission from Vermeersch AG.107

A B

C D


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determined, however, that the size of the exposure is lesssignificant than the quality of the capping technique inavoiding contamination and mechanical trauma to theexposure site and careful application of the medicamentto hemostatically controlled pulp tissue.74 Equallyimportant is the quality of the temporary or permanent

restoration to exclude microleakage.Contraindications. Contraindications to directpulp-capping therapy include a history of (1) sponta-neous and nocturnal toothaches, (2) excessive toothmobility, (3) thickening of the periodontal ligament,(4) radiographic evidence of furcal or periradiculardegeneration, (5) uncontrollable hemorrhage at thetime of exposure, and (6) purulent or serous exudatefrom the exposure.

Clinical Success

The salient features of a clinically successful direct pulp-

capping treatment (with or without bridging) are (1)maintenance of pulp vitality, (2) absence of sensitivity orpain, (3) minimal pulp inflammatory responses, and (4)absence of radiographic signs of dystrophic changes.

Permanent Teeth. Several investigators have pro-vided evidence that direct pulp capping cannot be suc-cessful in the presence of pulpal inflammation andidentify this condition as a contraindication to directpulp capping.2 Tronstad and Mjr capped inflamedpulps in monkey teeth with calcium hydroxide or ZOEand found no beneficial healing of the exposed pulpwhen calcium hydroxide was used.76 More recently,

however, other investigators have shown in animal

870 Endodontics

studies that pulp healing can take place irrespective ofthe presence of overt inflammation.77,78 Cottonobserved that when there is minimal pulp inflamma-tion, a bridge may form against the capping material,but when inflammation is more severe, the bridge is aptto form at a distance from the exposure.79

Dentin bridge formation has been considered to bethe sine qua non for success in response to direct pulp-capping procedures.73,8082 Weiss and Bjorvatn havedemonstrated, however, that a healthy pulp can existbeneath a direct pulp cap even in the absence of adentinal bridge.83 Kakehashi et al., in a germ-free ani-mal study, found pulp exposure healingwith bridgingeven when left uncovered84 (Figure 17-8). Seltzer andBender42 and Langeland et al.85 have shown that adentin bridge is not as complete as it appears, whichcan ultimately lead to untoward pulp reactions. Coxand Subay found that 89% of bridges formed in

response to calcium hydroxide direct pulp caps demon-strated tunnel defects, which allowed access ofmicroleakage products beneath the restoration into thepulp. They found recurrent pulp inflammationbeneath 41% of all bridges formed in the sample.86

It is generally considered that pulps inadvertentlyexposed and asymptomatic in the preoperative periodare more apt to survive when capped. The prognosis isfar less favorable if an attempt is made to cap aninflamed pulp infected from caries or trauma.87 Also,the wide-open apices and high vascularity of youngpermanent teeth enhance the successful outcome of

direct capping techniques.

Figure 17-8 Role of bacteria in dentin repair following pulp exposure. A, Germ-free specimen, obtained 14 days after surgery, with food

and debris in occlusal exposure. Nuclear detail of the surviving pulp tissue (arrow) can be observed beneath the bridge consisting of dentin

fragments united by a new matrix. B, Intentional exposure of a first molar in a control rat (with bacteria) 28 days postoperatively. Complete

pulp necrosis with apical abscess. A reproduced with permission from Kakehashi S et al.84 B reproduced with permission from Clark JW and

Stanley HR. Clinical dentistry. Hagerstown (MD): Harper & Row; 1976.

A B


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Primary Teeth. Kennedy and Kapala attributedthe high cellular content of pulp tissue to be responsi-ble for direct pulp-capping failures in primary teeth.88

Undifferentiated mesenchymal cells may give rise toodontoclastic cells in response to either the cariesprocess or the pulp-capping material, resulting in

internal resorption.Because of the pulp cellular content, increased

inflammatory response, and increased incidence ofinternal resorption, some pediatric dentists feel that thedirect capping procedure is contraindicated in primaryteeth.27,89,90 Starkey and others feel that a high degreeof success with direct pulp capping in primary teethcan be achieved in carefully selected cases using specif-ic criteria and treatment methods.9194

Treatment Considerations

Dbridement. Kalins and Frisbee have shown that

necrotic and infected dentin chips are invariablypushed into the exposed pulp during the last stages ofcaries removal.95 This debris can impede healing in thearea by causing further pulpal inflammation andencapsulation of the dentin chips. Therefore, it is pru-dent to remove peripheral masses of carious dentinbefore beginning the excavation where an exposuremay occur. When an exposure occurs, the area shouldbe appropriately irrigated with nonirritating solutionssuch as normal saline to keep the pulp moist.81

Hemorrhage and Clotting. Hemorrhage at theexposure site can be controlled with cotton pellet pres-sure. A blood clot must not be allowed to form after thecessation of hemorrhage from the exposure site as itwill impede pulpal healing.96 The capping materialmust directly contact pulp tissue to exert a reparativedentin bridge response. Hemolysis of erythrocytesresults in an excess of hemosiderin and inflammatorycellular infiltrate, which prolongs pulpal healing.74

Exposure Enlargement. There have been recom-mendations that the exposure site be enlarged by amodification of the direct capping technique known aspulp curettage or partial pulpotomy prior to the place-

ment of the capping material.3,93,96,97

Enlarging thisopening into the pulp itself serves three purposes: (1) itremoves inflamed and/or infected tissue in the exposedarea; (2) it facilitates removal of carious and noncari-ous debris, particularly dentin chips; and (3) it ensuresintimate contact of the capping medicament withhealthy pulp tissue below the exposure site.

