Endodontics

Calcifié metamorphosis: A challenge in endodonticdiagnosis and treatment

Faisal A, Amir, BDSVJames L. Gutmann, DDS^/D, E, Witherspoon, BDSc, MS^

Calcilic metamorphosis (CM) is seen commonly in the dental pulp after traumatic tooth injuries and is rec-ognized clinically as early as 3 months atter injury Calcitic metamorphosis is characterized by depositionot hard tissue within the root canai space and yellow discoloration of the clinical crown Opinion differsamong practitioners as to whether to treat these cases upon early detection ot CM or to observe themuntil symptoms or radiographie signs of pulpal necrosis are detected. In this review, the clinical, radio-graphic, and histopathologic appearance ot CM is described; a review ot the iiterature is presented toaddress these issues in an attempt to establish a sound rationale for treatment. Approximately 3,8% to24% of traumatized teeth develop varying degrees ot CM, Studies indicate that of these, approximately 1%to 16% will develop pulpal necrosis. Most ot the literature does not support endodontic intervention unlessperiradioular pathosis is detected or the involved tooth becomes symptomatfc. It may be advisable to man-age cases demonstrating CM through observation and periodic examination, (Quintessence int 200132-447-455)

Key words: calcific metamorphosis, calcification, pulp canal obliteration, pulp disease, trauma

Calcific metamorphosis (CM) is defined as a pulpalresponse to trauma that is characterized by depo-

sifion of hard tissue within tbe root canal space,' Ithas also been referred to as pulp canal obliteration, =-'CM is seen commonly after traumatic tootb injuries'̂and is recognized clinically as early as 3 months afterinjury, but in most instances it is not detected forabout 1 year.'-^ Altbougb tbe exact mecbanism of CMis still unknown, damage to tbe neurovascular supplyof tbe pulp is probably related significantly to thisprocess."'-'̂ Teeth presenting with radiographie evi-dence of CM are considered to be undergoing patbo-logic cbanges by some clinicians,^'^ In this respect, thediagnostic status and treatment planning decisionsregarding teeth with CM remain controversial,"'"*-'*

'Gradúale Student, Graduate Endodontics, Baylor College oí Denfisfry,Texas Am Ur!iversily System Heaith Science Center, Oalias, Tenas,

'Program Director, Graduate Endodontics, Bayior College of Dentistry,Teias ASM University System Health Science Center, Dallas, Texas,

'Assistant Professor, Graduate Endodoritics, Baylor College of Dentistry,Texas A&M University System Healih Science Center, Daiias, Texas,

Reprint requests: Dr James L Gutmann, Program Director, GraduateEnoodortlcs, Baylor Coilege of Dentistry, 3303 Gaston Avenue, Dalias,Texas 75346. E-maiI:jgutmann@taml>cd,edu

ETIOLOGY AND INCIDENCE

Calcific metamorphosis occurs commonly in yotmgadults because of trauma. It is evident usually in tbeanterior region of tbe moutb and can partially or totallyobliterate tbe canal space radiograpbically.'^'^-"*''-''Tbe clinical picture of CM has been described byPatterson and Mitchell'̂ as a tooth that is darker in huetban the adjacent teetb and exbibits a dark yellowcolor because of a decrease in translucency from agreater tbickness of dentin under tbe enamel (Fig 1),These autbors considered CM a pathologic conditionand recommended either root canal treatment orextraction of tbe tootb. It was reasoned tbat tbe pulpfissue involved should be regarded as a potential focusof infection and therefore sbould be removed, Histo-logically, bowever, no evidence of pulpal patbosis couldbe demonstrated as a result of poor fixation of tbe pulptissue. Table 1 summarizes studies tbat indicated tbefrequency of puip necrosis following CM,

Holcomb and Gregory!̂ examined 881 patietits andfound tbat 41 teeth in 34 pafients exhibited CM, repre-senting an incidence of 3,8%, Over a 4-year period, onlytbree of tbe 41 teetb (7,3%) developed periradicularrarefactions, Tbey concluded that CM may be a patho-logic deviafion from tbe normal pulp. As a result, tbeonly definitive criterion for choice of treatment for theseteeth was the appearance of a periradicular rarefaction.

