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Endodontic treatment of a tooth with pulp necrosis and severe inflammatory external apical root resorption in a single session: Is it possible? A case report

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Drs. Ricardo Machado, Emanuely da Silva Chrun, Luiz Fernando Tomazinho, and Lucas da Fonseca Roberti Garcia consider the possibility of endodontic treatment of a tooth with pulp necrosis and severe inflammatory external apical root resorption in a single session

Educational aims and objectives

This article aims to present a case of a tooth with pulp necrosis, periradicular lesion and severe inflammatory apical root resorption, where endodontic treatment was performed in a single session.

Expected outcomes

Endodontic Practice US subscribers can answer the CE questions to earn 2 hours of CE from reading this article. Take the quiz by clicking here. Correctly answering the questions will demonstrate the reader can:

  • Recognize certain characteristics of the external inflammatory apical root resorption process.
  • Realize differences in endodontic treatment with and without the use of an intracanal medication.
  • Discuss the use of calcium hydroxide as an intracanal medication.
  • Recognize the involvement of cementum and dentin in healing of external root resorption.
  • Identify the steps that lead to the success of pulp necrosis and severe inflammatory apical root resorption in a single session after a 6-month follow-up.

Root resorption is characterized by an unregulated function between blastic and clastic cells, normally responsible for the maintenance and remodeling of the periodontal support tissues. This condition may lead to tooth loss from uncontrolled cell activity if adequate treatment is not given (Andreasen, 1985).

Particularly in regards to external inflammatory apical root resorption, several studies have shown a positive correlation between this disease, pulp necrosis, and the presence of periradicular lesions (Campos, et al., 2013; Vier-Pelisser, et al., 2013). Thus, performing proper endodontic treatment may interrupt the external inflammatory apical root resorption process by neutralizing microbiological content and inhibiting clastic action (Barratto-Filho, et al., 2009).

The number of sessions required to properly reduce the microbial population of a contaminated root canal system is still a controversial issue among researchers (Kvist, et al., 2004; Molander, et al., 2007; Paredes-Vieyra, Enriquez, 2012). In recent years, several clinical and meta-analysis studies have been performed to compare endodontic treatment with and without the use of an intracanal medication and have reported similar results between these two treatment modalities (Kvist, et al., 2004; Molander, et al., 2007; Soltanoff, 1978). However, to date, no conclusive scientific evidence has been found on required use of an intracanal medication in cases of pulp necrosis, periradicular lesion, and severe associated inflammatory apical root resorption.

Thus, the purpose of this article is to report the clinical case of a tooth with pulp necrosis, periradicular lesion, and severe inflammatory apical root resorption, where endodontic treatment was performed in a single session. The 6-month follow-up shows clear signs of repair.

Case report

A 24-year-old male patient was referred to the endodontic specialization course at Ingá University, UNINGÁ, Rio Branco, AC, Brazil, for analysis of tooth No. 36. The patient related episodes of pain and swelling in this region a few months prior. Clinical examination revealed an extensive carious lesion and provisional sealing with temporary restorative material. Radiographic analysis showed communication of the temporary restorative material with the pulp chamber, periradicular lesions in both roots, and severe inflammatory apical root resorption in the distal root (Figure 1A).


Figures 1A-1C: A. Initial periapical radiograph of tooth No. 36, showing periapical lesions in both roots, and severe apical root resorption in the distal root (circle). B. Tooth No. 36 after filling of root canal system. C. Radiograph after 6-month follow-up, with clear evidence of tissue repair and containment of the resorptive process (arrow)

After conducting clinical and radiographic analysis, it was decided that endodontic treatment should be performed. Initially, the tooth was anesthetized with 4% articaine and adrenaline 1:100.000 (DFL Indústria e Comércio), followed by the placement of a rubber dam. Then the temporary restorative material and the carious lesion were removed with spherical 1016 and Endo™ Z burs (KG Sorensen) coupled with a high-speed device (Extra Torque 605C, KaVo). Four canal orifices were identified with endodontic probes (MB, ML, DB, and DL) and prepared with number two Gates-Glidden burs (Dentsply Sirona). Then each canal was irrigated with 2.5 ml of 2.5% sodium hypochlorite (Fórmula & Ação).

Afterwards, the working lengths were established at -0.5 (mesial canals) and -1.0 mm (distal canals) from the point indicated by the electronic apex locator (Mini Apex Locator, SybronEndo) as “0.0.”

A manual glide path was created in the mesial root canals, with size 15 and 20 K-type files (Dentsply/Maillefer), followed by preparation using the two-system (VDW) full-sequence technique. The size of the distal canals required manual preparation to be performed up to size 60 K-type file (Dentsply/Maillefer), following the principles of the crown-down technique. The patency of the root canals was maintained by using a size 20 K-type file (Dentsply/Maillefer) up to the main foramen. The canals were irrigated at each change of file, with 2.5 ml of 2.5% sodium hypochlorite, and a final irrigation was performed with 2.5 ml of 17% EDTA (Fórmula & Ação) for 3 minutes to remove the smear layer.

The root canals were dried with absorbent paper cones (Dentsply/Maillefer) and filled with gutta-percha cones (Dentsply/Maillefer) and Sealer 26 (Dentsply/Maillefer) (Figure 1B), using the lateral compaction technique.

Six months after the treatment, the patient returned for a follow-up and related no pain or any relevant symptomatology. Radiographic examination showed clear evidence of tissue repair and containment of the resorptive process (Figure 1C).

Discussion

Since no evidence of dental trauma, occlusal disharmony, or relevant associated systemic disease was observed in this case report, it was concluded that the severe inflammatory resorptive process evolved from carious lesion to pulp necrosis and periradicular disease. Complete necrosis of pulp tissue leads to colonization and proliferation of microorganisms within the root canal system, inducing periradicular inflammation, which promotes clastic cell activity, and, in turn, triggers an osseous and radicular resorptive process (Patel, et al., 2009).