Cvek98 and Zilberman et al.99 have described highlyfavorable results with this partial pulpotomy techniquefor pulp-exposed, traumatized, anterior teeth and cari-ous molars. After a 24-month waiting period, Mejare

and Cvek were able to show a 93.5% success rate of par-tial pulpotomy in permanent posterior teeth with deepcarious lesions with exposed pulps.100 Fuks et al. foundsimilar partial pulpotomy success rates above 90% inpermanent incisors with fracture-exposed pulps.101

Bacterial Contamination. Watts and Paterson102

and Cox103

have both emphasized the fact that bacter-ial microleakage under various restorations causes pul-pal damage in deep lesions, not the toxic properties ofthe cavity liners and/or restorative materials. The suc-cess of pulp-capping procedures is dependent on pre-vention of microleakage by an adequate seal. Cox et al.have shown that pulp healing is more dependent on thecapacity of the capping material to prevent bacterialmicroleakage rather than the specific properties of thematerial itself.104

Medications and Materials. Many medicamentsand materials have been suggested to cover pulp expo-

sures and initiate tissue healing and/or hard structurerepair. Calcium hydroxide, in one form or another, hasbeen singled out by a myriad of authors as the medica-ment of choice for pulp exposures.80,82,105,106

Antibiotics, calcitonin, collagen, corticosteroids, cyano-acrylate, formocresol, and resorbable tricalcium phos-phate ceramic have also been investigated, with varyingdegrees of success. These latter compounds, with theexception of formocresol, have not had sufficient clinicalimpact to be adopted as the material of choice in directpulp capping, especially in the pediatric age groups.

Calcium Hydroxide. Calcium hydroxide producescoagulation necrosis at the contact surface of the pulp.The underlying tissue then differentiates into odonto-blasts, which elaborate a matrix in about 4 weeks.107

This results in the formation of a reparative dentinbridge, caused by the irritating quality of the highlyalkaline calcium hydroxide, which has a pH of 11 to12.108 Stanley has identified that the dentin bridgingeffects of calcium hydroxide occur only when the agentis in direct contact with healthy pulp tissue.74 Tamburicet al. summarized the mineralizing effects of calciumhydroxide, which include cellular adenosine triphos-

phate activation resulting from calcium and hydroxylion enhancement of alkalinity in the mineralizationprocess.109

Yoshiba et al. provided immunofluorescence evi-dence of the possible contribution of calcium hydrox-ide to odontoblastic differentiation. They foundincreased amounts offibronectin, an extracellular gly-coprotein implicated in cell differentiation, amongmigrating fibroblasts and newly formed odontoblastsin areas of initial bridge calcification in response to cal-cium hydroxide. They noted that although calcium


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hydroxide was not unique in initiating reparativedentinogenesis, it demonstrated the most rapid tubulardentin formation in comparison to calcium phosphateceramics and tricalcium phosphate.110

Calcium hydroxide has significant antibacterialaction, which has been identified as an additional ben-

efit in capping procedures.111,112

Estrela et al. summa-rized the antibacterial properties of calcium hydroxide,which include hydrolyzing bacterial cell wall lipo-polysaccharides, neutralizing bacterial endotoxins, andreducing anaerobic organisms through carbon dioxideabsorption.113

There is some controversy as to the source of calci-um ions necessary for dentinal bridge repair at theexposure site. Sciaky and Pisanti114 and Attalla andNoujaim115 demonstrated that calcium ions from thecapping material were not involved in the bridge for-mation. Stark and his colleagues, however, believe that

calcium ions from the capping medicament do enterinto bridge formation.116 Holland et al. provided addi-tional evidence to support this concept.117

Seltzer and Bender identified the osteogenic potentialof calcium hydroxide.42 It is capable of inducing calcif-ic metamorphosis, resulting in obliteration of the pulpchamber and root canals. This fact has raised concernamong clinicians.42 Lim and Kirk, in an extensive reviewof direct pulp capping literature, found little support forpulp obliteration and internal resorption being a majorcomplication of pulp capping.81 Although internalresorption has been documented following calciumhydroxide pulpotomies in primary teeth, it does notappear to be a problem in permanent teeth.

Jeppersen, in a long-term study using a creamy mixof calcium hydroxide placed on exposed pulps of pri-mary teeth, reported a 97.6% clinical success and 88.4%histologic success.93 Although calcium hydroxide pasteshave been shown to be effective in promoting dentinbridges, their higher pH, water solubility, and lack ofphysical barrier strength led manufacturers to introducemodified calcium hydroxide cements that set quicklyand hard for lining cavities and pulp capping.

Various studies have shown successful results of upto 80% with calcium hydroxide pulp capping ofinvolved primary teeth with or without coronalinflammation.65,94,96,118 These investigations supportthe use of hard-set calcium hydroxide cements in placeof calcium hydroxide pastes without causing patholog-ic sequelae, such as internal resorption, associated withpulp-capping failure. For example, the so-callednecrobiotic and inflammatory zones are minimal,and dentin bridges seem to form directly under thesecommercial compounds instead of at a distance from

872 Endodontics

the paste forms.82,118,119 Antibacterial properties andphysical strength to support amalgam condensationhave been shown for the hard-set calcium hydroxidecements.51,103,120

After a clinical investigation of two formulas of ahard, self-setting calcium hydroxide compound

(Dycal), Sawusch found calcium hydroxide liners to beeffective agents for direct and indirect pulp capping inboth primary and young permanent teeth.65 He alsofound that failures in this study tended to be associat-ed with failed restorations and microleakage. Fuks etal. observed an 81.5% success in young permanentfractured teeth with pinpoint exposures when calciumhydroxide was the capping material of choice.121

With the advent of visible light-curing restorativeresins, it was inevitable that, in the interest of efficien-cy and improving the hardness of a cavity lining mate-rial, light-cured calcium hydroxide pulp-capping prod-

ucts were introduced. Stanley and Pameijer122 andSeale and Stanley,123 in histologic studies, found that acalcium hydroxide product (Prisma VLC Dycal, L. D.Caulk Co.), cured by visible light, maintained all of thecharacteristics of healing and bridge formation equiva-lent to the original self-curing Dycal. Lado, in an invitro study comparing the bacterial inhibition of thesenew light-cured products to the self-setting calciumhydroxide cements, also found no differences.112

