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he Effect of Pulp Obliteration on Pulpal Vitality ofrthodontically Intruded Traumatized Teeth

skar Bauss, PhD,* Johannes Röhling, DMD,† Alexander Rahman, DMD,‡

nd Stavros Kiliaridis, PhD§

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bstractimited information exists on the impact of pulp oblit-ration on pulpal vitality of orthodontically treatedraumatized teeth. Pulpal condition was examined in69 traumatized maxillary incisors after orthodontic

ntrusion (OT group) and in 193 traumatized maxillaryncisors without subsequent orthodontic treatmentC group). According to the degree of initial pulp oblit-ration, the teeth were divided into three categories:eeth without, teeth with partial, and teeth with totalulp obliteration. Teeth in the OT group revealed aignificantly higher rate of pulp necrosis than teeth inhe C group (p � 0.001). In addition, teeth in the OTroup with total pulp obliteration showed a signifi-antly higher rate of pulp necrosis than teeth withoutp � 0.001) or only partial pulp obliteration (p � 0.025).he results indicate that traumatized teeth with totalulp obliteration have a higher susceptibility to pulpalomplications during orthodontic intrusion than trau-atized teeth without or only partial pulp obliteration.

J Endod 2008;34:417– 420)

ey Wordsental trauma, orthodontic treatment, pulp necrosis,ulp obliteration

From *Private Practice, Hannover, Germany; †Private Prac-ice, Bielefeld, Germany; ‡Department of Conservative Den-istry and Periodontology, Medical School Hannover, Han-over, Germany; and §Department of Orthodontics, Universityental School of Geneva, Geneva, Switzerland.

Address requests for reprints to Dr Oskar Bauss, Luisen-trasse 10/11, 30159 Hannover, Germany. E-mail address:.bauss@praxisbauss.de.099-2399/$0 - see front matter

Copyright © 2008 by the American Association ofndodontists.oi:10.1016/j.joen.2008.01.006

c

OE — Volume 34, Number 4, April 2008

ard tissue apposition along the root canal walls is a physiological aging process. Itoccurs throughout the life of a tooth, and as a normal defense response to tooth

ear, it may also occur in the pulp at a slow pace (1, 2). However, hard-tissue appo-ition has been found to be accelerated considerably in the case of dental trauma (3, 4),utotransplantation (5, 6), or orthodontic tooth movement (7–10), leading to partialr total pulp obliteration.

Because a high prevalence of traumatized permanent incisors is found in candi-ates for orthodontic treatment (11), orthodontic movement of previously traumatized

eeth showing pulp obliteration is of particular importance in routine orthodonticherapy. However, only sparse attention has been paid so far to this issue. Two previousnvestigations reported no higher frequency of pulp necrosis after orthodontic treat-

ent of teeth with obliterated pulps although without further specification of the kindnd duration of orthodontic tooth movement performed (12, 13). In contrast, a signif-cant increase in pulp necrosis was observed after orthodontic derotation of autotrans-lanted immature third molars, and the authors suspected a correlation to progressiveulp obliteration of the transplants (14).

Of the possible force factors that can be applied to teeth during orthodonticreatment, intrusion is thought to have the greatest impact on the apical region.everal investigations reported an obvious reduction in pulpal blood flow afterpplication of intrusive forces (15–18). According to Andreasen and Andreasen 19), progressive obliteration implies reduction of the pulpal blood supply. There-ore, it might be assumed that previously traumatized teeth showing pulp obliter-tion have a higher susceptibility to pulpal complications during orthodontic in-rusion than orthodontically treated traumatized teeth without pulp obliteration orreviously traumatized teeth with pulp obliteration but without subsequent orth-dontic treatment. The aim of this study was to determine the influence of pulpbliteration on pulpal vitality of orthodontically intruded traumatized permanentpper incisors and to compare the pulpal condition with traumatized upper inci-ors without subsequent orthodontic treatment.