Some studies have advocated the use of calcium hydroxide as an intracanal medication in cases of open apices caused by incomplete apexogenesis, over-instrumentation, and/or apical resorptions (Mente, et al., 2009; Mente, et al., 2013). In addition to its antimicrobial activity, this substance acts as a physical-chemical barrier, preventing the proliferation of residual microorganisms, reinfection of the root canal by microorganisms originating from the oral cavity, and invagination of the granulation tissue of the area reabsorbed by the walls of the root canal. Furthermore, calcium hydroxide is capable of promoting necrosis of the resorptive cells present in Howship’s lacunae, thus neutralizing clastic cell acids, preventing the mineral dissolution of the root, and rendering the region unsuitable for acid hydrolases (Mohammadi, Dummer, 2011; Saad, 1989).

Healing of external root resorption, involving cementum and dentin caused by apical periodontitis also requires the recruitment of progenitor cells. Dentin-producing odontoblasts can be differentiated only from dental pulp stem cells (Gronthos, et al., 2000), and stem cells, from apical papilla (Sonoyama, et al., 2008). In mature teeth with apical periodontitis, the dental pulp is completely destroyed, and the apical papilla no longer exists. In addition, stem cells/progenitor cells in the periodontal ligament and alveolar bone marrow are not capable of differentiating into odontoblasts (Huang, Gronthos, Shi, 2009; Seo, et al., 2004). Therefore, the resorbed root dentin caused by the inflammatory process cannot be regenerated by odontoblasts and dentin formation (Ricucci. et al., 2014).

Resorbed root dentin is repaired by cementum and not by dentin (Lindskog, Blomlof, Hammarstrom, 1987). The mechanisms of repair by cementum formation, including the origin of cementoblasts and the molecules related to their recruitment and differentiation, remain unclear (Grzesik, Narayanan, 2002). Cementoblast progenitors have their origin in the periodontal ligament (usually in a paravascular location) or the endosteum (Liu, et al., 1997; McCulloch, 1993). In periradicular tissue healing, periodontal ligament cells adjacent to the affected root area may start to proliferate and populate the region in which the periodontal ligament and cementum were changed or lost by inflammation. It has been suggested that the cementum matrix and associated molecules can recruit cementum-forming stem/progenitor cells in the periodontal ligament (Grzesik, Narayana, 2002), and that the dentin matrix may also be able to signal progenitor cells in the periodontal ligament (Diekwisch, 2001) to differentiate into cementoblasts. Initially, cementoblast progenitors have to be selected, possibly by specific integrins and signaling events (Grzesik, Narayanan, 2002; Wu, et al., 1996). Then the selected cells adhere to the root surface and are activated by growth factors previously sequestered in the cementum and dentin matrix and released as a consequence of root resorption. These factors include bone morphogenetic proteins, transforming growth factor beta, insulin-like growth factor one, and epidermal growth factor (Grzesik, Narayanan, 2002; MacNeil, Somerman, 1999). Newly formed cementum usually covers areas of the root where cementum and dentin were lost (Ricucci, et al., 2014).

It seems much more “plausible biologically” that the entire immunological complex is activated after performing an adequate cleaning and shaping process of the root canal system and not only or necessarily after using calcium hydroxide. This argument is based on the absence of statistically significant differences in the success rates of necrotic teeth with radiographically visualized periradicular lesions treated with or without the use of this substance as an intracanal medication (Molander, et al., 2007; Paredes- Vieyra, Enriquez, 2012; Penesis, et al., 2008).

With this in mind, it was decided that appropriate endodontic treatment could be concluded in a single session, based on the certainty that correct cleaning and shaping could be performed, and that all the canals could be completely dried after this phase.

The success of this treatment was observed after the 6-month follow-up, at which time no pain, sinus tract, swelling, or discomfort was observed or related by the patient. Although it is thought that randomized clinical studies must be conducted to compare the results of endodontic treatment performed in a single or more sessions for teeth with pulp necrosis, periradicular lesion, and severe inflammatory apical root resorptions, the clinical case related in this article demonstrates the feasibility of performing endodontic treatments for these cases in a single visit.

Author Info

Ricardo Machado runs a clinical practice limited to endodontics in Navegantes, Santa Catarina, Brazil.
 
Emanuely Da Silva Chrun is from the department of Pathology, Health Sciences Center, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil.
 
Luiz Fernando Tomazinho is from the Department of Endodontics, Paranaense University, Umuarama, Paraná, Brazil.
 
Lucas Da Fonseca Roberti Garcia is from the Department of Dentistry – Endodontics Division, Health Sciences Center, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil.