Howerton and Cox reported the same results as Stanleyand Pameijer122 and Seale and Stanley123 usinglight-cured calcium hydroxide in monkeys.124

Alternative Agents to Calcium HydroxideSuggested for Direct Pulp Capping in Primary

and Permanent Teeth

Zinc OxideEugenol Cement. Glass and Zanderfound that ZOE, in direct contact with the pulp tissue,produced chronic inflammation, a lack of calcific bar-rier, and an end result of necrosis.80

Hembree and Andrews, in a literature review of ZOEused as a direct pulp-capping material, could find nopositive recommendations.125 Watts also found mild to

moderate inflammation and no calcific bridges in thespecimens under his study,126 and this was confirmedby Holland et al.127 Weiss and Bjorvatn, on the otherhand, noted negligible necrosis of the pulp in directcontact with ZOE but stated that any calcific bridgingof an exposure site was probably a layer of dentinalchips.83 They also found no apparent difference in thepulp reactions of primary and permanent teeth.

In spite of the reported lack of success with ZOEcement, Sveen reported 87% success with the cappingof primary teeth with ZOE in ideal situations of pulp


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exposure.128 He offered no histologic evidence, butTronstad and Mjr, comparing ZOE with calciumhydroxide, found ZOE more beneficial for inflamed,exposed pulps and felt that the production of a calcificbridge is not necessary if the pulp is free of inflamma-tion following treatment.76

Corticosteroids and Antibiotics. Corticosteroidsand/or antibiotics were suggested for direct pulp cap-ping in the pretreatment phase and also to be mixed inwith calcium hydroxide with the thought of reducingor preventing pulp inflammation. These agents includ-ed neomycin and hydrocortisone,129 Cleocin,130 corti-sone,131 Ledermix (calcium hydroxide plus pred-nisolone),132 penicillin,133 and Keflin (cephalothinsodium).134 Although many of these combinationsreduced pain for the most part, they were found only topreserve chronic inflammation and/or reduce repara-tive dentin. Also, Watts and Paterson cautioned that

anti-inflammatory compounds should not be used inpatients at risk from bacteremia.135 Gardner et al.found, however, that vancomycin, in combination withcalcium hydroxide, was somewhat more effective thancalcium hydroxide used alone and stimulated a moreregular reparative dentin bridge.136

Polycarboxylate Cements. These cements havealso been suggested as a direct capping material. Thematerial was shown to lack an antibacterial effect anddid not stimulate calcific bridging in the pulps of mon-key primary and permanent teeth.134 Negm et al.placed calcium hydroxide and zinc oxide into a 42%aqueous polyacrylic acid and used this combination fordirect pulp exposure in patients from 10 to 45 years ofage. This mixture showed faster dentin bridging overthe exposures in 88 to 91% of the patients when com-pared to Dycal as the control.137

Inert Materials. Inert materials such as isobutylcyanoacrylate138 and tricalcium phosphate ceramic139

have also been investigated as direct pulp-cappingmaterials. Although pulpal responses in the form ofreduced inflammation and unpredictable dentin bridg-ing were found, to date, none of these materials have

been promoted to the dental profession as a viabletechnique. At Istanbul University, dentists capped 44pulps, half with tricalcium phosphate hydroxyapatiteand half with Dycal (calcium hydroxide). At 60 days,none of the hydroxyapatite-capped pulps exhibitedhard tissue bridging but instead had mild inflamma-tion. Nearly all of the Dycal-capped pulps, however,were dentin bridged, with little or no inflammation.140

Collagen Fibers. Because collagen fibers areknown to influence mineralization, Dick andCarmichael placed modified wet collagen sponges with

reduced antigenicity in pulp-exposed teeth of youngdogs.141 Although the material was found to be rela-tively less irritating than calcium hydroxide, and withminimal dentin bridging in 8 weeks, it was concludedthat collagen was not as effective in promoting a dentinbridge as was calcium hydroxide. Fuks et al. did find

dentin bridges after 2 months in 73% of pulpotomizedteeth that had been capped with an enriched collagensolution.142 They felt that a different mechanism existsfor the production of a truer dentin when a collagensolution is used rather than with calcium hydroxidebecause no coagulation necrosis was seen.

Formocresol. Because of the clinical success offormocresol when used in primary pulp therapy suchas pulpotomies and pulpectomies, several investigatorshave been intrigued by the possibility of its use as amedicament in direct pulp-capping therapy. Arnoldapplied full-strength formocresol for 2 minutes over

enlarged pulp exposures in primary teeth and found a97% clinical success after 6 months.97 Ibrahim et al.reported the absence of inflammation along withdentin bridging in 15 experimental teeth when expo-sures were medicated with formocresol for 5 minutesand capped with a mixture of formocresol and ZOEcement.143 More recently, Garcia-Godoy obtained a96% clinical and radiographic success rate in humanexposed primary molars when capped with a paste ofone-fifth diluted formocresol mixed with a ZOE pasteand covered with a reinforced ZOE cement.144

Hybridizing Bonding Agents. Recent evidence hasshown that elimination of bacterial microleakage is themost significant factor affecting restorative material bio-compatibility.145,146 A major shortcoming of calciumhydroxide preparations is their lack of adhesion to hardtissues and resultant inability to provide an adequate sealagainst microleakage.9,147 Furthermore, calcium hydrox-ide materials have been found to dissolve under restora-tions where microleakage has occurred, resulting in bacte-rial access to the pulp.148 Currently, hybridizing dentinalbonding agents (such as AmalgamBond or C & BMetaBond, Parkell Products, Farmingdale, N.Y.) represent

the state of the art in mechanical adhesion to dentin withresultant microleakage control beneath restora-tions.9,149,150 Miyakoshi and et al. have shown the effec-tiveness of4-META-MMA-TBB adhesives in obtaining aneffective biologic seal.151 Cox et al. demonstrated thatpulps sealed with 4-META showed reparative dentindeposition without subjacent pulp pathosis.152,153

A number of investigators have proposed that sealingvital pulp exposures with hybridizing dentin bondingagents may provide a superior outcome to calciumhydroxide direct pulp-capping techniques.9,154 Because


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of their superior adhesion to peripheral hard tissues, aneffective seal against microleakage can be expected. Theseproposals have been made in spite of concerns with theeffects of acid etchant and resin materials on pulp tissue.