Materials and MethodsPatients with orthodontically treated traumatized maxillary incisors (OT group)

ere compared with a control group with patients with previous dental trauma to theaxillary incisors and no subsequent orthodontic treatment (C group).

he Orthodontically Treated Traumatized Teeth (OT) GroupThe original sample consisted of all patients of a private orthodontic practice who

ad presented between 1990 and 2004 with a class 2 division I malocclusion withncreased overjet and deep bite and had been treated orthodontically by intrusion of the

axillary incisors. From the original sample, all patients who had sustained dentalrauma to the maxillary incisors before the onset of orthodontic treatment were selectedor further examination. The presence of previous dental trauma was determined fromhe dental records made at baseline, which included a standardized questionnaire (11),nd the results of the pretreatment clinical and radiologic examination. During thelinical examination, the permanent incisors of all patients had been carefully examinedor the evidence of traumatic injury (rating of crown color or evidence of previousard-tissue injuries). In teeth with previous dental trauma, a sensitivity test with a

ryogenic spray (Provotest; Hoechst, Frankfurt, Germany) had been performed before

Pulp Obliteration and Vitality of Traumatized Teeth 417

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he onset of orthodontic treatment. In addition, pretreatment standard-zed periapical radiographs had been obtained for all traumatized teeth.hese records were considered as the initial records of the presentnvestigation (initial examination). At the end of the retention period,ostretention standardized periapical radiographs and sensitivity test-ng with a cryogenic spray were performed in all traumatized teeth.hese records were considered as the final records (final examination).nly traumatized teeth with positive sensitivity testing before the onset ofrthodontic treatment and without a history of multiple dental traumasere included in this investigation.

A total of 186 patients (130 males and 56 females) with 269raumatized permanent upper incisors were found to meet the inclusionriteria. Uncomplicated crown fractures were observed in 151 teeth anderiodontal injuries in the remaining 118 teeth (subluxation � 31,ateral luxation � 30, extrusive luxation � 28, and intrusive luxation �9). In cases of more than one type of injury to the same tooth, only theost serious one was used to categorize the tooth. The average age of

he patients at the time of trauma was 9.5 years (range, 6.5–15.1 years),nd the average age at the end of active orthodontic treatment was 15.0ears (range, 13.7–17.1 years).

Orthodontic treatment of the previously traumatized teeth hadeen started at the earliest 3 months after hard-tissue injuries and 12onths after periodontal tissue injuries (20). Orthodontic treatmentas performed with a preadjusted appliance with 0.018-inch slotrackets. Orthodontic intrusion of the maxillary incisors was performedy means of a 0.016 � 0.016-inch Elgiloy blue intrusion arch (Rockyountain Orthodontics, Denver, CO) from the maxillary tube of theaxillary right first molar to the maxillary left first molar. Interference

f premolars and canines was avoided by means of second-order bendshat bypassed these teeth. First molars were usually consolidated withhe premolars and canines with passive segmented arches. Intrusionorces were adjusted to approximately 15 g per tooth and checkedsually at each visit by using a light-force gauge (Haag-Streit, Bern,witzerland). After correction of the vertical malocclusion with intrusiveechanics, treatment was continued with continuous arch wire me-

hanics and class II elastics for further reduction of overjet. The intru-ion period averaged 5.7 months (range, 4.6 –7.2 months), and theotal treatment time with fixed appliances averaged 22.4 months (range,0.9 –30.4 months). After termination of active orthodontic treatment,etention was performed with removable appliances. The mean reten-ion period was 3.2 years (range, 2.8 –3.6 years).

raumatized Teeth without Subsequent Orthodonticreatment (C Group)

The C group included 173 patients (112 males and 61 females)ith a total of 193 traumatized permanent upper incisors. Standardizederiapical radiographs had been obtained directly after the trauma (ini-ial examination) and during the final follow-up (final examination).nclusion criteria for the control group were the absence of pulp oblit-ration on the initial radiographs, positive sensitivity testing during theirst 6 months after dental trauma, a minimum follow-up period of 3ears after dental trauma, no subsequent orthodontic treatment afterrauma, and no additional grinding or filling therapy of the traumatizedeeth. Uncomplicated crown fractures had occurred in 68 teeth, sub-uxation in 31, lateral luxation in 33, extrusive luxation in 30, andntrusive luxation in 31 teeth. The mean age of the patients at the time ofrauma was 9.3 years (range, 6.6 –16.4 years). The mean age at the timef re-examination was 14.7 years (range, 12.5–27.3 years).