References

  1. Andreasen JO. External root resorption: its implication in dental traumatology, paedodontics, periodontics, orthodontics and endodontics. Int Endod J. 1985;18(2):109-118.
  2. Baratto-Filho F, Leonardi DP, Zielak JC, Vanni JR, Sayao-Maia SM, Sousa-Neto MD. Influence of ProTaper finishing files and sodium hypochlorite on cleaning and shaping of mandibular central incisors – a histological analysis. J Appl Oral Sci. 2009;17(3):229-233.
  3. Campos MJ, Silva KS, Gravina MA, Fraga MR, Vitral RW. Apical root resorption: the dark side of the root. Am J Orthod Dentofacial Orthop. 2013;43(4):492-498.
  4. Diekwisch TG. The developmental biology of cementum. Int J Dev Biol. 2001;45(5-6):695-706.
  5. Gronthos S, Mankani M, Brahim J, Robey PG, Shi S. Postnatal human dental pulp stem cells (DPSCs) in vitro and in vivo. Proc Natl Acad Sci U S A. 2000;97(25):13625-13630.
  6. Grzesik WJ, Narayanan AS. Cementum and periodontal wound healing and regeneration. Crit Rev Oral Biol Med. 2002;13(6):474-484.
  7. Huang GT, Gronthos S, Shi S. Mesenchymal stem cells derived from dental tissues vs. those from other sources: their biology and role in regenerative medicine. J Dent Res. 2009;88(9):792-806.
  8. Kvist T, Molander A, Dahlen G, Reit C. Microbiological evaluation of one- and two-visit endodontic treatment of teeth with apical periodontitis: a randomized, clinical trial. J Endod. 2004;30(8):572-576.
  9. Lindskog S, Blomlof L, Hammarstrom L. Cellular colonization of denuded root surfaces in vivo: cell morphology in dentin resorption and cementum repair. J Clin Periodontol. 1987;14(7):390-395.
  10. Liu HW, Yacobi R, Savion N, Narayanan AS, Pitaru S. A collagenous cementum-derived attachment protein is a marker for progenitors of the mineralized tissue-forming cell lineage of the periodontal ligament. J Bone Miner Res. 1997;12(10):1691-1699.
  11. MacNeil RL, Somerman MJ. Development and regeneration of the periodontium: parallels and contrasts. Periodontol 2000. 1999;19:8-20.
  12. McCulloch CA. Basic considerations in periodontal wound healing to achieve regeneration. Periodontol 2000. 1993;1(1):16-25.
  13. Mente J, Hage N, Pfefferle T, Koch MJ, Dreyhaupt J, Staehle HJ, Friedman S. Mineral trioxide aggregate apical plugs in teeth with open apical foramina: a retrospective analysis of treatment outcome. J Endod. 2009;35(10):1354-1358
  14. Mente J, Leo M, Panagidis D, et al. Treatment outcome of mineral trioxide aggregate in open apex teeth. J Endod. 2013;39(1):20-26.
  15. Mohammadi Z, Dummer PM. Properties and applications of calcium hydroxide in endodontics and dental traumatology. Int Endod J. 2011;44(8):697-730.
  16. Molander A, Warfvinge J, Reit C, Kvist T. Clinical and radiographic evaluation of one-and two-visit endodontic treatment of asymptomatic necrotic teeth with apical periodontitis: a randomized clinical trial. J Endod. 2007;33(10):1145-1148.
  17. Paredes-Vieyra J, Enriquez FJ. Success rate of single- versus two-visit root canal treatment of teeth with apical periodontitis: a randomized controlled trial. J Endod. 2012;38(9):1164-1169.
  18. Patel S, Dawood A, Wilson R, Horner K, Mannocci F. The detection and management of root resorption lesions using intraoral radiography and cone beam computed tomography — an in vivo investigation. Int Endod J. 2009;42(9):831-838.
  19. Penesis VA, Fitzgerald PI, Fayad MI, Wenckus CS, BeGole EA, Johnson BR. Outcome of one-visit and two-visit endodontic treatment of necrotic teeth with apical periodontitis: a randomized controlled trial with one-year evaluation. J Endod. 2008;34(3):251-257.
  20. Ricucci D, Siqueira JF Jr, Loghin S, Lin LM. Repair of extensive apical root resorption associated with apical periodontitis: radiographic and histologic observations after 25 years. J Endod. 2014;40(8):1268-1274.
  21. Saad AY. Calcium hydroxide in the treatment of external root resorption. J Am Dent Assoc. 1989;118(5):579-581.
  22. Seo BM, Miura M, Gronthos S, et al. Investigation of multipotent postnatal stem cells from human periodontal ligament. Lancet. 2004;364(9429):149-155.
  23. Soltanoff W. A comparative study of the single-visit and the multiple-visit edodontic procedure. J Endod. 1978;4(9):278-281.
  24. Sonoyama W, Liu Y, Yamaza T, et al. Characterization of the apical papilla and its residing stem cells from human immature permanent teeth: a pilot study. J Endod.2008;34(2):166-171.
  25. Vier-Pelisser FV, de Figueiredo JA, Reis Só MV, Estivallet L, Eickhoff SJ. Apical resorption in teeth with periapical lesions: correlation between radiographic diagnosis and SEM examination. Aust Endod J. 2013;39(1):2-7.
  26. Wu D, Ikezawa K, Parker T, Saito M, Narayanan AS. Characterization of a collagenous cementum-derived attachment protein. J Bone Miner Res. 1996;11(5):686-692.

]

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    Pulp Necrosis

    Related terms:

    • Root Canal
    • Dentin
    • Endodontics
    • Periapical Periodontitis
    • Infection
    • Injury
    • Pain
    • Tooth
    • Fracture
    • bacterium

    Learn more about Pulp Necrosis

    Trauma management

    Angus C Cameron , … Sarah Raphael , in Handbook of Pediatric Dentistry (Fourth Edition) , 2013

    Incomplete root apex with a necrotic pulp (Figure 9.26)

    Pulp necrosis is unlikely to occur immediately after trauma that results in a complicated crown fracture. It is more likely to be diagnosed at follow-up examinations. If the pulp of a tooth with a complicated crown fracture becomes necrotic and infected, then removal of the pulp and subsequent root canal treatment is required. Although there is no difference in the prognosis of root canal treatment in immature teeth compared with mature teeth, the long-term survival of a tooth with an open apex may be compromised. This is caused by the thin dentine walls of the root, especially in the cervical third, and a shortened root which make the tooth susceptible to fracture during function or if there is further trauma to the tooth. Endodontic treatment of immature anterior teeth is complicated because of the inability to create an apical seat, the thin dentinal walls, and the difficulty in filling the root canal by traditional methods such as lateral compaction of gutta percha.

    Figure 9.26. (A) Open apex root canal treatment requiring an apexification procedure. (B,C) The long-term prognosis of these teeth is not ideal with some sustaining subsequent root fractures because of inherent weakness in the cervical region.

    Management

    The aim of management is to create an apical hard-tissue barrier against which the root canal filling can be placed. The formation of this apical hard tissue barrier is stimulated by using long-term intra-canal calcium hydroxide dressings (apexification).

    Technique (apexification)

    1.

    Administer local anaesthesia.

    2.

    Place rubber dam – this is mandatory for all root canal treatment.

    3.

    Prepare an access cavity through the palatal or lingual surface of the crown.

    4.

    Remove any necrotic pulp tissue from the canal with a barbed broach.

    5.

    Biomechanically prepare the canal to a level 1 mm short of the radiographic apex.

    6.

    The canal should be carefully instrumented to completely remove necrotic tissue and debris, while also preserving as much tooth structure as possible. The apical root, being very thin, is weak and may fracture if undue pressure is exerted. Very little instrumentation of the canal walls is required.