Snuggs et al. demonstrated that pulpal healingoccurred, with bridge formation, in exposed primate

teeth capped with acidic materials such as silicatecement and zinc phosphate cement. This was contin-gent on the fact of the biologic surface seal of the over-lying restoration remaining intact.147 Kashiwada andTakagi demonstrated 60 of 64 teeth to be vital and freeof any clinical and radiographic signs of pulp degener-ation 12 months after pulp capping with a resin bond-ing agent and composite resin. The pulp tissue was notexposed to acid conditioner during the technique.Selected third molars receiving this treatment were his-tologically studied and demonstrated dentin bridgeformation below the area of exposure.155

Heitman and Unterbrink studied a glutaraldehyde-containing dentin bonding agent, in direct pulp-cap-ping exposed pulps, in eight permanent teeth. Allexposed pulps were protected with calcium hydroxideduring application of the acid conditioner. After rins-ing away the calcium hydroxide dressing and condi-tioner, the bonding agent was applied directly to theexposed pulp tissue and surrounding dentin. All teethwere vital after a 6-month postoperative period.156

These results have been further substantiated by Coxand White and Bazzuchi et al.153,157 Kanca reported a4-year clinical and radiographic success with dentinbonding agent application following etching materialapplied directly to a fracture-induced exposed pulpand dentin in rebonding a tooth fragment.158

Conversely, other investigators provide conflictingevidence that does not support using dentin bondingagents in pulp-capping techniques. Stanley has statedthat acid conditioning agents can harm the pulp whenplaced in direct contact with exposed tissues.159 In aprimate tooth sample with pulp exposures treated withtotal-etch followed by application of a dentin bondingagent, Pameijer and Stanley found that 45% became

nonvital and 25% exhibited bridge formation after 75days. In the no etch calcium hydroxide pulp-cappingsample, 7% became nonvital and 82% exhibited bridgeformation after the same time period.160 After 1 year,Araujo et al. experienced a clinical and radiographicsuccess rate of 81% in primary tooth exposures etchedand capped with resin adhesives. Histologic assessmentof extracted sample teeth in advent of their exfoliationdemonstrated inflammatory infiltrate, microabscessformation, and no dentin bridging. Furthermore, bac-terial penetration occurred in 50% of the histologically

874 Endodontics

studied teeth. This occurred in spite of the final com-posite resin restorations being resealed at 6-monthintervals from the time of initial placement.161

Gwinnett and Tay, using light microscopic and elec-tron microscopic techniques, identified early and inter-mediate pulp responses to total-etch followed by a resin

bonding agent and composite resin restoration inhuman teeth. Some specimens demonstrated signs ofinitial repair with dentin bridge formation along theexposed site and reparative dentin adjacent to theexposed site. Other specimens demonstrated persist-ence of chronic inflammation with a foreign bodyresponse in the form of resin globules imbedded with-in the exposed pulp tissue that were surrounded bypulpal macrophages. This was also accompanied by amononuclear inflammatory infiltrate and an absenceof calcific bridge formation.162

Although using dentin bonding agents as a replace-

ment for calcium hydroxide in the direct pulp-cappingtechnique has been advocated,163 more long-term evi-dence and histologic evaluation are needed. Until suchevidence is available, the clinician would be prudent toemploy a combination of calcium hydroxide as amedicament for the exposed pulp followed by ahybridizing resin bonding agent for a successful micro-biologic seal.164,165 This concept is further substantiatedby Katoh et al., who reported improved direct pulp-cap-ping results with dentin bonding agents when they wereused in conjunction with calcium hydroxide.166,167

Cell-Inductive Agents. A number of cell-inductiveagents have been proposed as potential direct pulp-cap-ping alternatives to calcium hydroxide. These contempo-rary substances mimic the reciprocal inductive activitiesseen in embryologic development and tissue healing thatare receiving so much attention at this time.

Mineral trioxide aggregate (MTA) (Dentsply,Tulsa; Tulsa, Okla.) cement was developed at LomaLinda by Torabinejad for the purposes of root-endfilling and furcation perforation repair.168 The mate-rial consists of tricalcium silicate, tricalcium alumi-nate, tricalcium oxide, and silicate oxide. It is a

hydrophilic material that has a 3-hour setting time inthe presence of moisture. Major MTA advantagesinclude excellent sealing ability, good compressivestrength (70 MPa) comparable to IRM, and good bio-compatibility. Pitt Ford et al. documented superiorbridge formation and preservation of pulp vitalitywith MTA when compared with calcium hydroxide ina direct pulp-capping technique.169 They also report-ed normal cytokine activity in bone and cementumregeneration in response to MTA, which is indicativeof its cell-inductive potential.169


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Calcium phosphate cement has been developed forrepairing cranial defects following brain neurosurgery.The components of this material include tetracalciumphosphate and dicalcium phosphate, which react in anaqueous environment to form hydroxyapatite, the min-eral component of hard tissues. Chaung et al. histolog-

ically compared calcium phosphate cement with calci-um hydroxide as a direct pulp-capping agent. Althoughboth materials produced similar results with respect topulp biocompatibility and hard tissue barrier forma-tion, calcium phosphate cement was suggested as aviable alternative because of (1) its more neutral pHresulting in less localized tissue destruction, (2) itssuperior compressive strength, and (3) its transforma-tion into hydroxyapatite over time.170

Yoshimine et al. demonstrated the potential benefits ofdirect pulp capping with tetracalcium phosphatebasedcement. As with calcium phosphate cement, this materi-

al has the ability to be gradually converted into hydroxy-apatite over time. In contrast to calcium hydroxide, tetra-calcium phosphate cement induced bridge formationwith no superficial tissue necrosis and significant absenceof pulp inflammation.171

Summary: Direct Pulp Capping. Adherence toestablished criteria for case selection is important toachieve success. Although somewhat controversialbased on the previously reviewed studies, direct pulpcapping has been found to be less successful in pri-mary teeth than indirect pulp therapy or coronalpulpotomy. However, direct pulp capping tends to bemore successful in young permanent teeth.

