70601472

doi:10.1111/j.1365-2591.2011.01978.x

CLINICAL ARTICLE

Responses of immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/abscess to revascularization procedures M. Y.-H. Chen1, K.-L. Chen1, C.-A. Chen1, F. Tayebaty2, P. A. Rosenberg2 & L. M. Lin2 1

Department of Endodontics, Chi Mei Medical Center, Yong Kang and Liouying, Tainan, Taiwan; and 2Department of Endodontics, New York University College of Dentistry, New York, NY, USA

Abstract Chen MY-H, Chen K-L, Chen C-A, Tayebaty F, Rosenberg PA, Lin LM. Responses of immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/abscess to revascularization procedures. International Endodontic Journal, 45, 294–305, 2012.

Aim To report several types of response of immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscess to revascularization procedures.

Methodology Twenty immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscesses from 20 patients were included. The teeth were isolated with rubber dam, and pulp chambers was accessed through the crowns.

The canals were gently irrigated with 5.25% sodium hypochlorite with minimal mechanical debridement. Calcium hydroxide was used as an inter-appointment intracanal medicament and placed into the coronal half of the canal space. After resolution of clinical signs and symptoms, bleeding was induced into the canal space from the periapical tissues using K-files. The coronal canal space was sealed with a mixture of mineral trioxide aggregate (MTA) and saline solution. The access cavity was filled with composite resin. These immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/abscesses were followed up from 6 to 26 months.

Results Five types of responses of these immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/abscess to revascularization procedures were observed: type 1, increased thickening of the canal walls and continued root maturation; type 2, no significant continuation of root development with the root apex becoming blunt and closed; type 3, continued root development with the apical foramen remaining open; type 4, severe calcification (obliteration) of the canal space; type 5, a hard tissue barrier formed in the canal between the coronal MTA plug and the root apex.

Correspondence: Dr. Louis M. Lin, Department of Endodontics, New York University, College of Dentistry, 345 East 24th Street, New York, NY 10010, USA (e-mail: Lml7@nyu.edu).

294

International Endodontic Journal, 45, 294–305, 2011

ª 2011 International Endodontic Journal

Keywords: Hertwig’s epithelial root sheath, immature permanent teeth, pulp canal calcification, revascularization.

CLINICAL ARTICLE

Conclusions Based on this case series, the outcome of continued root development was not as predictable as increased thickening of the canal walls in human immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/abscess after revascularization procedures. Continued root development of revascularized immature permanent necrotic teeth depends on whether the Hertwig’s epithelial root sheath survives in case of apical periodontitis/abscess. Severe pulp canal calcification (obliteration) by hard tissue formation might be a complication of internal replacement resorption or union between the intracanal hard tissue and the apical bone (ankylosis) in revascularized immature permanent necrotic teeth.

Received 25 April 2011; accepted 3 October 2011

Introduction Traditionally, immature permanent teeth with apical periodontitis/abscess are treated by apexification (Rafter 2005). Apexification is a method to induce a calcified barrier in a root with an open apex or the continued apical development of an incompletely formed root in teeth with necrotic pulps (American Association of Endodontists 2003). After apexification procedures, the immature permanent teeth are usually filled with root canal sealer and gutta-percha. The disadvantages of apexification procedures are that the canal walls remain thin and continued root development might not occur (Iwaya et al. 2001, Banchs & Trope 2004), and such teeth are prone to fracture after root canal treatment. Recently, revascularization procedures have been recommended to treat immature permanent teeth with necrotic pulp tissue and/or apical periodontitis/abscess. The treatment procedures have been shown to result in increased thickening of the canal walls by deposition of hard tissue and encourage continued root development in immature permanent teeth with necrotic pulp tissue and/or apical periodontitis/abscess (Iwaya et al. 2001, Banchs & Trope 2004, Chueh & Huang 2006, Cotti et al. 2008, Jung et al. 2008, Shah et al. 2008, Chueh et al. 2009, Ding et al. 2009, Petrino et al. 2010). In several case reports and case series studies, a triple antibiotic mixture of ciprofloxacin, metronidazole and minocycline has been used to disinfect the canals in revascularization procedures (Iwaya et al. 2001, Banchs & Trope 2004, Jung et al. 2008, Ding et al. 2009, Petrino et al. 2010). In contrast, calcium hydroxide (Chueh & Huang 2006, Cotti et al. 2008) and formocresol (Shah et al.