    7.

    Irrigate thoroughly with 1% sodium hypochlorite to dissolve pulp tissue remnants and to disinfect the root canal system.

    8.

    Ledermix® paste should be placed as the initial dressing followed by calcium hydroxide to create a 50 : 50 mixture of these two medicaments. The mixture is very effective at reducing periapical inflammation, reducing pain and controlling infection within the root canal. The pastes can be inserted into the root canal using a spiral root filler in a low-speed handpiece, run at a very low speed.

    9.

    Place a small pledget of cotton wool in the coronal pulp chamber and then place a temporary restoration in the access cavity using a temporary filling material such as Cavit, or a double-layer temporary restoration using Cavit® and IRM®.

    10.

    After 4–6 weeks, the patient should be reviewed. If there are no symptoms or other problems, then under rubber dam isolation, the temporary filling material should be removed and the canal should be thoroughly irrigated to remove the previous dressing. After drying the canal, it should be re-dressed with a non-setting calcium hydroxide paste.

    11.

    Compress the calcium hydroxide with a cotton wool pellet to ensure good condensation in the canal and to allow contact with the apical tissues. Another temporary restoration should then be placed in the access cavity.

    12.

    Review the child every 3 months and change the calcium hydroxide dressing each time in the manner described above. The formation of an apical hard tissue barrier typically takes about 12 months but it may take up to 18 months. Once the barrier has formed, the canal should be filled with gutta-percha and cement. Root canal filling with gutta-percha is performed using either a warm vertical compaction technique, or lateral compaction. An impression of the apical seat may be made with heat-softened gutta-percha which is then cemented into the canal with a root canal cement. Whichever technique is used, it should be stressed that gentle pressure must be applied to avoid splitting the root or breaking the hard tissue barrier off the root and pushing it into the periapical tissues. Thermoplasticized gutta-percha delivery systems are often invaluable in these cases.

    13.

    Remove the gutta-percha and cement from within the crown part of the tooth. Gutta-percha can be easily removed with a hot instrument and then the remainder should be vertically compacted into the coronal third of the canal while it is still warm. The access cavity should be thoroughly cleaned by wiping it out with cotton pellets soaked in alcohol to remove the root canal cement. This should be repeated 2–3 times to ensure complete removal of the cement in order to avoid discolouration of the tooth.

    14.

    Restore the access cavity with a base of Cavit, followed by a glass ionomer cement to replace dentine and finally composite resin. The Cavit will facilitate any further access to the root canal system should it become necessary in the future.

    In immature teeth, occasionally a small root apex may develop, although the pulp otherwise appears necrotic. This is caused by surviving remnants of Hertwig's epithelial root sheath. Such a situation requires no management or change to the treatment being provided for the tooth.

    Review

    Review 6 months after the root filling has been completed and then annually for at least 5 years to monitor the tooth and the periapical tissues.

    Periapical radiographs at each review.

    Adjacent teeth should also be monitored in the usual manner following trauma.

    Filling an open apex tooth without apexification

    An alternative approach that has been advocated in recent years is the use of a material known as mineral trioxide aggregate (MTA) to fill the apical few millimetres of an open apex tooth without first having to use long-term dressings of calcium hydroxide. Although sometimes called ‘MTA apexification’, it is not an apexification procedure, since an apical hard tissue barrier is not formed prior to root filling the tooth. It is more accurate to consider this procedure as filling an open-ended root canal. MTA is a mixture of tricalcium silicate, dicalcium silicate, tricalcium aluminate, tetracalcium aluminoferrite, calcium sulfate and bismuth oxide. It is chemically very similar to Portland cement and has similar handling and physical properties.

    Initially, the root canal system must be cleaned and disinfected – this can be achieved through the use of irrigating solutions such as sodium hypochlorite and EDTAC, plus the use of an appropriate intra-canal medicament. The medicament chosen will depend on the presenting condition of the pulp or root canal. Ledermix paste may be used if there has been irreversible pulpitis, while either a 50 : 50 mixture of Ledermix paste and calcium hydroxides or just calcium hydroxide alone should be used if the root canal system had been infected.

    Once the canal has been disinfected and dried, the MTA can be placed in the apical few millimetres of the canal. Special instruments and magnification are required to achieve an adequate filling, as it is very technique sensitive and difficult to do. The MTA needs to be left to set for at least several days before the remainder of the canal can then be filled with conventional materials (such as gutta-percha and cement) and techniques (such as lateral compaction).

    It is claimed that this technique reduces the chances of root fractures occurring later since the dentine is not exposed to long-term calcium hydroxide. However, MTA releases calcium hydroxide and therefore the effects of this need further investigation. The other disadvantages of this procedure are the high costs of the material, the need for two appointments to do the root canal filling, the slow setting time and the technical difficulties of placing the material without any of it being pushed into the periapical tissues.

    New methods to manage open apex teeth with pulp necrosis and infection

    An emerging prospect for the management of teeth with incomplete root development where the pulp has necrosed and become infected is the concept of ‘pulp regeneration’ (Figure 9.27). The aim is to achieve revascularization of the root canal system and regeneration of tissue that is capable of producing what radiographically appears to be dentine. To date, several cases have been reported in the literature showing that this is feasible, especially in premolar teeth that had developmental defects such as dens evaginatus. The prospect of using this approach for traumatized teeth with an open apex is being researched and shows promise. Although there are no established guidelines published yet, the initial approach is to:

    Figure 9.27. Pulp revascularization. (A) Haemorrhage is induced into the canal by passing a file through the apex of this immature tooth. (B) Mineral trioxide aggregate (MTA) is placed over the clot at the level of the cemento-enamel junction (CEJ). (C) Periapical radiographs of an open-apex tooth treated with this new technique. Over 3 and 12 months, there has been further development and closure of the root apex.

    1.

    Disinfect the root canal system by using sodium hypochlorite irrigating solution, followed by.

    2.

    Antibiotics as an intracanal dressing. A triple antibiotic paste (ciprofloxacin, metronidazole and minocycline) has been advocated but some authors have reported only using one or two antibiotics.