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Fig 1 Ciinicai photograph oí a maxiiiary ielt centrai incisor withthe ciassic appearance of CM; note the dark yeilow discolorationwhen compared to the adjacent teeth

TABLE 1 Frequency of necrosis following calcific metamorphosis (CM) in permanentteeth

Study

Holcomb and Gregory 1967"Andreasen 1970'Stâihane and Hedegard 1975^Jacobsen and Kerekes 1977™Andreasen et ai 1987"Rcbertson et al 1996''

Meanobservationperiod (y)

41-12(3,4)13-2110-23(16.0)1-10(3.6)7-22(16)

No, of unitsstudied

88 patients189 iuxated teeth76 teeth with CM

122 traumatized teeth637 teeth82 traumatized teeth

No. ofteeth

with CM

4t4276

1229682

No. of teethwith puipainecrosis

3 (7%)3 (7%)

12(16%)16(13%)1 (1%)7 (8.5%)

Andreasen' conducted a follow-up study of 189 litx-ated permanent teeth with a mean observation periodof 3,4 years. Pulp canal obliteration was found in 42teeth (22'*/o) and was reiated significantly to the vari-able stage of root development. Calcific metamorpho-sis was more common iti teeth with incomplete rootdevelopment and crown fracture and was related tothe type of luxation injury, Calcific metatnorphosis wasconsidered to be an accelerated deposition of dentin inresponse to trauma, and early endodontic interventionwas not supported. In a similar study with a 5-year fol-low-up of 637 permanent incisors, only lS'i/o developedCM, and only lVo of those developed pulp necrosis,''

Stálhane and Hedegard' conducted a long-termstudy on 76 teeth with CM following trauma. Theteeth were examined 3 to 21 years after the accident.Twelve of the 76 teetb (16%) developed a periradicu-lar rarefaction during the observation period. Theauthors stated that in making treatment decisions, thesuccess rate enjoyed by modern endodontic treatmentmust be weighed against the percentage of teeth thatbecome necrotie secondary to CM. The possibility thatadditional trauma, subsequent earies, or orthodonticmovement could contribute to the periradicularchanges in these cases was highlighted.

Jacobsen and Kerekes^" conducted a follow-up studyof 122 traumatized teeth with radiographie evidence ofhard tissue formation in the pulp cavity for a mean of16 years after injury. Partial canal obliteration was iden-tified in 36% of the cases, with total canal obliterationin 64%. Of the total population studied, 13% eventuallydeveloped pulp necrosis. These findings support thoseof Holcomb and Gregory'-* in that the rationale forendodontie treatment should be the development of aperiradieular radiolucency.

A retrospective study of 517 traumatized teeth byRoek and Grundy'' showed that 16% of the teeth devel-oped CM, with CM mostly occurring in the youngerage group and résorption occurring in the older agegroup. Root canal treatment was recomtnended assoon as narrowing of the pulp chatnber shadow is seenradiographicaiiy, based on two clinical parameters: (IjOnce the guidance afforded by the pulp canal is lost, itis more difficult to prepare a post hole without pene-trating the periodontal ligament; and (2) should necro-sis occur in the retnaining apical tissue, the only possi-ble access may be surgical intervention.

One of the most recent studies that addressed CMconsisted of 82 traumatized permanent incisors thatwere followed for a period of 7 to 22 years (mean 16

448 Voiume 32, Number B, 2D01

years).-' lu liiat study, a clinical finding of yellow dis-coloration of the teeth was observed frequently.During the observation period, periradicular bonelesions suggesting pulp necrosis developed in seventeeth {8,5»b), The 20-year pulp survival rate was 84%,and no higher frequency of pulp necrosis wasobserved in teeth with CM that were subjected tocaries, new trauma, orthodontic treatment, or com-plete-crown coverage when compared to intact teeth.The conclusion that the incidence of pulp necrosis inteeth displaying CM seems to increase over time wasnot supported, and routine endodontic interventionon teeth with CM was not justified.

RADIOGRAPHIC INTERPRETATION

The radiographie appearance of CM is partial or totalobliteration of the pulp canal space with a normalperiodontal membrane space and intact lamina dura,̂A thickening of the periodontal ligament space orperiradieular radiolucency may be observed with orwithout subjective symptoms (Fig 2), Complete radi-ographie obliteration of the root canal space, however,does not necessarily mean the absence of the pulp orcanal space; in the majority of these cases there is apulp canal space with pulpal tissue,*''̂ '̂ '̂ i