lassification of Pulp ObliterationThe evaluation of pulp obliteration was performed on the pretreat-

ent and postretention periapical radiographs in the OT group and on i

18 Bauss et al.

he initial and final periapical radiographs in the C group. The degree ofulp obliteration was rated according to Jacobsen and Kerekes (3) as

otal obliteration (pulp chamber and root canal hardly or not discern-ble) or partial obliteration (pulp chamber not discernible and rootanal markedly narrowed but clearly visible). According to the pres-nce and degree of pulp obliteration, the teeth were divided into threeifferent categories: traumatized teeth without pulp obliteration, trau-atized teeth with partial, and traumatized teeth with total pulp oblit-

ration (Table 1).

valuation of Pulpal VitalityPulpal condition was examined clinically and radiologically. The

linical examination included rating of the crown color (normal orrayish) and sensitivity testing with a cryogenic spray. The radiologicxamination consisted of standardized periapical radiographs and con-ributed to the assessment of periapical radiolucencies. The followinglinical and radiologic criteria were used to define pulp necrosis: grayolor changes in the crown, loss of pulpal sensitivity, and periapicaladiolucency. All three diagnoses or loss of pulpal sensitivity in combi-ation with gray color changes in the crown or periapical radiolucencyere considered necessary before the diagnosis was made (19). In theT group, the evaluation of pulpal vitality was performed during the

nitial and final examination and during orthodontic treatment in case ofn indication of pulp necrosis (ie, gray color changes in the crown,ain, or swelling). In the C group, pulpal vitality was tested at the initialxamination, monthly during the first 6 months after injury, and at theime of the final examination.

tatistical AnalysisThe chi-square test or Fisher exact test were used to detect signif-

cant intergroup differences concerning the frequency of pulp necrosis.he significance level was set at � � .05. Statistical analysis was per-

ormed with SPSS 11.0 (SPSS Inc, Chicago, IL).

rror of the MethodWith respect to the radiographic assessment of pulp obliteration

nd periapical radiolucencies, 100 randomly selected periapical radio-raphs were re-evaluated within a 4-week interval by two examiners.fterwards, interexaminer agreement was calculated by using weightedappa statistics. A very good interexaminer agreement was determined

or the assessment of pulp obliteration (� � 0.83) and periapicaladiolucencies (� � 0.90).

ResultsDuring the final examination, signs of pulp necrosis were detected

n 10.4% of the teeth in the OT group (n � 28) and in 1.6% of the teethn the C group (n � 3), the difference being statistically significant (p �.001).

In the OT group, pulp necrosis was found in 4.9% (n � 10) of theeeth without initial pulp obliteration, in 14.7% (n � 5) of the teeth with

ABLE 1. Distribution of Teeth in Both Groups According to the Presence andegree of Pulp Obliteration

Examination GroupPulp Obliteration

Without Partial Total

OT-group (n � 269) 204 (75.9%) 34 (12.6%) 31 (11.5%)C-group (n � 193) 147 (76.1%) 21 (10.9%) 25 (13.0%)Total (n � 462) 351 (76.0%) 55 (11.9%) 56 (12.1%)

T group, initial examination; C group, final examination.

nitial partial, and in 41.9% (n � 13) of the teeth with initial total pulp

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bliteration. Teeth with total pulp obliteration revealed a significantlyigher rate of pulp necrosis than teeth without (p � 0.001) or onlyartial pulp obliteration (p � 0.025) (Fig. 1).

In the teeth without initial pulp obliteration, five of the cases with pulpecrosis were detected during orthodontic intrusion, and the remaining fiveases were diagnosed during orthodontic treatment after the intrusion pe-iod. In the teeth with partial pulp obliteration, three of the cases with pulpecrosis were determined during orthodontic intrusion, and two cases were

ound at the end of the retention period. In the teeth with total pulp obliter-tion, pulp necrosis was detected in 10 teeth during orthodontic intrusion.n the remaining three teeth, the diagnosis was made during active orth-dontic treatment after intrusion. In the orthodontically treated teeth withotal pulp obliteration, the incidence of pulp necrosis was significantlyigher during the intrusion period as compared with later treatmenttages (p � 0.017).

In the OT group, four teeth without signs of pulp obliteration on theretreatment radiographs revealed partial pulp obliteration at the finalxamination at the end of the retention period. In addition, two furthereeth with total pulp obliteration on the pretreatment radiographshowed a loss of pulpal sensitivity with normal crown color and anbsence of periapical radiolucencies during the final examination.