    3.

    At the next appointment, the antibiotic paste is removed and bleeding is induced in the periapical tissues by instrumenting through the apical foramen with a root canal file. The aim of this is to get blood within the canal which then clots to form a matrix for cell regeneration (Figure 9.27A).

    4.

    Once the clot has formed in the canal, a cement such as MTA is placed in the coronal part of the root canal followed by restoration of the crown of the tooth (Figure 9.27B).

    The tooth should then be reviewed after 6 and 12 months to determine whether there is further root development and hard tissue formation along the canal walls (Figure 9.27C). Research is currently being carried out to determine whether the procedure can be more predictable if stem cells, growth factors, tissue scaffolds or other tissue engineering techniques are used.

    It is important to understand that the above procedures for regeneration are largely based on case reports at present, and guidelines need to be established. Current recommendations are that regenerative procedures in traumatized infected incompletely developed permanent teeth should only be performed if the tooth is not suitable for apexogenesis, or root canal treatment and apexification.

    Read full chapter

    LUXATION INJURIES

    ASGEIR SIGURDSSON , CECILIA BOURGUIGNON , in A Clinical Guide to Dental Traumatology , 2007

    Pulpal

    Potential pulpal sequelae following luxation injuries include pulp necrosis and pulp canal obliteration, each of which occurs in 35% to 40% of all luxated teeth.37,42

    In an 11-year follow-up study of teeth that sustained luxation injuries, Andreasen3 concluded that pulpal healing could be divided into 3 groups according to the degree of injury directed to the pulp: mild, moderate, or severe. A mild injury seldom caused pulp necrosis. A moderate injury typically caused pulp canal obliteration. And a severe injury often provoked pulp necrosis.

    There is usually no need for endodontic treatment in cases of mild injury because the pulp is likely to survive undisturbed. However, in cases in which the canal space begins to calcify, it has been questioned if endodontic treatment is necessary as a “preventive” measure.8,34 Investigations50,51 have evaluated teeth with calcified (obliterated) canal spaces after luxation injuries. They found that just over half of these teeth responded normally to pulp testing at the end of the observation period (7 to 22 years). Furthermore, 40% of these teeth did not show any clinical or radiographic signs of pulp necrosis. When compared with normal intact teeth, there was not a higher frequency of pulp necrosis in teeth with calcified canals, even when these teeth were subjected to subsequent caries, new trauma, orthodontic movement, or crown coverage.8,50 For these reasons, prophylactic endodontic intervention on a routine basis does not seem justified. Also observed in this study of calcified canals was an increased frequency of yellow crown discoloration50 (Fig. 5-18). This was primarily attributed to a lack of translucency caused by the increased thickness of pulp chamber dentin and the fact that tertiary dentin is usually darker in color compared with normal dentin.50 This yellowish discoloration may cause an esthetic problem that external bleaching will not easily correct. Veneers or full coverage crowns are still the most predictable esthetic treatment options for these teeth. If the pulp of the calcified and discolored tooth becomes necrotic, endodontic treatment will be necessary, and the yellowish discoloration can then be improved with internal bleaching.

    Figure 5-18. A, 18-year-old male with a history of severe luxation of maxillary left lateral incisor 10 years previously. The tooth shows a complete pulpal calcification. B, Clinically, the tooth shows a yellowish discoloration of the crown.

    A rare pulpal reaction to trauma is internal root resorption (Fig. 5-19). It has been reported to occur in only about 2% to 3% of all traumatic injuries.10 To properly diagnose this, a minimum of two periapical radiographs are necessary, whereby the radiographs are exposed with varied horizontal angulations (mesial and distal) (Fig. 5-20). If the resorptive defect presents the same radiodensity as the root canal space and stays located in the center of the tooth in both opposite angulations, then it is likely that the defect is internal root resorption. These resorption lesions expand at the expense of the canal and tend to be symmetrically located within the root canal space.6 Histologically the pulp tissue seems to undergo a transformation such that it starts resembling granulation tissue, with giant cells resorbing the internal walls of the root.5 The treatment recommendation is to initiate root canal therapy as soon as possible. Once the blood supply to the main pulpal tissue is removed by the endodontic treatment, the resorptive tissue will cease to proliferate, providing that it has not broken through the lateral walls of the root.

    Figure 5-19. Patient with a history 2 years ago of trauma to the right maxilla. In the lateral incisor, note the extensive intracanal root destruction secondary to internal root resorption.

    Figure 5-20. A and B, Radiographs exposed from two different horizontal angulations aiming to diagnose internal vs. external root resorption. C and D, This resorption is external because the resorptive defect moves in the opposite direction of the cone. E and F, This resorption is internal because the defect remains centered in the root irrespective of the angulation.

    (A and B, Courtesy Dr. C. Barthel.)

    Read full chapter

    The perio–endo interface

    K Gulabivala , … Y-L Ng , in Endodontics (Fourth Edition) , 2014

    Pulpo-periapical inflammation and periodontal wound healing

    Teeth subjected to acute dentoalveolar trauma followed by pulp necrosis exhibit compromised periodontal healing with marginal epithelial down-growth on their roots. Likewise, wound healing after periodontal or apical surgery may also be compromised in the presence of root-canal infection, resulting in attachment loss or recession. Many factors influence this, including gingival tissue thickness (gingival biotype), alveolar bone level, surgical trauma to the flap (or alternatively, the quality of flap protection), effectiveness of flap repositioning and adequacy of suturing. Mean attachment loss after periapical surgery is greater in the absence of periapical healing (being indicative of persistent root-canal infection).

    Some periodontists may request root-canal treatment on teeth with “doubtful” pulp status when regenerative surgery is planned in the site. The rationale is to eliminate possible sources of infection to maximize the potential for successful periodontal outcome. The desire to eliminate potential, unconfirmed root-canal infection must be tempered by the knowledge that extrusion of root-canal treatment materials may have an equally negative impact on periradicular healing (Fig. 12.22) and, therefore, the prognosis of subsequent periodontal surgery. Equally, some periodontists may request root-canal treatment on teeth with “doubtful” pulp status when implant fixture placement is planned in an adjacent site.