2008) have also been used effectively as intracanal medicaments to disinfect the canals of immature permanent teeth with necrotic pulp tissue and apical periodontitis/abscess in revascularization procedures.

The nature of hard tissue formed in the canal space in conjunction with continued root development of human immature permanent teeth with necrotic pulp tissue and/or apical periodontitis/abscess following revascularization procedures is not known, because no histological studies are available. Histologically, in animal studies, the hard tissue formed in the canal spaces was described as bone-like or cementum-like tissues, and continued root development was attributed to apical cementum deposition after revascularization procedures of immature necrotic teeth with apical periodontitis (Thibodeau et al. 2007, Bezerra da Silva et al. 2010, Wang et al. 2010, Yamauchi et al. 2011).

The purpose of this case series is to present several types of response of human immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/ abscess to revascularization procedures.

ª 2011 International Endodontic Journal

International Endodontic Journal, 45, 294–305, 2011

295

CLINICAL ARTICLE

Materials and methods Twenty immature permanent teeth with infected necrotic pulps and apical periodontitis/ abscess from 20 patients were included in this case series study. The demography of the patients, signs and/or symptoms, and pulpal and periapical status of involved teeth were recorded (Table 1). Ten of the 20 teeth were premolars; three maxillary premolars had a carious pulp involvement and seven mandibular premolars had a Dens Evaginatus with subsequent pulp infection. The remaining 10 teeth were maxillary incisors, all of which had a history of traumatic injury followed by pulp infection. The ages of patients ranged from 8 to 13 years. The teeth did not respond to pulp sensibility tests with ice, heated gutta-percha and electric current from a Vitality Scanner (SybronEndo, Glemdora, CA, USA). Twelve teeth had a draining sinus tract. Radiographically, all teeth demonstrated evidence of periapical osteolytic lesions caused by root canal infection. This case series study was approved by the Institutional Review Board of Chi Mei Medical Center, Tainan, Taiwan, and New York University School of Medicine, New York, NY, USA. To make sure that no vital tissue was present in the canals, local anaesthesia was not administered initially. The tooth was isolated with a clamp and rubber dam. The operating field including tooth, clamp and surrounding rubber dam was disinfected with a swab with 5% Tincture of iodine (Rougier, Ontario, Canada) using Q tips. Access to the pulp chamber was made through the crown with a sterile carbide no. 4 round bur and the canal was identified. The pulp chamber was irrigated with 5.25% sodium hypochlorite solution (Sultan Healthcare, Hackensack, NJ, USA) in a 3 mL Luer Lock syringe with a 27-G irrigating needle tip (Henry Schein, Melville, NY, USA). An initial K-file or a gutta-percha cone (Henry Schein) was introduced into the canal to determine working length. If the patients felt pain when files were introduced into the canals, a local anaesthetic, lidocaine HCl 2% and epinephrine 1:100 000 (Novocol Pharmaceutical, Cambridge, ON, Canada), was immediately given by local infiltration. In eight of 20 teeth, the patients reported pain when files were introduced into the canals close to the apical third of the root canal. All

Table 1 Demography of the patients, signs and/or symptoms, and pulpal and periapical status of the involved teeth Case #

Age

Sex

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

10 9 8 10 13 10 10 11 10 8 11 11 10 12 10 10 7 10 10 13

M F M F F M F M F F F M M F F M F M F M

Tooth #

Signs/symptoms

Pulpal status

PA lesion

Sensitivity*

35 24 45 15 45 35 35 45 21 11 35 22 12 11 21 22 11 21 21 14

S ST ST ) ) S S S ST ST ST ) ST ) ST S ST ST ST ST

N N N N N N N N N N N N N N N N N N N N

+ + + + + + + + + + + + + + + + + + + +

12 mm 13 mm 8 mm ) ) ) ) 10 mm 12 mm ) ) 11 mm ) 14 mm 12 mm ) ) ) ) )

S, swelling; ST, sinus tract; N, necrosis; PA, periapical; *, depth of file in the canal that patient felt pain.