Fig 2 Periradicular radiogiaph of multiplemandibuiar incisors wifh varying degrees ofCM demohsfrates different outcomes. Themandibuiar righl lateral incisor shows com-plete oblitération and normai lamina dura,as well as complete pulpal obliteration anddnvelopmenf of a periradicuiar radiolu-cency. The mandibular leff central incisorshews parliai puipal obliteration and devel-cpmenl of a periradicular lesion, (Casecourtesy cf Dr Anthony McNaught,)

HISTOPATHOLOGY

Histopathologic studies designed to assess the pulpalstatus of teeth with CM have failed to show anyinflammatory component indicative of a pathologicprocess,^'''''^ This may be a resuit of multiple causes,including but not limited to poor tissue fixation, speci-men sectioning, and the investigator's interpretation.On the other hand, Patterson and Mitchell'^ consid-ered CM a pathologic process but could not prove ithistologically hecause they based their conclusion onone case with a poorly fixed pulpal tissue.

The pulps of 20 maxillary permanent incisors wereevaluated microscopically by Lundberg and Cvek,'' Theteeth were treated endodontically because of progres-sive hard tissue formation in the canal space. The tissuechanges were characterized by a varied increase in col-lagen content and a marked decrease in the number ofcells, Osteoid tissue with included cells was found adja-cent to mineralized areas in the pulp, with only onepulp showing moderate lymphocytic inflammatoryinfiltrate because of further trauma. They concludedthat tissue changes in the pulps of teeth with CM donot indicate the necessity for root canal treatment,

Torneck^ described CM as a tertiary dentinresponse to trauma that is highly irregular in pattern

and calcification and contains a maze of small irregu-lar spaces and cul-de-sacs that extend from the pulpchamber to the apical foramen. Such irregularitieswere iess common when the rate of calcification wasslower, with the dentin deposition occurring only onthe periphery of the pulp space. The dentin structurewas also more regular, heing principally of a tubulartype that is supported at times hy a small but Identifi-able pulp in the more central portion of the root,

Fischer^' indicated that CM was a response totrauma with progressive hard tissue formation, withmaintenance of vital tissue and a pulp space observedup to the apical foramen [Fig 3), He argued, however,that such cases require root canal treatment becauseof reduced cellular content leading to decreased ahihtyfor healing, therefore making the pulpai tissue moresusceptible to infection.

The histopathoiogic appearance of pulp canal oblit-eration in traumatized primary incisors shows threetypes of calcific tissue occluding the pulp lumen:dentin like, bone like, and fibrotic." Recently, Holan^described tube-like structures that extended along theentire length of the pulp canal. These were separatedfrom the root dentin by normal pulp tissue but con-nected to the dentin in some of the sites evaluated. The

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Fig 3 (left) Histologie section of a tooth vM\i evidence ot com-plete pulp canal obliteration radiographically shows irregulardeposition ot te'tiary dentin along the length of tne pulp coronal totne apical foramen. Note tne gaps indicating tnat compiete oblit-eration did not exist (Original magnification xlOO, hematcxylin-eosin stain.)

Fig 4 (below) Transverse section cf a tootfi shows concentricdeposition of tertiary dentin. with entrapped ceils giving rise to ancstecdentirt-iii<e appearance. [Originai rnagnification '16: lierra-ic/ylin-eosin stain.̂

structures had a histologie appearance of osteodentin,with celiular inclusions in ring-like formations (Fig 4).

MECHANISM OF HARDTISSUE FORMATION

The mechanism of hard tissue formation during CM isnot yet clear. Several hypotheses have been proposedto explain this phenomenon, Torneck* hypothesizedthat the deposition of hard tissue is either as a resiiltof stimulation of the pre-existing odontohlasts or byloss of their regulatory mechanism. On the otherhand, Andreasen and Andreasen' described CM as aresponse to severe injury to the neurovasciilar supplyto the pulp, which after healing leads to accelerateddentin deposition and is closely related to the loss andre-establishmcnt of the pulpal neural supply. Neithermechanism has been proven or studied, and furtherinvestigation is required to provide an evidence-basedunderstanding of this occurrence,

Calcific metamorphosis is characterized by anosteoid tissue that is produced by the odontoblasts atthe periphery of the pulp space or can be produced byundifferentiated puipai cells that undergo differentia-tion as a result of the traumatic injury. This results in asimultaneous deposition of a dentin-like tissue alongthe periphery of the pulp space (root canal walls) andwithin the pulp space proper (root canal). These tis-sues can eventually fuse with one another, producingthe radiographie appearance of a root canal space thathas become rapidly and completely calcified.