    Fig. 12.22. (a) Extrusion of root-filling material in mandibular molar; (b) delayed apical healing associated with the extrusion

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    The restorative–endo interface

    K Gulabivala , Y-L Ng , in Endodontics (Fourth Edition) , 2014

    Relatively intact teeth

    Unrestored anterior teeth may require endodontic treatment because of pulp necrosis caused by traumatic injury (Fig. 14.14), severance of blood supply during surgery (Fig. 14.15), periodontal involvement (Fig. 14.16) or tooth transplantation (Fig. 14.17). Restoration of such teeth would normally be confined to the access cavities (Fig. 14.18) and may be achieved satisfactorily with composite restorative material. In such cases, “reinforcement” of the tooth by placement of a post or dowel remains controversial (Fig. 14.19). The rationale for post placement is based on the belief that the root-treated tooth is inherently weak and that the post would provide a degree of reinforcement by distributing some of the stresses to the root. The scientific support for this is equivocal. It appears that whether a tooth is made more resistant to fracture by placement of a dowel is dependent on the type of loading. It is widely accepted that where a post is not required to aid retention then it should not be placed. If one is placed then it should be at the expense of the minimal amount of tooth tissue. The need for a post is a subjective clinical assessment based on the amount and distribution of remaining dentine after preparation of the tooth for the selected restoration. In Figure 14.20, sufficient dentine cores remained after crown preparation to render post/cores unnecessary whereas, in Figure 14.21, loss of tooth tissue in the three teeth was variable. The gold posts and cores supplemented residual dentine cores. The idea of “reinforcement” has recently been resurrected with the possibility of using adhesive luting cements to bond posts made of materials similar in physical properties to dentine (carbon-fibre or glass-fibre posts). There is, as yet, no long-term clinical evidence to support this concept.

    Fig. 14.14. Pulp necrosis following trauma

    Fig. 14.15. Pulp necrosis caused by orthognathic surgery

    Fig. 14.16. Bone loss around a non-vital mandibular premolar, which has not responded to endodontic treatment – lesion of primary periodontal origin

    Fig. 14.17. Pulp in 3 damaged by transplantation

    Fig. 14.18. Intact teeth requiring root-canal treatment may be restored with composite material

    Fig. 14.19. “Reinforcement” of intact root-filled teeth prepared for crowns is unnecessary

    Fig. 14.20. (a) Adequate dentine cores remaining after crown preparation of root-filled canines render posts or cores unnecessary; (b) buccal view of prepared left canine

    Fig. 14.21. As much tooth tissue should be retained as possible, supplemented with a metal core as necessary

    Previously unrestored, root-treated teeth sometimes require more extensive restoration than simple access filling, for example, if the crown requires realignment or if its discoloration cannot be dealt with by bleaching alone. The most conservative restoration likely to satisfy aesthetic and functional requirements should be selected so as not to weaken the tooth further. Such restorations may include composite or porcelain veneers (Fig. 14.22), with or without tooth preparation, according to the prevailing preoperative condition. The least conservative preparation is for a ceramometal or pure ceramic crown but, even using this design, the tooth should be prepared to review the need for supplementation of retention by a dowel.

    Fig. 14.22. (a) Porcelain veneers – buccal view; (b) porcelain veneers – palatal view

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    ALVEOLAR FRACTURES

    RADHIKA CHIGURUPATI , KENNETH H. DAWSON , in A Clinical Guide to Dental Traumatology , 2007

    ENDODONTIC IMPLICATIONS

    Teeth within the fractured alveolar segment show varied responses to injury, including reversible pulpitis, irreversible pulpitis, canal calcification, pulp necrosis, and root resorption. The most detrimental sequelae to teeth are pulp necrosis and resorption.37 Investigators have evaluated the prognosis of permanent teeth in the line of mandibular fractures.36 They found that pulpal necrosis was more frequent in cases in which the fracture line ran through the apex or when there is a dislocation of the fracture segment. When the alveolar fracture is apical to the root tips or when the apices of teeth are open, the vascular supply to the teeth is less at risk. Another study has also shown that a minor luxation, an intact crown, and immaturity of the root positively influence pulpal and periodontal healing.20

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    Dental anomalies

    Michael J Aldred , … Richard P Widmer , in Handbook of Pediatric Dentistry (Fourth Edition) , 2013

    Dens invaginatus (Figures 11.20, 21)

    Maxillary lateral incisors may have a developmental invagination of the cingulum pit with often only a thin hard-tissue barrier between the oral cavity and the pulp. Pulp necrosis often occurs soon after eruption of the affected tooth and may lead to a canine fossa abscess or cellulitis. This anomaly may occur in other teeth such as the maxillary central incisors and canines.

    Figure 11.20. (A,B) Maxillary canine fossa cellulitis from an infected dens invaginatus. (B) Because of root canal morphology and the severity of the infection the tooth was removed. The patient required hospital admission, with high-dose intravenous antibiotics and surgical drainage of the abscess under general anaesthesia.

    Figure 11.21. (A) Dens invaginatus in a maxillary first premolar tooth. (B) Ultimately, the prognosis is related to the ability to adequately instrument and obturate the canals of these teeth. Temporary endodontic dressings can be placed in such teeth to relieve symptoms and treat infection but it is almost impossible to obturate such canals. (C) Dens evaginatus. (D) Dens evaginatus where the tubercle has fractured off and the tooth has become necrotic. This child presented in acute pain with a facial cellulitis. The radiograph (E) shows the periapical area.

    Alternative terminology

    Invaginated odontome, dens in dente (used to describe the extreme variant, but is a misnomer), dilated odontome.

    Frequency

    Primary dentition~0.1%
    Permanent dentition~4%

    More common in males.

    Management

    If newly erupted, the palatal fissures should be sealed as a preventive measure.

    If caries is evident, then place an acid-etched retained composite resin restoration with minimal preparation.

    If symptomatic and the root canal morphology is favourable, endodontic treatment can be undertaken.