PULPOTOMY

Pulpotomy is the most widely used technique in vitalpulp therapy for primary and young permanent teethwith carious pulp exposures. A pulpotomy is defined asthe surgical removal of the entire coronal pulp pre-sumed to be partially or totally inflamed and quite pos-sibly infected, leaving intact the vital radicular pulpwithin the canals.2 A germicidal medicament is thenplaced over the remaining vital radicular pulp stumps

at their point of communication with the floor of thecoronal pulp chamber. This procedure is done to pro-mote healing and retention of the vital radicular pulp.Dentin bridging may occur as a treatment outcome ofthis procedure depending on the type of medicamentused (Figure 17-9). Additional variables thought toinfluence treatment outcome include the medicationtype, concentration, and time of tissue contact.

Indications. According to Dannenberg, pulpo-tomies are indicated for cariously exposed primaryteeth when their retention is more advantageous than

extraction and replacement with a space maintainer.172

Pulpotomy candidates should demonstrate clinical andradiographic signs of radicular pulp vitality, absence ofpathologic change, restorability, and at least two-thirdsremaining root length. Pulpotomized teeth shouldreceive stainless steel crowns as final restorations to

avoid potential coronal fracture at the cervical region.Pulpotomy is also recommended foryoung permanentteeth with incompletely formed apices and cariouslyexposed pulps that give evidence of extensive coronaltissue inflammation.

Contraindications. According to Mejare, con-traindications for pulpotomy in primary teeth existwhen (1) root resorption exceeds more than one-thirdof the root length; (2) the tooth crown is nonrestorable;(3) highly viscous, sluggish, or absent hemorrhage isobserved at the radicular canal orifices; as well as (4)marked tenderness to percussion; (5) mobility with

locally aggravated gingivitis associated with partial ortotal radicular pulp necrosis exists; and (6) radiolucen-cy exists in the furcal or periradicular areas.173

Figure 17-9 Dentin bridge following calcium hydroxide pulpoto-

my with LIFE. (Courtesy of SybronEndo/Kerr Orange, Ca.)


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Persistent toothaches and coronal pus should also beconsidered contraindications.

Treatment Approaches for Primary Teeth. Ranly, inreviewing the rationale and various medicaments thathave guided the historical development of the pulpoto-my procedure, provided three categories of treatment

approaches. Devitalization was the first approach to beused with the intention of mummifying the radicularpulp tissue.174 The term mummifiedhas been ascribedto chemically treated pulp tissue that is inert, sterilized,metabolically suppressed, and incapable of autolysis.174

This approach involved the original two-sittingformocresol pulpotomy, which resulted in completedevitalization of the radicular pulp. Also included werethe 5-minute formocresol and 1:5 diluted formocresoltechniques, which both result in partial devitalizationwith persistent chronic inflammation.174,175

The preservation approach involved medicaments

and techniques that provide minimal insult to the ori-fice tissue and maintain the vitality and normal histo-logic appearance of the entire radicular pulp.Pharmacotherapeutic agents included in this categoryare corticosteroids, glutaraldehyde, and ferric sulfate.Nonpharmacotherapeutic techniques in this categoryinclude electrosurgical and laser pulpotomies.174

The regeneration approach includes pulpotomyagents that have cell-inductive capacity to eitherreplace lost cells or induce existent cells to differentiateinto hard tissueforming elements. Historically, calci-um hydroxide was the first medicament to be used in aregenerative capacity because of its ability to stimu-late hard tissue barrier formation. The calcium hydrox-ide pulpotomy is predicated on the healing of pulp tis-sue beneath the overlying dentin bridge. Recently, itsregenerative capacity has been questioned owing to thefact that calcium hydroxide tissue response is morereactive than inductive. Examples of true cell-inductiveagents include transforming growth factor- (TGF-)in the form of bone morphogenetic proteins,176,177

freeze-dried bone,178 and MTA.168,169 These materialsare more representative of the regeneration category

and provide the direction for future research in vitalpulp therapy.174

Formocresol Pulpotomy

Formocresol was introduced in 1904 by Buckley, whocontended that equal parts of formalin and tricresolwould react chemically with the intermediate and endproducts of pulp inflammation to form a new, colorless,and non-infective compound of a harmless nature.179

Buckleys formula, formocresol, consists of tricresol,19% aqueous formaldehyde, glycerine, and water.*

876 Endodontics

The formocresol pulpotomy technique currentlyused is a modification of the original method reportedby Sweet in 1930.180 By 1955, Sweet claimed 97% clini-cal success in 16,651 cases.181 It should be noted, how-ever, that in this report, about one half of the primaryteeth exfoliated early.