296

International Endodontic Journal, 45, 294–305, 2011

ÂŞ 2011 International Endodontic Journal

CLINICAL ARTICLE

canals were gently irrigated, with copious amounts of 5.25% sodium hypochlorite solution, to prevent extrusion through the open apex into the periapical tissues.

Mechanical instrumentation was minimal. Calcium hydroxide (Henry Schein) mixed with sterile saline solution was used as intracanal medication and placed into the coronal half of all canals. The maximum interval of calcium hydroxide treatment was 4 weeks as suggested by Bystro¨m et al. (1985) and Sjogren et al. (1991). The access cavity was closed with a sterile cotton pellet and an intermediate restorative material (IRM) (Dentsply International, Milford, DE, USA). If clinical signs and/or symptoms continued to persist, the same treatment protocol was repeated. After resolution of clinical signs and/or symptoms, under local anaesthesia the tooth was isolated and access cavity was re-entered. The cotton pellet was removed and calcium hydroxide was gently flushed out of the canal with 5.25% sodium hypochlorite solution. The canal was dried with sterile coarse paper points (Henry Schein). Under a Zeiss surgical microscope (Carl Zeiss Meditac Inc., Dublin, CA, USA), bleeding was induced into the canal space by irritating the periapical tissues using sterile stainless steel endodontic hand K-files (Dentsply Maillefer, Ballaigues, Switzerland).

In six cases, bleeding could not be satisfactorily induced into the coronal portion of the canal space. The coronal canal space of all teeth was carefully sealed with a thick mixture of ProRoot mineral trioxide aggregate (MTA) (Dentsply Tulsa Dental, Tulsa, OK, USA) and sterile saline solution to approximately 3–4 mm below the surface of the access opening, which was delivered with an amalgam carrier. A moist cotton pellet was then placed coronally against the unset MTA. The access cavity was restored with an IRM. Two to 3 days later under a surgical microscope, the cotton pellet and IRM in the pulp chamber was removed and the MTA was tested with an endodontic explorer to ensure that the material had set. The access cavity was sealed with a light-cured composite resin, Amelogen Plus (Ultradent, South Jordan, UT, USA). The revascularized immature permanent teeth were clinically and radiographically followed up from 6 to 26 months.

Results The results of revascularization procedures in 20 immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscess were summarized in Table 2.

All 20 revascularized immature permanent necrotic teeth with either apical periodontitis or abscess showed radiographic evidence of periapical wound healing and clinical evidence of resolution of signs and symptoms.

Five types of responses of immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscess to revascularization procedures were observed in the present case series: type 1, there was increased thickening of the canal walls and continued root maturation (Fig. 1); type 2, there was no significant continuation of root development and the root apex became blunt and closed (Fig. 2); type 3, there was continued root development and the apical foramen remained open (Fig. 3); type 4, there was severe calcification (obliteration) of the canal space (Fig. 4); type 5, there was a hard tissue barrier formed in the canal space between the coronal MTA plug and the root apex (Fig. 5).

All 20 revascularized immature permanent necrotic teeth with apical periodontitis/ abscess demonstrated radiographic evidence of increased thickening of the canal walls.