    If the internal anatomy is complex and the root canal is not negotiable then, in the event of infection, extraction is necessary. The presence of this anomaly should be carefully considered during orthodontic treatment planning.

    The same tooth on the opposite side should be carefully assessed for the same problem.

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    Biological and clinical rationale for root-canal treatment and management of its failure

    K Gulabivala , Y-L Ng , in Endodontics (Fourth Edition) , 2014

    Microscopy studies

    Several microscopy surveys (light, dark-field, fluorescent, confocal, TEM and SEM) of teeth have shown the pattern of bacterial invasion and associated pulp necrosis. A “synthesized view” is presented below based on the observations from these studies.

    Bacterial invasion usually begins in the coronal part of the tooth and root and is concentrated there (Fig. 3.30). The distribution from here into the canal system is associated with two factors: the presence or absence of pulp chamber exposure; and the presence or absence of a periapical lesion. As a rule, bacteria are evident lining the canal wall in biofilms, which are discontinuous (covering 30–50% of the surface area) and variable in thickness (Fig. 3.31), with thinner and less coverage in teeth with intact pulp chambers. The biofims may also extend along other surfaces, such as necrosing pulp tissue (Fig. 3.32) and degenerating vascular channels. Bacteria appear in smaller numbers in the root canals as the apical terminus is reached in teeth with intact pulp chambers (Fig. 3.31) but where the pulp chambers are cariously exposed, the canals are more evenly coated with a bacterial plaque. Even then, the plaque is not continuous over the entire surface (Fig. 3.33). In teeth without periapical lesions, vital pulp tissue may be present apically and, if so, the intensity of the infection tapers off towards it (Fig. 3.34). In teeth with periapical lesions, the infection follows one of several courses: in some, the colonization is concentrated in the coronal and middle portions of the root; in others, the colonization is concentrated in the coronal and apical portions (Fig. 3.35); in yet others, the distribution is concentrated in the middle and apical portions. This might suggest a variation in nutritional sources in the canal systems. The patterns confirm the diversity perspective that each infection is unique.

    Fig. 3.30. Bacterial distribution in the coronal part of the tooth and root

    Fig. 3.31. Sparse and discontinuous canal wall coverage with biofilm (red staining) of a tooth with intact pulp chamber and apical periodontitis. Bacterial distribution (in red) as revealed by in situ hybridisation using universal (EUB) and streptococcal (Strep) rRNA probes. Attempts 1 & 2 are separately stained sections

    Fig. 3.32. Bacterial biofilm extending along necrosing pulp tissue. Bacteria (yellow arrow) within necrotic tissue (black arrow) (×40 top and ×100 bottom)

    Fig. 3.33. Canals evenly coated with a discontinuous bacterial plaque in a tooth with exposed pulp and apical periodontitis. Bacterial distribution (in red) as revealed by in situ hybridisation using universal (EUB) and streptococcal (Strep) rRNA probes. Attempts 1 & 2 are separately stained sections

    Fig. 3.34. Vital pulp tissue present in the infected canal of a tooth without periapical lesion. Bacterial distribution (in red) as revealed by in situ hybridisation using universal (EUB) and streptococcal (Strep) rRNA probes. Attempts 1 & 2 are separately stained sections

    Fig. 3.35. Bacterial colonization concentrated in the coronal and apical portions of root canal. Bacterial distribution (in red) as revealed by in situ hybridisation using universal (EUB) and streptococcal (Strep) rRNA probes. Attempts 1 & 2 are separately stained sections

    Microscopy studies can only reveal bacterial morphotypes, so the description is limited (Fig. 3.36). A significantly greater percentage of coccoid and rod forms are noted in the coronal rather than the apical parts of canals, whereas the distribution of motile rods does not differ. In contrast, the percentage of filaments and spirochaetes are slightly higher in the apical than the coronal parts of the canal (Fig. 3.37). A significant correlation is noted between the size of the apical radiolucency and the percentage of spirochaetes present. Occasionally, yeasts or fungi may also be evident, sometimes in the process of budding (Fig. 3.38).

    Fig. 3.36. Different bacterial morphotypes in biofilm seen under TEM

    Fig. 3.37. Greater percentage of filaments and spirochaetes in the apical than the coronal parts of the canal

    Fig. 3.38. Budding yeasts present in infected root canal

    TEM observation of the apical portions (5 mm) of cariously exposed teeth confirms that the bulk of the microbiota exists as a loose collection of a variety of morphologically distinct forms consisting of cocci, rods and filamentous forms (see Fig. 3.13). Nair's first description (1987) was that the bacteria appeared suspended in an apparently moist canal lumen, with less frequent, dense aggregates observed sticking to the dentinal wall of the root canal or existing free among vast numbers of PMNs in the canal lumen. In acute cases, the PMNs can penetrate in vast numbers to line the biofilm on the canal wall and even extend to the coronal part of the canal (Richardson et al., 2009) (Fig. 3.39a,b). At higher magnification, these PMNs can be seen to be actively phagocytosing the intracanal bacteria (Fig. 3.39c).

    Fig. 3.39. PMNs (a = light microscopy, b = SEM) lining the biofilm on the canal wall and (c) actively phagocytosing the intracanal bacteria

    The dense aggregates were described as clusters of morphologically uniform cells. The interbacterial spaces were described as filled with an amorphous extracellular matrix. Independent of these tooth-adhering monobacterial aggregates, the dentinal wall was described as covered by single or multilayered bacterial condensations containing various morphotypes. The filamentous forms were often adherent perpendicular to the canal wall with coccoid forms arranged in strings in the same direction. Cocci occasionally attach to the filaments to give a corncob appearance (Fig. 3.40). Nair modified his interpretation later (personal communication) that the majority of the bacteria were probably in biofilm form.