Ten Cate''* identified this process as the depositionof tertiary or reparative dentin in response to irritationor trauma. Reparative odontoblasts are somehow ableto differentiate from dental pulp cells in the absence ofany epithelial influence. During the development ofthe tooth, the undifferentiated ectomesenehymal cellof the dental papilla divides into two daughter cells.One daughter cell is influenced by the epithelial cellsand differentiates into an odontoblast, while the sec-ond daughter cell that is not exposed to the epithelialinfluence persists as a subodontoblast cell, whichunder certain influences differentiates into odonto-biast-like cells and deposits dentin-like hard tissue.

Reparative dentin or tertiary dentin is deposited atspecific sites in response to injury, and rate of deposi-tion depends on the degree of injury. The more severethe injury, the more rapid the rate of dentin deposi-tion, with possibly as much as 3,5 jjm in a single day.This results in accelerated hard tissue formation thattraps some pulpal cells and gives the histologieappearance of osteodentin with an irreguiar tubularpattern {Figs 5 and 6), Evidence indicates that repara-tive dentin is produced by odontoblast-like cells andincorporates type I and III collagen in its matrix,which exhibits diminished phosphophoryn content."*

The cells constituting this hard tissue originate fromcell divisions in deeper layers of the pulp, and the typeof cells that divide has not been established. Theymight be undifferentiated perivascular cells, pulpalfibroblasts, or cells formed from the odontohlast lin-eage but not exposed to the final epithelial influence.̂ *

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Fig 5 (ieñ) Irregular linear caloilication with highly irregular tubu-lar pattern and gnarled appearance oí the reparative dentin.{Originai magnilioation x100, hematoxyhn-eosin stain.]

Fig 6 (beiow) Histoiogic seotior shows locai aeposition ol repar-ative dentin as a response lo a localized injury lo the pulp Notethe naiufe ot localized deposition compared to calcilic metamor-phosis, in which (he reparative dentin tormation is more linear andinvoives the entire pulp canal. (Original magnification x25:Brown-Brenn stain.)

These newly differentiated cells first express a mixtureof collagen (including types J, II, 111, and IV), whichforms a matrix surface. The deposition of fibronectinon predentin provides the mechanism for positioningthe cells that then produce a matrix of type I and IIcollagen that accepts mineral in the absence of phos-phophoryn. There is much discussion as to whetherthe mineralized tissue so formed is truly dentin,because the original odontoblasts express type I colla-gen and phosphophoryn,'^

MANAGEMENT OF CANALS WITHCALCIFIC METAMORPHOSIS

The management of canals with CM is similar to themanagement of pulpal spaces with any form of calcifi-cation. Usually, the teeth involved with CM are ante-rior teeth that were subjected to trauma at a youngage. The literature supports the fact that most teethwith the radiographie appearance of CM exhibit a per-sisting narrow pulp canal space that is not usuallydetectable radiographicaliy.^'''-'^'^'''^''^^ Even underthese circumstances, most canals can be located andnegotiated.'•"a

To locate the calcified orifice, the practitioner firstmentally visualizes and projects the normal spatial rela-tionship of the pulp space onto a radiograph of the cal-cified tooth. Then, the two-dimensional radiographieimage is correlated with the three-dimensional morphol-ogy of the tooth.^ Thereafter, access preparation is initi-

ated, with the rotary instrument directed toward thepresumed location of the pulpal space. This approachrequires knowledge of the normal pulp chamher loca-tion, tooth canal anatomy, and the long axis of the roots.Accurate radiographs are essential for preoperative visu-alization and periodic assessment of bur penetrationand orientation. Finally, the practitioner must be able torecognize the calcified orifice when it has been reached.

Normal root anatomy

In the past, textbooks on root canal morpbology haveoften overlooked an important anatomic fact: Thecanal space is always located in tbe cross-sectionalcenter of the root. Similarly, the pulp chamber is (orwas, before calcification) located in the cross-sectionalcenter of the crown^' (Fig 4).

In a tooth with a calcified pulp chamber, the dis-tance from the occlusal surface to the projected pulpchamber floor is measured from the preoperativeradiograph. An access cavity of normal size and shapeis created in the crown to a depth equal to that of thepulp chamber floor in a noncalcified tooth.