Fifteen revascularized immature permanent necrotic teeth with apical periodontitis/ abscess showed radiographic evidence of continued root development with an average follow-up time of 19.6 months. Five revascularized immature permanent necrotic teeth with apical periodontitis/abscess did not demonstrate significantly continued root development and formed a blunt, a closed apex or an open apex with an average follow-up time of 16.4 months. Four revascularized immature permanent necrotic teeth

ª 2011 International Endodontic Journal

International Endodontic Journal, 45, 294–305, 2011

297

CLINICAL ARTICLE

Table 2 Revascularization and radiographic assessment of outcomes Case # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

Calcium hydroxide + + + + + + + + + + + + + + + + + + + +

Follow-up time, months 7 9 6 26 25 7 9 12 8 7 25 6 7 11 9 9 12 12 10 12

Healing of PA lesion

Thickening of canal walls

Significantly continued root development

Crown discolouration

+ + + + + + + + + + + + + + + + + + + +

++ + + + ++ ++ + + + + ++ + + + + + + + + +

) + + ) ) + + ) + + + + + + + + + + + )

) ) + ) ) ) ) ) ) ) ) ) ) ) ) ) + ) ) )

++, markedly increased thickening of the canal walls.

[Correction added after online publication, 29 November 2011: Column six heading amended.]

with apical periodontitis/abscess exhibited radiographic evidence of severe pulp canal calcification (obliteration) by hard tissue formation with an average follow-up time of 16 months. In two cases of revascularized immature permanent necrotic teeth with apical periodontitis/abscess (cases 16 and 17), a hard tissue barrier was formed in the canal space between the coronal MTA plug and the root apex.

It should be pointed out that all average follow-up times mentioned above are only applicable to the present study, because the follow-up time schedule, such as 3, 6, 9 and 12 months, could not be controlled owing to unreliability of the patients. Therefore, increased thickening of the canal walls and/or continued root development in some cases might occur before or might occur after the follow-up times listed in Table 2.

Eight of 20 immature permanent necrotic teeth with apical periodontitis/abscess were painful when files were introduced into the apical third of the canal. Of these eight teeth, six teeth showed continued root development after revascularization procedures. The remaining 12 revascularized immature permanent necrotic teeth with apical periodontitis/ abscess were not painful when files were introduced into the apical third of the canal. Of these 12 teeth, nine teeth demonstrated continued root development after revascularization procedures. Those immature permanent necrotic teeth with apical periodontitis/ abscess painful to files introduced into the canals did not appear to show better outcome in terms of increased thickening of the canal walls nor any continued root development as compared to those immature permanent necrotic teeth with apical periodontitis/abscess not painful to files after revascularization procedures. However, the sample size was too small to draw any statistical conclusion.

Discussion As suggested by Bystro¨m et al. (1985) and Sjogren et al. (1991), calcium hydroxide is effective in killing microorganisms in the teeth with infected root canals. Therefore, it was

298

International Endodontic Journal, 45, 294–305, 2011

ª 2011 International Endodontic Journal

(c)

(b)

CLINICAL ARTICLE

(a)

(d)

Figure 1 Case 8. Tooth 45. Increased thickening of the canal walls and continued root maturation after revascularization. (a) Preoperative radiograph. (b) Postoperative radiograph right after revascularization. (c) Six-month follow-up radiograph. (d) One-year follow-up radiograph.

used as intracanal medication between inter-appointment visits for immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscess during revascularization procedures in the present case series. Calcium hydroxide has been used effectively in many revascularization cases of immature permanent necrotic teeth with apical periodontitis/abscess as an inter-appointment intracanal medicament (Chueh & Huang 2006, Cotti et al. 2008, Chueh et al. 2009, Cehreli et al. 2011). It was reported that calcium hydroxide and triple antibiotic paste, when used as an intracanal medicament in immature teeth with necrotic pulps, can help promote further development of the pulp– dentine complex after revascularization (Bose et al. 2009). Control of root canal infection provides a favourable environment for pulp and periapical cells to participate in tissue repair and regeneration after injury (Kakehashi et al. 1965).

In eight revascularization cases of immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscess, the patients felt pain when the files

ª 2011 International Endodontic Journal

International Endodontic Journal, 45, 294–305, 2011

299

CLINICAL ARTICLE

(a)

(b)

(c)

(d)

Figure 2 Case 3. Tooth 45. No significant continuation of root development and the root apex became blunt and closed. (a) Preoperative radiograph. (b) Postoperative radiograph. (c) Seven-month follow-up radiograph. (d) Thirteen-month follow-up radiograph.

