REVIEW

Apexification
Shikha Dogra1, Mukunda KS2, ArunA3 ,Shwetha M Rao4

1 Senior Lecturer, Department of Pedodontics, SSDC, Tumkur, Karnataka, India 2 Reader, Department of Pedodontics, SSDC, Tumkur, Karnataka, India 3 Senior Lecturer, Department of Conservative Dentistry, SSDC, Tumkur, Karnataka, India 4 Post Graduate Student, Department of Pedodontics, SSDC, Tumkur, Karnataka, India

ABSTRACT
An immature tooth that develops pulpal or periapical disease presents special problems. Because the apex has not yet completely formed, conventional root canal treatment procedures would be unpredictable. This paper reviews the rationale and techniques for treatment of the non-vital immature tooth. The treatment of choice for necrotic teeth is apexi? cation, which is induction of apical closure to produce more favourable conditions for conventional root canal ? lling. The most commonly advocated medicament is calcium hydroxide, although recently considerable interest has been expressed in the use of mineral trioxide aggregate. KEYWORDS : apexi? cation; calcium hydroxide; mineral trioxide aggregate; multiple visit Apexification; one-visit apexi? cation

JOURNAL OF DENTAL SCIENCES AND RESEARCH Vol. 3, Issue 1, Pages 41-44

INTRODUCTION Endodontic treatment of immature necrotic teeth with necrotic pulps and open apex involves induction of apical closure by apexification procedures to create optimal conditions for conventional root canal filling[1]. Apexification therapy is initiated when clinical and radiographic evidence of pulpal necrosis has been unequivocally established and the incompletely formed root has an apical diameter greater than coronal diameter. Apexogenesis, in contrast refers to vital pulp therapy to encourage continued physiological root and apex formation with its normal dentin and cementum composition[2]. ROOT DEVELOPMENT Root development begins when enamel and dentin formation has reached the future cementoenamel junction. At this stage the inner and outer enamel epithelium form Hertwig's epithelial root sheath[3]. Hertwig's epithelial root sheath is responsible for determining the shapeoftheroots. Theepithelial diaphragm surrounds the apical opening to thepulp andeventuallybecomestheapical foramen. An open apex is found in the developing roots of immature teeth until
Address for correspondence: Dr. Shikha Dogra E-mail: shi 2978@rediffmail.com Access this article online Website: http://www.ssdctumkur.org/jdsr.php

apical closure occurs approximately 3 years after eruption of permanent tooth[3]. The root sheath of Hertwig is usually sensitive to trauma but because of the degree of vascularity and cellularity in the apical region, root formation can continue even in the presence of pulpal in? ammation and necrosis[4]. It is thought to provide a source of undifferentiated cells that could give rise to further hard tissue formation. It may also protect against the in growth of periodontal ligament cells into the root canal, which would result in intracanal bone formation and arrest of rootdevelopment [5]. Complete destruction of Hertwig's epithelial root sheath results in cessation of normal root development. Once the sheath has been destroyed there can be no further differentiation of odontoblasts. However, hard tissue can be formed by cementoblasts that are normally present in the apical region and by ? broblasts of the dental follicle and periodontal ligament that undergo differentiation after the injury to become hard tissue producing cells[7]. There are two types of biological repairs that have been described in the literature following apexification : 1. Continued root growth[8] 2. Occlusion of apex with calcified material[9]. APEXIFICATION

Non plagiarized Content declaration provided by author

Yes

In the past, techniques for management of the open apex in non-vital teeth were confined to custom ? tting the ? lling material[10], paste ? lls[11] and apical surgery[12].
41