Histology. In spite of regional popularity, the mul-tiple-visit pulpotomy did not receive wide acceptancebecause it was regarded as a nonvital or devitalizationmethod. In addition, histologic studies to support itsuse were also lacking. It became overshadowed by theso-called vital pulpotomy for primary teeth usingcalcium hydroxide, which at that time was supportedby clinical and histologic evidence. Interest informocresol was renewed, however, with a reportedincrease in clinical failures and radiographic evidenceof internal resorption with calcium hydroxide, even inthe presence of dentinal bridging.188 At the same time,

improved clinical and histologic success rates werereported with formocresol.182

In spite of histologic studies that showed formalin,creosol, and paraformaldehyde to be connective tissueirritants, it was recognized early that formocresol is anefficient bactericide. It was also found to have theability to prevent tissue autolysis by the complexchemical binding of formaldehyde with protein.However, this binding reaction may be reversible asthe protein molecule does not change in its basicoverall structure.175

Massler and Mansukhani conducted a detailed his-

tologic investigation of the effect of formocresol on thepulps of 43 human primary and permanent teeth inmultiple treatment intervals.183 Fixation of the tissuedirectly under the medicament was apparent. After a 7-to 14-day application, the pulps developed three dis-tinctive zones: (1) a broad eosinophilic zone of fixa-tion, (2) a broad pale-staining zone with poor cellulardefinition, and (3) a zone of inflammation diffusingapically into normal pulp tissue. After 60 days, in a lim-ited number of samples, the remaining tissue wasbelieved to be completelyfixed, appearing as a strand ofeosinophilic fibrous tissue.183

Emmerson et al. also described the action offormocresol on human pulp tissue.184 They reported

*The formocresol used in this technique may be obtained under the

trade name Buckleys Formocresol (Roth,Chicago,IL). Composition:

35% cresol, 19% formalin in a vehicle of glycerine and water at a pH

of approximately 5.1. To dilute formocresol to one-fifth strength,

thoroughly mix three parts of glycerine with one part of distilled

water. Add these four parts to one part of concentrated commercial

formocresol compound.


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that the effect on the pulp varied with the length oftime formocresol was in contact with the tissue. A5-minute application resulted in surface fixation ofnormal tissue, whereas an application sealed in for 3days produced calcific degeneration. They concludedthat formocresol pulpotomy in primary pulp therapy

may be classified as either vital or nonvital, dependingon the duration of the formocresol application.

Formocresol versus Calcium Hydroxide. Doyle etal. compared the formocresol pulpotomy techniquewith the calcium hydroxide technique in primarycanines and found the formocresol technique to be95% clinically successful at the end of 1 year.182

Although fixation of pulp tissue and some loss of cellu-lar definition were seen histologically, healthy, vital tis-sue existed in the apical third. The calcium hydroxidetechnique was considered to be 61% clinically success-ful, and dentin bridge formation was seen in 50% of

the cases examined.Spedding et al. also studied these two medicaments

in monkeys and produced essentially the same resultsas Doyle and colleagues.185 Law and Lewis evaluatedthe clinical effectiveness of the formocresol techniqueover a 4-year period and reported a 93 to 98% successrate. Their failure rate was greatest between the firstand second years.186

Formocresol versus Zinc OxideEugenol. Bergercompared the pulpotomy effects of using aone-appointment formocresol medication with thoseof ZOE paste alone on the amputated pulps of carious-ly exposed human primary molars.187 Periods of eval-uation ranged from 3 to 38 weeks postoperatively.Clinically and radiographically, 97% of the formocre-sol-treated teeth were judged successful, whereas only58% of the teeth treated with ZOE were consideredsuccessful. Histologically, 82% of the formocresolgroup was judged successful, compared to total failurewith ZOE.187

An intriguing part of this study was the finding of atotal absence of cellular detail in the apical third at 3weeks, but by 7 weeks, connective tissue of a granular

type had ingrown through the apical foramen. In spec-imens obtained after longer postoperative periods,granulation tissue progressively replaced the necroticpulp tissue up to the coronal area. Small areas ofresorption of the dentinal walls were also beingreplaced by osteodentin.187

Spamer also conducted a histologic study ofcaries-free human primary canines following aone-appointment formocresol pulpotomy in whichthe final pulp covering was ZOE.188 Again, the threetypical zones were distinguishable, including the api-

cal one-third tissue, which was normal and free ofinflammatory reaction. Initially, Spamer observed anacute inflammatory reaction, succeeded by a chronicinflammatory response, proliferation of odonto-blasts, and an increase in collagen fibers. By 6months, deposition of mature dentin and vital tissue

was seen throughout.188

Formocresol Pulpotomy Outcomes: Primary Teeth.Rolling and Thylstrup reported a clinical 3-year fol-low-up study of pulpotomized primary molars usingformocresol.189 Their results showed a progressivelydecreasing survival rate of 91% at 3 months, 83% at 12months, 78% at 24 months, and 70% at 36 monthsafter treatment. These investigators concluded thatalthough their rate of success was less than previousstudies had shown, the formocresol method must beconsidered an acceptable clinical procedure comparedwith other methods. Possibly, bacterial microleakage

over the longer time span accounted for their decreas-ing success rate.

Rolling and coworkers, in later studies, investigatedthe morphologic and enzyme histochemical reactionsof pulpotomies done with formocresol in human pri-mary molars for periods ranging from 3 to 24 monthsand 3 to 5 years.190,191 In these studies, a wide range ofpulpal reactions occurred, from normal pulps to totalchronic inflammation. In most instances, however, thepulp tissue in the apical region was vital with minimalinflammation, which was in agreement with manyother studies. It was concluded from both studies thatthe formocresol method should be regarded as only ameans to keep primary teeth with pulp exposures func-tioning for a relatively short period of time.

Magnusson investigated therapeutic (ie, formocre-sol) pulpotomies and stated that his histologic exami-nations revealed early capricious diffusion of themedicament through the pulp tissue, producing chron-ic inflammation and no healing in the apical areas alongwith a small percentage of internal resorption.192 Froma biologic standpoint, Magnusson felt that formocresolwas biologically inferior to calcium hydroxide in the

pulpotomy technique as the latter manifested true signsof healing but in a low percentage in primary teeth.192

Ranley and Lazzari concluded, however, that variationsin the interpretation of histologic studies withformocresol, on either vital or nonvital tissue,are attrib-utable to the length of exposure of the radicular tissueto the drug, but there is no true healing.193

In general, the results of many histologic studies onthe formocresol pulpotomy have shown that severaldistinct zones are usually present in the pulp followingthe application of the medicament:


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1. Superficial debris along with dentinal chips at theamputation site

2. Eosinophil-stained and compressed tissue3. A palely stained zone with loss of cellular definition4. An area offibrotic and inflammatory activity5. An area of normal-appearing pulp tissue considered

to be vital

Formocresol Addition to Sub-base. Beaver et al.investigated the differences in pulp reactions between a5-minute application of formocresol using sub-bases ofeither ZOE cement alone or with the addition offormocresol.194 There was no appreciable difference ina histologic reaction of the remaining radicular pulptissue under either of these two types of sub-bases.