(a)

(b)

(c)

(d)

Figure 3 Case 7. Tooth 35. Continued root development and the apical foramen remained open. (a) Preoperative radiograph. (b) Postoperative radiograph. (c) Five-month follow-up radiograph. (d) Ninemonth follow-up radiograph.

were introduced into the apical portion of the canal without local anaesthesia. When tissue is inflamed, sprouting of sensory nerve fibres and release of neuropeptides occur (Khayat et al. 1988, Byers et al. 1990). In addition, inflammatory mediators and pro-inflammatory cytokines released by cells participating in the immuno-inflammatory response can sensitize sensory nerve fibres (Hargreaes 2002). Therefore, the inflamed tissue is more sensitive to mechanical stimulation. Nevertheless, it is not known whether pain was caused by the presence of remaining inflamed vital pulp tissue, apical papilla or ingrowth

300

International Endodontic Journal, 45, 294–305, 2011

ÂŞ 2011 International Endodontic Journal

(b)

(c)

(d)

CLINICAL ARTICLE

(a)

Figure 4 Case 1. Tooth 35. Severe calcification of the canal space. (a) Preoperative radiograph. (b) Postoperative radiograph. (c) Seven-month follow-up radiograph. (d) Twenty-six-month follow-up radiograph.

of periodontal ligament (PDL) tissue in the apical portion of the canal space. In terms of increased thickening of the canal walls and/or continued root development, the immature permanent necrotic teeth with apical periodontitis/abscess painful to files introduced into the canals did not demonstrate better outcomes than the immature permanent necrotic teeth with apical periodontitis/abscess not painful to files introduced into the canals after revascularization procedures. One possibility is that irrigation with copious amounts of 5.25% sodium hypochlorite solution might have damaged apical vital tissue (Rosenfeld et al. 1978, Gordon et al. 1981) and possibly progenitor/stem cells after revascularization procedures.

Radiographic evidence of hard tissue deposition on the canal walls of all immature permanent teeth with necrotic pulp tissue and either apical periodontitis or abscess after revascularization procedures was observed in the present case series and other human revascularization studies (Iwaya et al. 2001, Banchs & Trope 2004, Chueh & Huang 2006, Cotti et al. 2008, Jung et al. 2008, Shah et al. 2008, Chueh et al. 2009, Ding et al. 2009, Petrino et al. 2010, Cehreli et al. 2011). The nature of the hard tissue formed on the canal walls in human immature permanent necrotic teeth with apical periodontitis/abscess after revascularization is speculative because no histological studies are available. In animal studies, the tissues in the canal space of immature teeth with necrotic pulp and apical periodontitis/abscess following revascularization procedures were described as osteoid or cementoid tissue and periodontal ligament-like tissue (Thibodeau et al. 2007, Bezerra da Silva et al. 2010, Wang et al. 2010, Yamauchi et al. 2011).

Six immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscess in the present study did not show continued root development.

Ding et al. (2009) showed that all 12 revascularized immature permanent necrotic teeth in their study had complete root development with a closed apex after a minimum of 1-year follow-up. Chueh et al. (2009) showed that 21 out of 23 revascularized immature permanent necrotic teeth in their study had complete root development; 14 had a conical root apex; and seven had a blunt root apex at a follow-up period over 6 to 108 months.

A blunt root apex might be considered as apical closure without significant increase in root length. In the case series study of Petrino et al. (2010), only three of six revascularized

ÂŞ 2011 International Endodontic Journal

International Endodontic Journal, 45, 294–305, 2011

301

CLINICAL ARTICLE

(a)

(b)

(c)

(d)

Figure 5 Case 17. Tooth #11. A hard tissue barrier (arrow) formed inside the canal space between the coronal mineral trioxide aggregate (MTA) plug and the root apex. (a) Preoperative radiograph. (b) Postoperative radiograph. (c) Four-month follow-up radiograph. (d) One-year follow-up radiograph.