Journal of Dental Sciences and Research

A number of authors[10] have described the use of custom ? tted gutta-percha cones, but this is not advisable as the apical portion of the root is frequently wider than the coronal portion, making proper condensation of the gutta-percha impossible. Sufficient widening of the coronal segment to make its diameter greater than that of the apical portion would signi? cantly weakens the root and increases the risk of fracture. The disadvantages of surgical intervention include the difficulty of obtaining the necessary apical seal in the young pulp less tooth with its thin, fragile, irregular walls at the root apex. Apicoectomy further reduces the root length resulting in a very unfavourable crown root ratio. The limited success enjoyed by these procedures resulted in signi? cant interest in the phenomenon of continued apical development or establishment of an apical barrier, ? rst proposed in the 1960s[13]. Most of these techniques involve removal of the necrotic tissue followed by debridement of the canal and placement of a medicament. However, it has not been conclusively demonstrated that a medicament is necessary for induction of apical barrier formation. Nygaard- Ostby hypothesized that laceration of the periapical tissues until bleeding occurred might produce new vital vascularised tissue in the canal. He suggested that this treatment may result in further development of the apex[14]. Much of the early work in the area of induced apical closure focused on the use of antiseptic and antibiotic pastes. A number of investigators15demonstrated apical closure using an antiseptic paste as a temporary ? lling material following root canal debridement and Ball[16] successfully reproduced these results using an antibiotic paste. CALCIUM HYDROXIDE Although a variety of materials have been proposed for induction of apical barrier formation, calcium hydroxide has gained the widest acceptance. The use of calcium hydroxide was ? rst introduced by Kaiser[13] in 1964 who proposed that this material mixed with camphorated parachlorophenol (CMCP) would induce the formation of a calci? ed barrier across the apex. This procedure was popularised by Frank who emphasized the importance of reducing contamination within root canal by instrumentation and medication and decreasing the canal space temporarily with absorbable paste seal. Calcium hydroxide can be mixed with a number of different substances (Camphorated mono chlorophenol, d i s t i l l e d w a t e r, s a l i n e , a n e s t h e t i c s o l u t i o n s , chlorhexidene, cresatin) to induce apical closure[16]. The mechanism by which calcium hydroxide induces the formation of a solid apical barrier are not fully understood. Some attribute its action solely to its
42

antibacterial activity, while others emphasize its high pH or its direct effect on the apical and periapical soft tissues[17]. The alkaline pH and calcium ions might play a role either separately or synergistically. The calcium required for apical bridge formation comes through the systemic route as demonstrated by Pisanty and Sciacky[18]. Siqueira and Lopes[17] discussed the mechanism of its antimicrobial activity in detail. Calcium hydroxide assists in the debridement of the root canal, as it increases the dissolution of necrotic tissue when used alone or in combination with sodium hypochlorite. Frank in 1966 published three case histories of apical closure induced by calcium hydroxide. He assumed that the apical closure was related to Hertwig's epithelial root sheath. Mitchell and Shankwalker[19] studied the osteogenic potential of calciumhydroxide and other materials when implanted into the connective tissue of rats. Of the[11]materials used in comparative studies, only three gave any evidence of induced calcification. They concluded that calcium hydroxide had a unique potential to induce formation of heterotopic bone in this situation. TECHNIQUE Since in the vast majority of cases non vital teeth are infected, the first phase of treatment is to disinfect the root canal system to ensure periapical healing. The canal length is estimated with a parallel preoperative radiograph and confirmed radiographically with the first endodontic instrument. The root length cannot be determined with apex locator as it is not reliable in teeth with open apices[20]. Preparation of the canal owing to the thin dentinal walls is performed very lightly and with copious irrigation using 0.5% sodium hypochlorite (NaOCl). Lower strength of NaOCl is used because of the increased danger of extruding NaOCl through open apex. The canal is dried with paper points and a creamy mix of calcium hydroxide is spun into the canal with lentulospiral. The calcium hydroxide is left in the canal for at least one week to be effective in accomplishing disinfection[21]. At the second visit, a thick paste of calcium hydroxide will be packed in the root canal. Ca(OH)2 placement methods vary from injection of paste, using lentulo spirals and condensation or even using packed dry powder. Many authors consider a continuous intimate contact of calcium hydroxide with apical and periapical tissue as desirable[22]. Therefore it should be beneficial to use calcium hydroxide placement method that will provide the best retention of the material in the canals. Metzger[22] et al concluded from their study that injection

Vol. 3, Issue 1, February 2012

of calcium hydroxide paste was the easiest method to use. However, the injected paste was poorly retained in the canals. Condensation of calcium hydroxide with hand pluggers was the most demanding and time consuming procedure, yet retention of the paste in the canals was superior to retention with either of the two methodsfilling with lentulo spirals and injection method used[23]. Reports vary as to the time required to achieve the goal of apical barrier formation. Heithersay achieved apical closure in the time range of 14 to 75 months. Chawla[23] used calcium hydroxide paste and achieved closure within 6 to 12 months. Kleier[24] found closure of apex within 1 to 30 months. There are various factors that influence the time taken for apical barrier formation: 1. Size of the apical foramen at the start of treatment Teeth with apices < 2 mm in diameter has significant shorter time[23]. 2. Age - Since less calcified material would be needed to occlude a narrow apex as compared to wide apex; it is understandable that the former would require shorter period for apexification[23]. 3. Infection - some studies have reported that presence of periapical radiolucency at the start of treatment, increases the barrier formation time, whereas others have not[23]. 4. Inter appointment painful symptoms - may delay time taken for apical healing[24]. 5. Frequency of Ca(OH)2 dressings - there is no census on how frequently the dressing should be changed to induce apical healing. Some favour refilling every 36 months, others favour refilling only if there is radiographic evidence of root resorption of paste or only after determining mechanically if the hard tissue barrier formed is adequate. MULTIPLE VERSUS SINGLE VISIT APEXIFICATION The traditional use of calcium hydroxide apical barriers has been associated with unpredictable apical closure, time taken for barrier formation, patient compliance, risks of re-infection resulting from the difficulty in creating long term seals with provisional restorations and susceptibility to root fractures arising from the presence of thin roots or prolonged exposure of the root dentin to Ca(OH)2[25] .Thus there is increasing popularity with one visit apexification techniques. One visit Apexification has been defined as the non surgical condensation of a biocompatible material into the apical end of root canal. The rationale is to establish an apical stop that would enable the root canal to be filled immediately. Torneck[26] and others have indicated that