    Fig. 3.40. Cocci attached to the filaments giving a corncob appearance

    Deposits resembling bacterial plaque are also evident in the apical 2 mm of the root canal. Epithelial cells or a wall of PMNs often plugs the apical canal terminus. In acute cases, there may be a massive apical biofilm filling the entire circumference of the canal (Fig. 3.41). In those cases where the microbial front extends into the periapical lesion, there may be extensive tissue necrosis and acute PMN response. In the latter instance, the chronic granulomatous tissue immediately around the tooth apex may be lysed and occupied by an apparently young apical plaque. SEM or LM views reveal scalloped root resorption (Fig. 3.42) with multilayered bacterial plaque embedded in an extracellular matrix. Such extraradicular extension of bacteria (Fig. 3.43) is, however, rare; one microscopy study showing a prevalence of about 6%.

    Fig. 3.41. Massive apical biofilm filling the entire circumference of the canal of a tooth associated with acute apical periodontitis

    Fig. 3.42. Apical root resorption with multilayered bacterial plaque embedded in an extracellular matrix

    Fig. 3.43. Extraradicular extension of bacteria

    Bacterial penetration into dentine is only evident in the presence of pulp necrosis. Tubule colonization has been shown to be facilitated by the adherence of specific bacteria to the Type 1 collagen present in dentinal tubules (Fig. 3.44). The predentine is easily and commonly infected but the calcified dentine less so. Bacterial penetration into dentine around the root canal is confined to the close proximity of the root canal (Fig. 3.45), where nutrients are available and bacteria are able to grow and multiply (Fig. 3.46). In some teeth, bacteria may be evident penetrating up to a third or a half of the depth of dentinal tubules where they end in a vital periodontal membrane. Only in cases where the tubules end in necrotic periodontal tissue are the bacteria observed along the entire length of the dentinal tubules (Fig. 3.47). Dentine tubule infection is less evident in the apical part because of the sparcity of tubules but may be deeper, particularly in cariously exposed teeth. Cementum is rarely infected except in the presence of extraradicular infection.

    Fig. 3.44. Bacterial cells attached to collagen fibres in dentinal tubules

    Fig. 3.45. (a) Adequate root filling demonstrated on radiograph; (b) periapical surgery and root resection of the tooth shown in (a) (arrowed) shows stained root dentine; (c) resected root showing stained/infected dentine (2.82); (d) histological view of the root end shown in (c), showing infected dentinal tubules (S)

    Fig. 3.46. Bacteria in tubule with evidence of cell division

    Fig. 3.47. Presence of bacterial clusters in the root dentine, slightly coronal to the periapical area shown in Figure 3.12. Note part of the apical plaque is visible peripheral to the cementum (CE) and clusters of bacteria (BA) existing in apparently disintegrating dentinal tubules. Original magnification ×5300; inset ×12 800

    (from Nair, 1987)

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    Cysts

    J. Marley , C.G. Cowan , in Oral and Maxillofacial Surgery (Second Edition) , 2007

    Inflammatory cysts (radicular and residual)

    These are the most common of all jaw cysts and the main issue is to combine the removal of the cyst with eradication of the cause, i.e. the products of pulp necrosis. This may mean either retaining the tooth with a combination of endodontic therapy and surgery or removal of the associated tooth at the time of the enucleation. Residual cysts are treated with enucleation alone. A decision regarding retaining teeth requires careful assessment of all factors, the state of the dentition and periodontal tissues, significance of the loss of the tooth on the dentition and the patient's attitude to treatment. The size of the cyst and the degree of infection will also influence treatment options.

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    Management of pulpal and periradicular disease

    In Restorative Dentistry (Second Edition) , 2007

    PULP DISEASE

    Irritation from any of the sources mentioned above causes some degree of inflammation. The response of the pulp depends on the severity of the insult and the resultant inflammation could be either transient (reversible) or irreversible, eventually proceeding to pulp necrosis.

    There is an inconsistent relationship between clinical symptoms and histological findings in pulpal disease. Diagnoses are therefore usually based on patient symptoms and clinical findings. Pulpal disease may result in changes to both the soft and hard tissues.

    Soft tissue changes

    Reversible pulpitis is a transient condition which may be precipitated by caries, erosion, attrition, abrasion, operative procedures, scaling or mild trauma. The symptoms are usually as follows:

    pain does not linger after the stimulus is removed

    pain is difficult to localise (as the pulp does not contain proprioceptive fibres)

    normal periradicular radiographic appearance

    teeth are not tender to percussion (unless occlusal trauma is present).

    Treatment involves covering up exposed dentine, removing the stimulus or dressing the tooth as appropriate. Reversible pulpitis may progress to an irreversible situation.

    Irreversible pulpitis usually occurs as a result of more severe insults of the type listed above. Typically it may develop as a progression from a reversible state. The symptoms are as follows:

    pain may develop spontaneously or from stimuli

    in the latter stages, heat may be more significant

    response lasts from minutes to hours

    when the periodontal ligament becomes involved, the pain will be localised

    a widened periodontal ligament may be seen radiographically in the later stages.

    Treatment of irreversible pulpitis involves either root canal therapy or extraction of the tooth.

    Hyperplastic pulpitis

    This is a form of irreversible pulpitis otherwise known as a pulp polyp. It occurs as a result of proliferation of chronically inflamed young pulp tissue. Treatment involves root canal therapy or extraction.

    Pulp necrosis

    Pulp necrosis occurs as the end result of irreversible pulpitis and treatment involves root canal therapy or extraction.

    Hard tissue changes

    Pulp calcification

    Physiological secondary dentine is formed after tooth eruption and the completion of root development. It is deposited on the floor and ceiling of the pulp chamber rather than on the walls and, with time, can result in occlusion of the pulp chamber. Tertiary dentine is laid down in response to environmental stimuli as reactionary or reparative dentine. Reactionary dentine is a response to a mild noxious stimuli, whereas reparative dentine is deposited directly beneath the path of injured dentinal tubules as a response to strong noxious stimuli. Treatment is dependent upon the pulpal symptoms.

    Internal resorption

    Occasionally, pulpal inflammation may cause changes that result in dentinoclastic activity. Such changes result in resorption of dentine, and clinically a pink spot may be seen in the later stages if the lesion is coronal. Radiographic examination reveals a punched-out outline that is seen to be continuous with the rest of the pulp cavity. Root canal therapy will result in arrest of the resorptive process, but where destruction is very advanced extraction may be required.

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