immature permanent teeth with necrotic pulps showed obvious continued root development at a follow-up period of time from 6 months to 1 year. However, Shah et al. (2008) in their case series demonstrated that increased root length was observed in 10 of 14 revascularized immature permanent necrotic teeth and thickening of lateral dentinal walls was evident in 8 of 14 revascularized immature permanent necrotic teeth at a follow-up period of time from 0.5 to 3.5 years. A retrospective evaluation of radiographic outcomes in immature teeth with necrotic root canal systems treated with regenerative endodontic procedures also indicated that only a certain percentage of cases showed increase in root length (Bose et al. 2009). Continued root development does not appear to be a predictable outcome of immature permanent necrotic teeth with apical periodontitis/abscess after revascularization procedures in humans. Yamauchi et al. (2011) also demonstrated that continued apical development was not a constant finding in dog’s teeth after revascularization procedures of immature necrotic teeth with apical periodontitis.

302

International Endodontic Journal, 45, 294–305, 2011

ª 2011 International Endodontic Journal

CLINICAL ARTICLE

A root consists of dentine and cementum. Root dentine is formed by root odontoblasts differentiated from ectomesenchymal cells in the apical papilla upon receiving inductive signal from the Hertwig’s epithelial root sheath (HERS) (Sonoyama et al. 2008). Cementum is formed by cementoblasts differentiated from ectomesenchymal cells in the dental follicle after receiving inductive signal from the HERS (ZeichnerDavid et al. 2003, Sonoyama et al. 2007). In addition, stem cells in the PDL are also capable of differentiation into cementoblasts (Seo et al. 2004). A functional root cannot be formed without cementum because acellular cementum and cellular cementum provide primary and minor anchorage of PDL fibres to the alveolar socket, respectively (Nanci 2007). The viability of the HERS, apical papilla and dental follicle or PDL is likely to be dependent on the severity and duration of apical periodontitis/abscess in immature permanent necrotic teeth. Experimentally, if immature teeth of monkeys were extracted and either the entire or half of the HERS was removed before autotransplantation, total or partial arrest of root formation would occur. In contrast, if the HERS was not injured before autotransplantation, normal physiological root development would take place (Andreasen et al. 1988). Therefore, the HERS must survive in apical periodontitis/abscess in order to regulate root development in immature permanent necrotic teeth after revascularization. Continued root development appears to be due to apical cementum deposition after revascularization procedures of immature necrotic teeth with apical periodontitis in animal studies (Thibodeau et al. 2007, Bezerra da Silva et al. 2010, Wang et al. 2010, Yamauchi et al. 2011).

Severe pulp canal calcification (obliteration) by hard tissue formation was observed in four immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscess in the present study. Chueh et al. (2009) also reported two cases of complete and 21 cases of partial pulp canal obliteration in their case series of 23 revascularized immature permanent necrotic teeth. Pulp canal calcification (obliteration) by hard tissue formation can be caused by traumatic injury to the teeth, root fractures, replantation, pulp necrosis and periodontal disease (Andreasen & Andreasen 1994).

However, the mechanism of pulp canal calcification (obliteration) in revascularized immature permanent necrotic teeth with apical periodontitis/abscess is not clear.

Clinically, the outcome of pulp canal calcification (obliteration) by hard tissue formation in revascularized immature permanent necrotic teeth with apical periodontitis/abscess is unknown. It is also not known whether the outcome of pulp canal calcification (obliteration) in revascularized immature permanent necrotic teeth with apical periodontitis is similar to pulp canal calcification (obliteration) caused by traumatic injury to immature permanent teeth with possible development of pulp necrosis and apical periodontitis (Robertson et al. 1996). If the hard tissue formed in the canal space of revascularized immature permanent necrotic teeth with apical periodontitis/abscess is bone-like tissue, there will be a possibility that internal replacement resorption or union between intracanal hard tissue and apical alveolar bone (ankylosis) might occur. In addition, if there is a carious attack, can revascularized immature permanent necrotic teeth respond like normal teeth?