when apical closure takes place clinically with Ca(OH)2, there is not complete bridging of the apex histologically. Periapical inflammation persists about the apices of many teeth because necrotic tissue exists in corners and crevices of the bridge. A major target area of biomedical research is a mechanism to restore lost bone. A resorbabletricalcium phosphate ceramic has been developed. Koenig's, Brilliant and Driskell[27] found that use of this material induced apical closure in vital teeth of primates with open apices. Regeneration of periodontal ligament occurred around the apices of teeth and it was associated with minimal inflammatory response. Harbert documented the long term success of using a tri calcium phosphate plug as an apical barrier for one step apexification. In other studies teeth with open apices were obturated using an apical barrier with dentin and Ca(OH)2 plugs or dentin chips and hydroxyappatite[28]. There is increasing popularity with one visit apexification technique using Mineral Trioxide Aggregate (MTA) as osteoconductive apical barrier. MTA is relatively non cytotoxic and stimulates cementogenesis. This Portland cement based material generates a highly alkaline aqueous environment by leaching of calcium and hydroxyl ions, rendering it bioactive by forming hydroxyappatite in presence of phosphate containing fluids. Unlike the extended use of Ca(OH)2 in immature roots, prolonged filling of these roots with MTA did not reduce their fracture resistance[29]. Torabinejad[30] reported the ingredients in MTA as tri calcium silicate, tricalcium aluminate, tricalcium oxide and silicate oxide with some other mineral oxides that were responsible for the chemical and physical properties of aggregate. The powder consists of fine hydrophilic particles that set in the presence of moisture. The hydration of the powder results in a colloidal gel with a pH of 12.5 that will set in approximately 3 hours. MTA has a compressive strength equal to intermediate restorative material and Super EBA but less than that of amalgam. It is commercially available as ProRoot MTA (Dentsply Tulsa Dental, Tulsa) and has been advocated for use in the immediate obturation of open root apex. MTA has the ability to induce cementum like hard tissue when used adjacent to the periradicular tissues. MTA is a promising material as a result of its superior sealing property, its ability to set up in the presence of blood and its biocompatibility. Moisture contamination at the apex of tooth before barrier formation is often a problem with other materials used in apexification. As a result of its hydrophilic property, the presence of moisture does not affect its sealing ability. Shabahang[31] et al examined hard tissue formation and inflammation histomorphologically after treating open apices in canine teeth with osteogenic protein-1, MTA and
43

Journal of Dental Sciences and Research

calcium hydroxide. MTA induced hard tissue formation with the most consistency, but the amount of hard tissue formation and inflammation was not statistically different among the three materials. MTA has demonstrated the ability to stimulate cells to differentiate into hard tissue forming cells and to produce a hard tissue matrix. A number of animal studies have demonstrated a more predictable healing outcome when MTA is used when compared with teeth treated with calcium hydroxide[32]. In a prospective human outcome study, 57 teeth with open apices were obturated with MTA in one appointment. Forty three of these cases were available for recall at 12 months, of which 81% of cases were classified as healed[33]. Despite its good physical and biologic properties, extended setting time has been a main disadvantage. Calcium chloride was used with intention to stimulate hardening process of MTA. Studies have shown that not only the sealing ability but its physicochemical property was improved by addition of CaCl2 . CONCLUSION Introduction of techniques for one-visit apexi? cation provide an alternative treatment option in these cases. Success rates for calcium hydroxide apexi? cation are high although risks such as reinfection and tooth fracture exist. Prospective clinical trials comparing multiple and one-visit apexi? cation techniques are required. REFERENCES
1. Mafter M. Apexification: a review. Dent Traumatol 2005;21: 1-8 2. American Association of Endodontic. Glossary of endodontic terms, 7th edition Chicago: American Association of Endodontics 2003 3. Bhasker SN. Orban's oral histology and embryology, 11thedn. St. Louis: Mosby-Year Book; 1991. 4. Andreasen JO, Hjorting-Hansen R. Intra-alveolar rootfractures: radiographic and histologic study of 50 cases. J Oral Surg 1967;25:41426. 5. Pindborg JJ. Clinical, radiographic and histologic aspectsof intra-alveolar fractures of upper central incisors. ActaOdontolScand 1956;13:417. 6. Torneck CD. Effects of trauma to the developing permanent dentition. Dent Clin N Am 1982; 26:481504. 7. Frank AL. Therapy for the divergent pulpless tooth by continued apical formation, J Am Dent Assoc 1966;72:87-9 8. Burley MA. Root formation following traumatic loss of an immature incisor-a case report. Br Dent J 1976;14:315-316 9. Ham JW, Patterson SS, Mitchell DF. Induced apical closure in immature pulpless teeth in monkey. OralSurg 1972;33: 438-449 10. Stewart DJ. Root canal therapy in incisor teeth with openapices. Br Dent J 1963; 114:24954. 11. Friend LA.Treatment of immature teeth and non-vitalpulps.J Br EndodSoc 1967; 1:2833.
44