A second important aspect of normal root canalanatomy is the geometric pattern of canal orificesfound in the pulp chambers of teeth with multiplecanals.̂ *" These geometric patterns and their potentialvariations must be mentally projected onto the calci-fied pulp chamber floor, with consideration for tbedirection of the canals as they leave the pulp chamber.This requires an astute integration of two-dimensional

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radiograpbic findings witb three-dimensional tootbanatomy, coupled with a safe and dexterous move-ment of tbe rotary instrument on the pulpal floor.

Maxillary central and lateral incisors and canines

In maxillary incisors, the root canal is located in tbecross-secfional center of tbe root̂ ^ (Fig 4), If estbeticsand structural integrity were disregarded, the ideallocation of tbe access preparation wouid be tbrougbtbe incisai edge; bowever, the standard access prepa-ration for this tooth is in the exact center of the pala-tal surface of the crown buccolingually and incisogin-givally. At an angle of roughly 45 degrees to the longaxis, bur pcnctrafion of 3 to 4 mm will generally ititer-sect with tbe pulp cbamber in average-sized teetb. In acalcified cbamber, however, confinued penetration at45 degrees to the long axis will eventually pass overthe canal entirely and result in perforation of thelabial root surface below tbe gingival attachment,Tberefore, when tbe cbamher is calcified and thecanal has not been located after 3 to 4 mm of penetra-fion, the bur must be rotated to be as parallel to thelong axis of the tooth as possible to prevent perfora-tion. Penetration proceeds down tbe lingual aspect oftbe access preparation, with frequent explorafion forthe orifice with the DG-16 endodonfic explorer. Indeep excavafions, the bur may be changed to a long-shank No, 2 round bur witb frequent visual and radi-ograpbic reassessment of direcfion,

Mandibular incisors and canines

The most common canal morphology for these teetb isa single canal; however, a second canal, if present, willalmost invariably be found lingual to the first.^^'*' Inincisors and canines, second canals are parficularlydifficult to locate (even wbere minimal calcification ispresent) because of anguiation of the anatomic crownor the location of tbe standard access cavity on thelingual aspect. After tbe main canal is located anddebrided, it is important to widen the orifice linguallyand probe for the second orifice using a No, 8 or 10 Kfile with an abrupt curve placed 1 or 2 mm from tbefip of tbe file. If tbe canal is not located with tbis tech-nique, the use of No, 2, 3, and 4 Gates-Glidden drillson the lingual surface may be very helpful in uncover-ing the orifice of a lingual canal, Tbe drill is used inthe manner of tbe round bur and is drawn up tbe lin-gual surface in a sweeping motion, Witb tbe advent ofcanal-orifice shapers, the technique of increasing theorifice has been enhanced.

Location and penetration

The most important instrument for orifice location is Sthe DG-16 explorer. In firm probing during excavation Ïof the pulp chamber floor, the explorer will not pene- IItrate and "stick" in solid dentin; bowever, if an orificeis present, firm pressure will force tbe instrumentslightly into the orifice, and it will resist dislodgment, 'or sfick. To minimize perforafion, reconfirm the !oca-fion of the canal radiographicaiiy, leaving the explorer :in place. At this point, a fine instrument, usually a No,8 or 10 K file, is placed into the orifice, and an attemptis made to negotiate the canal. Some practifioners pre-fer to use a No, 6 K file initially to negotiate the canal; *however, these instruments are very fine and lack stiff- Sness in their shafts. If the canal is bigbly calcified or 'packed witb necrotic debris, the No, 6 K file will bendand curl instead of penetrating. An alternative optionis to use instruments with reduced fiutes, such as aCanal Pathfinder (JS Dental), or instruments withgreater shaft strength, such as the Pathfinder CS(Kerr), which are more likely to penetrate even bigblycalcified canals. Here also, tbe canal Orifice Shapers(Dentspiy) will enbance rapid canal penetrafion,

Wben faced witb trying to locate the canal orifice,many practitioners bave chosen to use magnification ititbe form of enhanced glasses or a microscope,Altbougb it may be advantageous to be able to see theposition of tbe orifice under magnification, tbisapproacb will not aid tbe clinician who does not lmowwbere to look for tbe orifice, Tbe anatomic features oftbe pulp chamber floor are an essential tool for locat-ing the orifices and sbould be preserved as much aspossible. Examining tbe color changes in tbe floor withbigb magnification will aid in locating canal orifices.