It is not known why a hard tissue barrier was formed in the canal space between the coronal MTA plug and the root apex in two cases. Histologically, Wang et al. (2010), in an animal study, also described bridge formation at the apical third of the canal by ingrowth of intracanal cementum in revascularized immature necrotic teeth with apical periodontitis.

Conclusion Based on the present case series, the outcome of continued root development was not as predictable as increased thickening of the canal walls in immature permanent teeth with

ÂŞ 2011 International Endodontic Journal

International Endodontic Journal, 45, 294–305, 2011

303

CLINICAL ARTICLE

infected necrotic pulp tissue and either apical periodontitis or abscess after revascularization procedures. Continued root development of revascularized immature permanent necrotic teeth depends on whether the HERS survives in case of apical periodontitis/ abscess. Severe pulp canal calcification (obliteration) by hard tissue formation might be a complication of internal replacement resorption or union between intracanal hard tissue and apical alveolar bone (ankylosis) in revascularized immature permanent teeth.

Disclaimer Whilst this article has been subjected to Editorial review, the opinions expressed, unless specifically indicated, are those of the author. The views expressed do not necessarily represent best practice, or the views of the IEJ Editorial Board, or of its affiliated Specialist Societies.

References American Association of Endodontists (2003) Glossary of Endodontic Terms, 7th edn. Chicago, IL: American Association of Endodontists.

Andreasen JO, Andreasen FM (1994) Textbook and Color Atlas of Traumatic Injuries to the Teeth, 3rd edn. Copenhagen: Munksgaard.

Andreasen JO, Kristerson L, Andreasen FM (1988) Damage of the Hertwig’s epithelial root sheath: effect upon root growth after autotransplantation of teeth in monkeys. Endodontics and Dental Traumatology 4, 145–51.

Banchs F, Trope M (2004) Revascularization of immature permanent teeth with apical periodontitis: new treatment protocol? Journal of Endodontics 30, 196–200.

Bezerra da Silva LA, Nelson-Filho P, Bezerra da Silva RA et al. (2010) Revascularization and periapical repair after endodontic treatment using apical negative pressure irrigation versus conventional irrigation plus triantibiotic intracanal dressing in dog’s teeth with apical periodontitis. Oral Surgery Oral Medicine Oral Pathology Oral Radiology Endodontology 109, 779–87.

Bose R, Nummikoski P, Hargreaves K (2009) A retrospective evaluation of radiographic outcomes in immature teeth with necrotic root canal systems treated with regenerative endodontic procedures.

Journal of Endodontics 35, 1343–9.

Byers MR, Tayler PE, Khayat BG et al. (1990) Effects of injury and inflammation on pulpal and periapical nerves. Journal of Endodontics 16, 78–84.

Bystro¨m A, Claesson R, Sundqvist G (1985) The antibacterial effect of camphorated paramonochlorophenol, camphorated phenol and calcium hydroxide in the treatment of infected root canals.

Endodontics and Dental Traumatology 1, 170–5.

Cehreli ZC, Isbitiren B, Sara S, Erbas G (2011) Regenerative endodontic treatment (Revascularization) of immature necrotic molars medicated with calcium hydroxide: a case series. Journal of Endodontics 37, 1327–30.

Chueh L-H, Huang GT-J (2006) Immature teeth with periapical periodontitis or abscess undergoing apexogenesis: a paradigm shift. Journal of Endodontics 32, 1205–13.

Chueh J-H, Ho Y-C, Kuo J-C, Lai W-H, Chen Y-HM, Chiang C-P (2009) Regenerative endodontic treatment for necrotic immature permanent teeth. Journal of Endodontics 35, 160–4.

Cotti E, Mereu M, Lusso D (2008) Regenerative treatment of an immature traumatized tooth with apical periodontitis: report of a case. Journal of Endodontics 34, 611–6.

Ding RY, Cheung GS-P, Chen J et al. (2009) Pulp revascularization of immature teeth with apical periodontitis: a clinical study. Journal of Endodontics 35, 745–9.