12. Ingle JI.Endodontics.Philadelphia:LeaandFebiger;1965:504. 13. Kaiser HJ. Management of wide open apex canals with calcium hydroxide. Presented at the 21st Annual Meeting of the American Association of Endodontists, Washington DC April 17 1964. 14. Nygaard-Ostby B. The role of the blood clot in endodontictherapy. ActaOdontolScand 1961; 19:32346. 15. Holland R,deSouza V,TugliaviniRL,MilaneziLA.Healing process of teeth with open apices: histologic study.Bull Tokyo Dent Coll 1971;12:3338. 16. Ball JS. Apical root formation in non-vital immature permanent incisors. Report of a case. Brit Dent J 1964;116:166-7 17. Siqueira JF, Lopes HP. Mechanism of antimicrobial activity of calcium hydroxide: a critical review.IntEndod J1999;32:361 18. Pisanti S, Sciaky I. Origin of calcium in the repair of wall after pulp exposure in the dog. J Dent Res 1964;43:641-644 19. Mitchell DF and ShankwalkerGB.Osteogenic potential of calcium hydroxide and other materials in soft tissue and bone wounds. J Dent Res 1958;37:1157-1163 20. HulsmannM,PieperK.use of an electronic apex locator in treatment of teeth with incomplete root formation.Endod Dent Traumatol 1989;5:238 21. Bakland LK. Traumatic dental injuries.In: Ingle JI, BaklandLK,Endodontics, 4th ed. Baltimore: Williams and Wilkins 1994:764-814 22. Metzger Z, Solomonov M, Mass E. Calcium hydroxide retention in wide root canals with flaring apices.DentTraumatol 2001;17:86-92 23. KleirDJ,Barr ES.A study of endodontically apexifiedteeth. Endod Dent Traumatol 1991;7:112-117 24. Walia T, Chawla H, Gauba K. Management of wide open apices in non vital permanent teeth with calcium hydroxide paste. JClinPediatr Dent 2000 ;25(1):51-56 25. Andreasen JO, Farik B, Munksgaard EC. Long term calcium hydroxide as a root canal may increase risk of root fracture. Dent Traumatol 2002;18:134-7 26. Torneck CD, Smith JS, Grindall P. Biologic effects of endodontic procedures on developing incisor teeth. Oral Surg 1973;35:541 27. Koenigs JF, Brilliant D, Driskell TD. Induced apical closure of permanent teeth in adult primates using a resorbable form of tricalcium phosphate ceramic.JEndod 1975; 3(1):102-106 28. Brandell DW, Torabinajed M, Bakland L K. Demineralised dentin, hydroxyappatite and dentin chips as apical plugs.Endod Dent Traumatol 1986;2:210-4 29. Rebecca L, Martin BS, Francesca M et al.Sealing properties of mineral trioxide aggregate orthograde apical plugs and root fillings in an in vitro apexification model. J Endod 2007;33:272-275 30. Torabinejad M, ChivianN.Clinical applications of mineral trioxide aggregate.JEndod 1999;25:197-205 31. Shabahang S, TorabinejadM.Treatment of teeth with open apices using mineral trioxide aggregate. Pract Periodont Aesthet Dent 2000;12:315-20 32. El-Meligy OA, Avery DR. Comparison of Apexification with mineral trioxide aggregate and calcium hydroxide. Pediatr Dent 2006;28:248-53 33. Simon S, Rillard F, Berdal A et al ,The use of mineral trioxide aggregate in one visit Apexification treatment: a prospective study. IntEndod J 2007;40:186-97