Because of curvature in tbe coronal 1 or 2 mm ofmany canals, it is necessary to remove tbe cervicalledge or bulge,^' If tbe orifice still cannot be negofi-ated with a flne instrument, drill 1 or 2 mm into thecenter of the orifice with a No, 2 round bur on slowspeed and use the explorer to re-establisb the canalorifice. When counter sinking or trougbíng in an areawhere an orifice is located, be sure tbat tbe pulpcbamber is dry. The slow-speed rotating bur willremove white denfin chips tbat accumulate in the ori-fice. After a light stream of air is blown into thecbamber, tbese denfin cbips appear as wbite spots ontbe dark floor of tbe cbamber and serve as markersfor exploration or furtber counter sinking. Uponentry, tbe file is carefully rotated and teased apicallyaround tbe canal curves, Chelating agents such asREDTA (Roth Drug), RC-prep (Premier DentalProducts), and Glyde (Dentsply) are seldom of valuein locating the orifice but can be useful during canalnegotiation,^^

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Penetration and negotiation

Once the orifice bas been located, it is advisable toenlarge the coronal third to improve tactile sensationand better apical penetration, A 21-nim No, 8 K file isthe initial instrument of choice to negotiate the calci-fied canal. A No, 10 K file is usually too large, and aNo, 6 K fiîe is too weak to apply any firm apical pres-sure, particularly if curved. Likewise, the use ofnickel-titanium files is contraindicated for this pur-pose because of lack of strength in the long axis ofthe file. The 21-mm-long K file Is fiexible enough tortegotiate around curvatures of calcifications. If thecanal is longer than 21 mm, it is simple to change toa 25-mm instrument once 21 mm of penetration hasbeen achieved. Before the file is inserted into thecanal, a small curve is placed in its apical 1 mm. Thepoint on the rubber stop is tben aligned with thecurve. In negotiating the fine-curved canal, thecurved instrument must be directed along the path-way the canal is most likely to follow; consequently,it is vitally important to know what direction thecurve in the instrument is pointed. This is easilyaccomplished by observing the rubber stop on theinstrument shaft.

Heipful considerations

' Irrigate copiously at all times with 2,5% to 5.25%NaOCl, which enhances dissolution of organicdebris.'' lubricates tbe canal, and keeps dentinchips and pieces of calcified material in solution,

• Advance instruments slowly in calcified canals,• Clean the instrument on withdrawal and inspect it

before reinserting it into the canal.• Do not remove the instrument when it has reached

the approximate canal, rather, obtain a radiographto ascertain the position of the file,

• Do not use acids (hydrochloric acid) or alkalis(sodium hydroxide) to aid in canal penetration,

• Use chelating pastes or solutions to assist in canalpenetration.

• Use ultrasonic instruments in the pulp chamber toloosen debris in the canal orifices.

• Flare tbe canai orifice in a crown-down fashionand enlarge the negotiated canal space to improvetactile perception in continued canal penetration.

• Use of newer, nickel-titanium rotary orifice-pene-trating instruments should be considered whenpossible.

Prognosis

The prognosis of teeth with CM treated with nonsurgi-cal root canal treatment has been investigated by Cvek

et aV^ They examined 54 nonvital incisors with post-traumatically reduced pulpal lumina with a follow-upof 4 years. Healing was found in 80%. They filled thecanals with resin-chloroform and gutta-percha points.This couid be another factor involved in decreasingthe success rate, because considerable shrinkage ingutta percha oeeurs when chloroform evaporates,"There have been no studies that compare the relativesuccess rates of calcified canals treated using a surgi-cal approach,

Adherenec to the principles of radiographie inter-pretation, recognition of the presence of CM withpathologic sequelae, and use of the techniques des-eribed in managing tbese cases will in many casesresult in successful management of a case tbat mayhave been deemed untreatable (Figs 2 and 7 to 9),

SURGICAL ENDODONTIC CONSIDERATIONS

Often, symptomatic teeth that exhibit complete CMradiographiealiy or in which the canals cannot benegotiated must be treated with periradicularsurgery,'''^' Subsequent to trauma, a rapid, disorga-nized calcification tbat cbaracterizes CM can occur;pulpal remnants may become entrapped in tbis calcifi-cation. Ultimately, these pockets of tissue necrose butare contained within tbe dentin. Once a root-endresection is performed, many of the pockets ofnecrotic tissue may be opened to the periradicular fis-sues, resuiting in persistent chronic infiammafion withpossible sinus tract involvement subsequent tosurgery.'''^ Fven a second root-end resection does notsolve the problem, and ultimately extraction mayoccur If this situation truly exists, very little can bedone short of complete root-end fill of the entire rootface, as suggested many years ago by Castenfeldt, '̂ orpossibly using a surface layer of glass ionomer or alayer of composite.̂ '"^^ Presently advocated teebniquesof preparing a concave root face, followed by a dentinbonding agent and resin composite root-end fill,appear promising and may negate the problem of con-taminated tissue debris at the resected root end,'̂ '*"