Gordon TM, Damato D, Christner P (1981) Solvent effect of various dilutions of sodium hypochlorite on vital and necrotic tissue. Journal of Endodontics 7, 466–9.

Hargreaes KM (2002) Pain mechanisms of the pulpodentin complex. In: Hargreaves KM, Goodis HE, eds. Dental Pulp. Chicago: Quintessence, pp. 181–203.

Iwaya SI, Ikawa M, Kubota M (2001) Revascularization of an immature permanent tooth with apical periodontitis and sinus tract. Dental Traumatology 17, 185–7.

304

International Endodontic Journal, 45, 294–305, 2011

ª 2011 International Endodontic Journal

ª 2011 International Endodontic Journal

International Endodontic Journal, 45, 294–305, 2011

CLINICAL ARTICLE

Jung I-Y, Le S-J, Hargreaves KM (2008) Biologically based treatment of immature permanent teeth with pulp necrosis: a case series. Journal of Endodontics 34, 876–87.

Kakehashi S, Stanley HR, Fitzgerald RJ (1965) The effect of surgical exposures of dental pulps in germfree and conventional rats. Oral Surgery Oral Medicine Oral Pathology 20, 340–9.

Khayat BG, Byers MR, Taylor PE et al. (1988) Responses of nerve fibers to pulpal inflammation and periapical lesions in rat molars demonstrated by calcitonin gene- related peptide immunohistochemistry. Journal of Endodontics 14, 577–87.

Nanci A (2007) Ten Cate’s Oral Biology, 7th edn. St. Louis: Mosby.

Petrino JA, Boda KK, Shambarger S et al. (2010) Challenges in regenerative endodontics: a case series. Journal of Endodontics 36, 536–41.

Rafter M (2005) Apexification: a review. Dental Traumatology 21, 1–8.

Robertson A, Andreasen FM, Bergenholtz G et al. (1996) Incidence of pulp necrosis subsequently to pulp canal obliteration from trauma of permanent incisors. Journal of Endodontics 22, 557–60.

Rosenfeld EF, James GA, Burch BS (1978) Vital pulp tissue response to sodium hypochlorite. Journal of Endodontics 4, 140–6.

Seo B-M, Mirura M, Gronthos S et al. (2004) Investigation of multipotent postnatal stem cells from human periodontal ligament. The Lancet 364, 149–55.

Shah N, Logani A, Bhaskar U et al. (2008) Efficacy of revascularization to induce apexification/ apexogenesis in infected, nonvital, immature teeth: a pilot clinical study. Journal of Endodontics 34, 919–25.

Sjogren U, Fidgor D, Spangberg L et al. (1991) The antimicrobial effect of calcium hydroxide as a shortterm intracanal dressing. International Endodontic Journal 24, 119–25.

Sonoyama W, Seo B-M, Yamaza T, Shi S (2007) Human Hertwig’s epithelial root sheath cells play crucial roles in cementum formation. Journal of Dental Research 86, 594–9.

Sonoyama W, Liu Y, Yamaza T et al. (2008) Characterization of the apical papilla and its residing stem cells from human immature permanent teeth: a pilot study. Journal of Endodontics 34, 166–71.

Thibodeau B, Teixeira F, Yamauchi M et al. (2007) Pulp revascularization of immature dog teeth with apical periodontitis. Journal of Endodontics 33, 680–9.

Wang X, Thibodeau B, Trope M et al. (2010) Histological characterization of regenerated tissues in canal space after the revitalization/revascularization procedure of immature dog teeth with apical periodontitis. Journal of Endodontics 36, 56–63.

Yamauchi N, Yamauchi S, Nagaoka H et al. (2011) Tissue engineering strategies for immature teeth with apical periodontitis. Journal of Endodontics 37, 390–7.

Zeichner-David M, Oishi K, Su Z et al. (2003) Role of Hertwig’s epithelial root sheath cells in tooth root development. Development Dynamics 228, 651–63.

305

This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy.

Users should refer to the original published version of the material.