An alternative procedure reported clinically and his-tologically successful is to incorporate dilutedformocresol into the ZOE dressing and then place it on

the pulpal stumps instead of a moistened formocresolcotton pellet.17,195,196 Ranly and Pope have shown invitro and in vivo that formocresol can leach out from aZOE sub-base when the two substances are com-bined.197 They have suggested that the initial applica-tion of a formocresol-saturated cotton pellet on thepulp might be an unnecessary step.

Formocresol Dilution. Venham suggested thatformocresol might be reduced to one-quarter strengthin the pulpotomy application.198 The combined investi-gations of Straffon and Han199,200 and Loos et al.201 onthe histologic and biochemical effects of formocresolintroduced new thinking in this type of pulp therapy.Straffon and Han concluded from a study of connectivetissue in hamster pulps exposed to formocresol that themedicament does not interfere with a prolonged recov-ery of connective tissue and may even suppress the ini-tial inflammatory reaction. In a later report, they con-cluded that formocresol at 1:5 strength might be equallyeffective and possibly a less damaging pulpotomy agent.Loos and colleagues concurred with the previous workin a further study of diluted formocresol.201 Morawa andcolleagues, in a 5-year clinical study of 70 cases, found

that the formocresol pulpotomy, using a 1:5 concentra-tion, was as effective as a full concentration and also hasthe advantage of reduced postoperative complications inthe periradicular region. In onlyfive teeth was there lim-ited radicular internal resorption.202

Fuks and Bimstein used this one-fifth dilution offormocresol in a clinical and radiographic study of pri-mary teeth over a period of 4 to 36 months.203 The clin-ical success rate was reported at 94.3%, and 39% of 41cases showed a slightly higher rate of premature rootresorption. Twenty-nine percent had radiographic evi-

878 Endodontics

dence of a root canal obliteration process. In a laterstudy with rhesus monkeys, using full-strengthformocresol compared with a 20% dilution, theseinvestigators found the same premature root resorp-tion but a milder pulpal inflammatory response withthe diluted concentration.204 Garcia-Godoy, however,

did not find any differences histologically between full-strength and a one-fifth dilution of formocresol whenapplied in several ways over the amputated pulps.195

Outcomes. Citing an 80% success rate of primarymolars pulpotomized with formocresol, Wright andWidmer also found early root resorption of the pulpo-tomized molars in comparison to the untreatedantimeres.205 The permanent successors, however, werenot found to erupt significantly earlier, as has been pre-viously reported.

The hard tissue deposition or calcification of theroot canal walls following a formocresol pulpotomy

has also been observed radiographically in severalother studies.203,206,207 These findings imply that theuse of formocresol does not result in a complete loss ofpulp vitality.

More recently, the findings of a retrospective radi-ographic study of the formocresol pulpotomy tech-nique with a post-treatment time ranging from 24 to87 months were reported by Hicks et al.196 In thisstudy, a ZOE paste into which full-strength formocre-sol was incorporated was placed in the pulp chamberafter coronal amputation followed by restoration witha stainless steel crown. Based on radiographic evalua-tion criteria, which included abscess formation, radi-olucencies, pathologic root resorption, calcific meta-morphosis, and advanced or delayed exfoliation, theprocedure was considered to be successful in 93.8% ofthe cases. Coll et al. compared the techniques offormocresol pulpotomy versus pulpectomy in primaryincisors. They concluded that the pulpotomy was thepreferred technique for these teeth.67

Formocresol Pulpotomy Technique in Primary Teeth

Correct diagnosis is essential to ensure the clinician

that inflammation is limited to the coronal pulp.208

Biopsy studies of pulp tissue removed from the open-ing of root canals under pulpotomies have demonstrat-ed the unreliability of clinical assessments in primaryteeth.192 Radiographic examinations are therefore nec-essary to confirm the need for pulpotomy therapy inprimary teeth. It is judicious to take bitewing and peri-radicular radiographs so that the depth of caries maybe observed and the condition of the periradicular tis-sues determined. Mejare found only a 55% success ratein primary molars with either coronal or total chronic


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pulpitis that were treated by formocresol pulpotomyafter 212years.209

One-Appointment Pulpotomy. Indications. Thismethod of treatment should be carried out only onthose restorable teeth in which it has been determinedthat inflammation is confined to the coronal portion of

the pulp. When the coronal pulp is amputated, onlyvital, healthy pulp tissue should remain in the rootcanals (Figure 17-10).

Contraindications. Teeth with a history of spon-taneous pain should not be considered. If profusehemorrhage occurs on entering the pulp chamber, theone-step pulpotomy is also contraindicated. Othercontraindications are pathologic root resorption, rootsthat are two-thirds resorbed or internal root resorp-tion, interradicular bone loss, presence of a fistula, orpresence of pus in the chamber (Figure 17-11).

Procedure.

1. Anesthetize the tooth and tissue.2. Isolate the tooth to be treated with a rubber dam.3. Excavate all caries.4. Remove the dentin roof of the pulp chamber with a

high-speed fissure bur (Figure 17-12, A).5. Remove all coronal pulp tissue with a slow-speed

No. 6 or 8 round bur (Figure 17-12, B). Sharp spoonexcavators can remove residual tissue remnants.