SUMMARY

Approximately 3.8% to 24% of traumatized teethdevelop varying degrees of calcific metamorphosis.Although tbere are different opinions on the manage-ment of pulps exhibiting canal obliteration, studiesindicate that the incidence of puipai necrosis in theseteeth is between 1% and 16%, Histoiogic examinationof puipai tissue from teetb demonstrating closure oftbe pulpal lumina revealed no significant inflammation

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Fig 7 Per,radicular radiograph showswoikihg-length determination and success-ful negotiation of Ihe canal space. (Casecourtesy of Dr Anthony McNaught.)

Fig 8 Postoperaiive raoiograph of caseshown in Fig 7 with successful cleaning,shaping, and obiuration of the canal space.(Case courlesy of Dr Anthony McNaught.)

Fig 9 Six-month iollow-up radiographshows decrease in size of Ihe periradicularlesions and reformation of the lamina duracompared to the preoperative radicgraph(see Figs 2 and 7). (Case courfesy ot DrAnthony McNaughf.)

that would warrant root canal treatment. Most of theliterature does not support endodontic interventionunless periradicular pathosis is detected or theinvolved tooth becomes symptomatic. Because theoverall failure rate of nonsurgical root canal treatmetitis between 10% and 19%, it may be advisable to man-age cases demonstrating calcific metamorphosisthrough ohservation and periodic examination. If thepulp tissue becomes necrotic and a periradicular radi-oiucency develops, nonsurgical root canal treatmenthas been shown to be successful 80% of the time.

REFERENCES

1, American Association of Endodontisls, Glossary; Contem-porary Terminology for Endodontics, ed 6. Chicago: AAE,1998,

2, Andreasen J, Andrcasen F. Textbook and Color Atlas ofTraumatic Injuries to Teeth, ed 3, Copenhagen: Munks-gaard, 1994.

3, Oikarinen K, Gundlach K, Pfeifer G, Late complication ofluxation injuries, Endod Dent Traumatol 1987;5:2f)6-303,

4, Robertson A, Andreasen F, Bergenholtz G, Andreasen J,Noren J Incidence of pulp necrosis subsequent to pulpcanal obliteration from trauma of permanent incisors.J Endod 1996:22:557-560,

5. Stâlhane 1, Hedegard B, Traumatized permanent teeth inchildren aged 7-15 years. Part II, Swed Dent J 1975;68:157-169.

6. Holan G. Tube-hke mineralization in the dental pulp ottraumatized primary incisors, Endod Dent Traumatol 1998;14:279-284.

7. Andreasen J, Luxation of permanent teeth due to trauma.Scand J Dent Res 1970;78:273-286,

8. TOI neck C. The clinical significance and management of cal-cific pulp obliteration. Alpha Omegan 1990;83:50-54,

9. Rock W, Grundy M. The effect of luxation and subluxafionupon the prognosis of traumatized incisor teeth. J Dent1981;3:224-230,

10, Robertson A, A retrospective evaluation of patients withuncomplicated erown fractures and luxation injuries, EndodDent Traumatol 1998; 14:245-256,

11, Yaacob HB, Hamid JA. Pulpal calcifications in primaryteeth: A light microscope study, J Pedodont 1986;10:254-264,

12, Andreasen K Pulpal Healing After Tooth Luxation and RootFractures in the Permanent Dentition [thesis]. Copenhagen:University of Copenhagen, 1995,

13, Patterson S, Mitchell D, Calcific metamorphosis of the den-tal pulp. Oral Surg Oral Med Oral Pathol 1965:20:94-101,

14, Holcomb J, Gregory W, Calcific metamorphosis of the pulp:Its incidence and treatment. Oral Surg Oral Med OralPathol 1967:24:825-830,

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15. Schindler WG, Gullickson DC. Rationale for the manage-ment of calcific metamorphosis secondary to traumaticinjuries. J Endod 1988:14:408-412.

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