DiscussionThe present investigation indicates that previously traumatized

eeth have a higher susceptibility to pulpal complications during orth-dontic intrusion. In addition, previously traumatized teeth with totalulp obliteration have a higher risk for pulp necrosis during orthodon-ic intrusion than traumatized teeth without or only partial obliteration.

Numerous investigations have shown that orthodontic tooth move-ent can affect the blood supply to the dental pulp (10, 21–23). Mc-onald and Pitt Ford (24) showed that blood flow changes within theulp during application of a tipping force have dynamic changes andhat an initial decrease in blood flow is followed by a reactive hyperemiao compensate for the lack of perfusion. However, orthodontic intrusions considered to have the greatest impact on the apical region and thusn pulpal blood supply. Previous studies have already shown an obviouseduction of pulpal blood flow and marked histologic changes in theulp as a result of intrusive forces (15–18, 25). In contrast to tippingorces (24) or brief intrusive forces (26), the reduction of pulpal blood

igure 1. The frequency of pulp necrosis in dependence on the degree of initialulp obliteration in the orthodontically treated traumatized teeth (OT group).**p � 0.001; *p � 0.05.

low without reactive hyperemia was observed during application of a o

OE — Volume 34, Number 4, April 2008

ontinuous intrusive force of 50 g for 6 days (17). Because an intrusiveorce of 50 g has been shown to cause an apical tooth displacement ofbout 40 �m (27), which is considered to be large enough to constrictlood vessels 30 to 150 �m in diameter (28), Sano et al (18) con-luded that a significant compression of the apical vessels occurs be-ause of the apical displacement of the tooth. Our results indicate thathe pulpal circulatory system of traumatized teeth without or with onlyartial pulp obliteration seems to be capable of compensating for theeduction of pulpal blood flow during orthodontic intrusion. In con-rast, the vascular supply of teeth with total pulp obliteration seems to bensufficient to maintain an adequate blood supply to the pulp duringpplication of intrusive forces. Possible explanations for these findingsight be a reduced number of pulpal blood vessels and the constriction

r rupture of the neurovascular bundle.Pulp obliteration is caused by progressive hard-tissue apposition

long the pulp chamber that gradually diminishes the pulpal lumen29). Thus, it is very likely that this hard-tissue formation also leads torogressive compression and finally to constriction of the existing pul-al vessels, resulting in an impaired blood supply to traumatized teethith total pulp obliteration. In addition, progressive hard-tissue appo-

ition might also lead to constriction of the apical foramen and thus toompression of the neurovascular bundle. This might cause strangula-ion or even rupture of the apical vessels during orthodontic tooth

ovement and especially during orthodontic intrusion.Partial pulp obliteration revealed no detrimental effect on the pul-

al vitality of orthodontically intruded teeth. In contrast to total pulpbliteration, partial obliteration involves primarily the pulp chamber,hereas the root canal and probably also the apical foramen show onlycertain narrowing. Therefore, only limited constriction of the apical

essels might be concluded in teeth with partial obliteration as com-ared with teeth with total obliteration. This might allow the pulpalirculatory system of these teeth to react adequately and to maintain aufficient pulpal perfusion during orthodontic intrusion.

Four new cases of partial pulp obliteration were detected in therthodontically treated traumatized teeth at the end of the retentioneriod. Because pulp canal obliteration represents the response of aital pulp to a severe injury to its neurovascular supply (20), a possiblexplanation might be a temporarily diminished pulpal blood flow dur-ng orthodontic therapy of these teeth. Previous investigations have al-eady determined pulp obliteration as a potential side effect of orth-dontic treatment and a connection to impaired pulpal blood flowuring tooth movement was suspected (7–10). In addition, Andreasent al (2) reported an increased incidence of pulp obliteration afterrthodontic band fixation of traumatized teeth, and they assumed thatand application might have caused displacement of the root with com-ression of the apical vessels.

The loss of pulpal sensitivity was observed in two orthodonticallyreated teeth with total pulp obliteration during the final examination.isturbances in sensitivity reaction have been previously reported in

eeth with total pulp obliteration and long observation periods, and aorrelation to the narrowing of the pulp cavity has been suspected (3).ecause both teeth in the present investigation showed observationeriods of more than 5 years, progressive hard-tissue apposition during

he observation period probably could explain the loss of pulpal sensi-ivity in these teeth. An additional cause might be an altered response toulp-test stimuli because of orthodontic tooth movement. It has beenhown that orthodontic forces have some effect on the pulpal nerves andhat higher response thresholds to sensitivity testing are to be expectedn orthodontically treated teeth (30, 31).