6. Achieve hemostasis with dry cotton pellets underpressure.

7. Applydiluted formocresol to the pulp on a cottonpellet for 3 to 5 minutes210 (Figure 17-12, C).

8. Place a ZOE cement base without incorporation offormocresol (Figure 17-12, D).

9. Restore the tooth with a stainless steel crown.

Two-Appointment Pulpotomy. Indications. Thetwo-appointment technique is indicated if there is (1)evidence of sluggish or profuse bleeding at the ampu-tation site, (2) difficult-to-control bleeding, (3) slightpurulence in the chamber but none at the amputationsite, (4) thickening of the periodontal ligament, or (5)a history of spontaneous pain without other con-traindications. The two-step pulpotomy can also beused when shorter appointments are necessary to facil-

itate patient management problems. Miyamoto sug-gested the two-appointment technique for uncoopera-

Figure 17-10 One-appointment formocresol pulpotomy. A, Root of the pulp chamber and coronal pulp removed. Cotton pellet with

formocresol in place for 5 minutes. B, Successful formocresol pulpotomy 1 year following treatment.(A courtesy of Dr. Constance B. Greeley;

B courtesy of Dr. Mark Wagner.)

Figure 17-11 Final failure of formocresol pulpotomy, mandibular

first primary molar. Root resorption and interradicular bone loss

(arrows) prior to treatment forecast eventual failure. The tooth was

extracted. Reproduced with permission from Law DB, Lewis TM,

Davis JM. An atlas of pedodontics. Philadelphia: WB Saunders;

1969.

A B


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tive children to minimize chair time, especially for the

initial operative visit.211

Contraindications. This technique should not bedone for teeth that are (1) nonrestorable, (2) soon to beexfoliated, or (3) necrotic.

Procedure.

1. The steps are the same as for the one-appointmentprocedure through step 6.

2. A cotton pellet moistened with diluted formocresolis sealed into the chamber for 5 to 7 days with adurable temporary cement.

880 Endodontics

3. At the second visit, the temporaryfilling and cotton

pellet are removed and the chamber is irrigated withhydrogen peroxide.4. A ZOE cement base is placed.5. The tooth is restored with a stainless steel crown. As

previously stated, Verco and Allen found no differ-ence in the success rate between one-stage andtwo-stage procedures.212

Avram and Pulver surveyed Canadian, American,and selected dental schools throughout the world aswell as a limited number of pediatric dental specialists

Figure 17-12 Step-by-step technique in one-appointment formocresol pulpotomy. A, Exposure of pulp by roof removal. B, Coronal pulp

amputation with a round bur. Hemostasis with dry cotton or epinephrine. C, Application of formocresol for 1 minute. Excess medicament

is expressed from cotton before placement. D, Following formocresol removal, zinc oxideeugenol base and stainless steel crown are placed.

A B

C D


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to determine medicament choice and clinician attitudetoward pulpotomy therapy prevalent at the time ofinvestigation.213 The most prevalent medicament usedin pediatric dental departments (40.8%) wasfull-strength formocresol, followed by 36% for the 1:5dilution. This 1:5 dilution was used by 50% of the pedi-

atric specialists, whereas 42% used-full strengthformocresol. Primosch et al. surveyed predoctoralpediatric dentistry programs in 53 US dental schools todetermine the prevalence and types of primary toothpulp therapy techniques taught in those institutions.Formocresol was the most widely taught pulpotomymedicament, with 71.7% of the programs using dilut-ed formocresol and 22.6% full-strength formocresol.Zinc oxideeugenol was the base material of choice for92.4% of all programs surveyed. 69

Clinical experience has shown that pulpotomizedprimary molars are susceptible to cuspal and cervical

fracture. For this reason, the restoration of choice is awell-fitted stainless steel crown. Additional advan-tages of this restoration include elimination of recur-rent decay, elimination of intracoronal restorationfracture, and reduction of microleakage. Althoughcomposite resin restorations, incorporating thedentin bonding agents, have been proposed forpulpotomized primary molars, more studies are indi-cated to determine their effectiveness relative to stain-less steel crowns.

PULPOTOMY FOR YOUNG PERMANENT TEETH

Treatment of severely decayed and pulpally involvedyoung permanent teeth in the child or adolescent cre-ates a dilemma. Complete endodontic therapy and acast full-crown restoration have been considered to bethe ideal treatment. However, this is time consumingand, in many instances, beyond the family financialresources. Most importantly, canal obturation forincompletely formed roots and open apices presentsunique problems with conventional endodontic tech-niques. The relatively thin dentin walls of the largeobturated canals place the tooth at greater risk for root

fracture over time. In these instances, the treatmentobjective is to maximize the opportunity for apicaldevelopment and closure, known as apexogenesis, andenhance continual root dentin formation. Theseobjectives can occur only if the radicular pulp is main-tained in a healthy statethe intent of the pulpotomytechnique. Although calcium hydroxide has been themost recommended pulpotomy medicament for pul-pally involved vital young permanent teeth withincomplete apices, formocresol has also been proposedas an alternative.

Formocresol

The well-documented success with formocresol pulpo-tomies in primary teeth has led a number of cliniciansto extrapolate the use of this medication in young per-manent teeth with avital or, in some instances, nonvi-tal pulp status at the start of operative treatment.

Canosa reported the widespread use of formocresolpulpotomy in Cuba for all restorable molars with vitalpulps only. Restorable necrotic molars, as well as pre-molars and anterior teeth, received full root canal ther-apy. She reported an empirical success rate of 75% withformocresol pulpotomies. Those cases that failed weretreated by endodontic cleaning, shaping, and filling(I Canosa, personal communication, March 1994).

Ibrahim et al. studied the use of formocresol as apulpotomy medication in the permanent teeth of twodogs and a monkey for up to 20 weeks.214 Radio-graphically, no evidence of apical pathosis was seen.

Histologically, calcification in the canal, continued api-cal closure, and partial bridging were noted. Areas ofinflammation were replaced with connective tissue.

Using formocresol, Tras

pediatric tics - chap 17 - ingle

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