In conclusion, orthodontic intrusion of previously traumatizedeeth displaying total pulp obliteration seems to be very hazardous. The

rthodontist should be aware of this risk, and the treatment plan should

Pulp Obliteration and Vitality of Traumatized Teeth 419

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e adapted accordingly. However, even if orthodontic intrusion isvoided, late pulp necrosis can not be ruled out during the progress ofrthodontic treatment. Finally, because the amount of pulp obliterationight not be representative of the degree of trauma, it is not possible to

raw any conclusions concerning the influence of the type of trauma. Inddition, because all data came from only one orthodontic practice,urther investigations are necessary to confirm the results obtained inhe present study.

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the human tooth. Oral Surg Oral Med Oral Pathol 1966;21:180 –9.2. Andreasen FM, Yu Z, Thomsen BL, Andersen PK. Occurrence of pulp canal obliter-

ation after luxation injuries in the permanent dentition. Endod Dent Traumatol1987;3:103–5.

3. Jacobsen I, Kerekes K. Long-term prognosis of traumatized permanent anterior teethshowing calcifying processes in the pulp cavity. Scand J Dent Res 1977;85:588 –98.

4. Andreasen JO. Luxation of permanent teeth due to trauma. A clinical and radio-graphic follow-up study of 189 injured teeth. Scand J Dent Res 1970;78:273– 86.

5. Bauss O, Engelke W, Fenske C, Schilke R, Schwestka-Polly R. Autotransplantation ofimmature third molars into edentulous and atrophied jaw sections. Int J Oral Max-illofac Surg 2004;33:558 – 63.

6. Andreasen JO, Paulsen HU, Yu Z, Bayer T, Schwartz O. A long-term study of 370autotransplanted premolars. Part II. Tooth survival and pulp healing subsequent totransplantation. Eur J Orthod 1990;12:14 –24.

7. Delivanis HP, Sauer GJR. Incidence of canal calcification in the orthodontic patient.Am J Orthod 1982;82:58 – 61.

8. Popp TW, Årtun J, Linge L. Pulpal response to orthodontic tooth movement in ado-lescents: a radiographic study. Am J Orthod Dentofacial Orthop 1992;101:228 –33.

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0. Malmgren O, Malmgren B, Goldson L. Orthodontic management of the traumatizeddentition. In: Andreasen JO, Andreasen FM, eds. Textbook and Color Atlas of Trau-matic Injuries to the Teeth. 3rd ed. Copenhagen: Mosby; 1992:587– 631.

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2. Vandevska-Radunovic V, Kristiansen AB, Heyeraas KJ, Kvinnsland S. Changes in bloodcirculation in teeth and supporting tissues incident to experimental tooth movement.Eur J Orthod 1994;16:361–9.

3. Derringer KA, Jaggers DC, Linden RWA. Angiogenesis in human dental pulp followingorthodontic tooth movement. J Dent Res 1996;75:1761– 6.

4. McDonald F, Pitt Ford TR. Blood flow changes in permanent maxillary canines duringretraction. Eur J Orthod 1994;16:1–9.

5. Raiden G, Missana L, Santamaria de Torres E, Kozuszko S, Pedroso R. Pulpal re-sponse to intrusive orthodontic forces. Acta Odontol Latinoam 1998;11:49 –54.

6. Barwick PJ, Ramsay DS. Effect of brief intrusive force on human pulpal blood flow.Am J Orthod Dentofacial Orthop 1996;110:273–9.

7. Picton DCA. The effect of normal vertical tooth mobility of the rate of thrust and thetime interval between thrusts. Arch Oral Biol 1963;8:291–9.

8. Takahashi K, Kishi Y, Kim S. A scanning electron microscope study of the bloodvessels of dog pulp using corrosion resin casts. J Endod 1982;8:131–5.

9. Cvek M. Endodontic management and the use of calcium hydroxide in traumatizedpermanent teeth. In: Andreasen JO, Andreasen FM, Andersson L, eds. Textbook andColor Atlas of Traumatic Injuries to the Teeth. 4th ed. Oxford: Blackwell Publishing;2007:598 – 657.

0. Burnside RR, Sorenson FM, Buck DL. Electric vitality testing in orthodontic patients.Angle Orthod 1974;44:213–7.

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