Roberto Gustavo Sánchez-Lara y Tajonar1*, Itzel Athziry Carre Espinoza2 and Ángel Daniel Gutiérrez Dávila3
Received: April 18, 2023; Published: April 28, 2023
*Corresponding author: Roberto Gustavo Sánchez-Lara y Tajonar, Resident of department of Endodontics, Faculty of Medicine, Universidad Autónoma de Querétaro, Santiago de Querétaro 76176, Mexico
DOI: 10.26717/BJSTR.2023.50.007898
The objectives of endodontics are the prevention and cure of periapical disease (Apical Periodontitis); which is achieved by cleaning and disinfection of the root canal system and subsequent obturation of root spaces by filling with inert materials, avoiding reinfection and persistent inflammation [1]. The purpose of the treatment is no longer the preservation of the pulp, but the prevention and/or cure of apical periodontitis [2]. Apical periodontitis is an inflammatory disease of the periapical tissues in the presence of bacteria inside the root canals. It has been solidly demonstrated that bacteria inside the canals are the main etiological factor of apical periodontitis [3-7]. It has recently become relevant that the microbial communities attached to the dentin walls or biofilm induce the pathobiology of apical periodontitis and are the cause of post-treatment disease [7-13]. Filling the canal space to working length has been a fundamental component of root canal treatment to seal and isolate the periapical tissues from biofilm and irritants remaining after confirmation and cleaning as well as to eliminate the possibility of further contamination. Several authors have shown that the quality of the root canal filling contributes significantly to the success of endodontic treatment [14-18].
The lateral canals of the main root canal are formed after localized fragmentation of Hertwig’s epithelial sheath occurs during the process of root maturation, leaving a small space, or when blood vessels persist from the dental sac through the dental papilla. Dentinogenesis does not occur in this specific area, resulting in a canal containing small blood vessels and sometimes nerves. Although the branches contain connective tissue and blood vessels, this is not usually considered a collateral blood supply and therefore contributes little, if anything, to pulpal function [19]. Lateral canals comprise potential pathways through which bacteria and/or their products from the necrotic root canal could reach the periodontal ligament and cause disease, and likewise, bacteria from periodontal pockets could reach the pulp. Lateral canals are difficult to reach, clean, disinfect and obturate during treatment. Their potential clinical importance has long drawn the attention of clinicians and researchers as to how and whether these branches should be addressed and what is the fate of the tissue present in them after treatment [19]. According to our evidence, even if there are lateral canals where periradicular lesions have developed, if the main canal is well obturated, these apical periodontitis repair by instrumenting and obturating the main canal, without the need for these lateral canal spaces to be filled with gutta-percha.
A 30-year-old female patient presented for consultation on November 15, 2004, with a diagnosis of symptomatic apical periodontitis, previous failed treatment of dental organ (OD) 21 (Figure 1).
Clinical Procedure
Endodontic retreatment was performed in an appointment on November 30, 2004. The patient was anesthetized with articaine-epinephrine 1/200.000 (Septodont), then the tooth was isolated with a 6” X 6” Hygenic rubber dam and Hu-friedy staples, disinfection of the operative field with cotton swab and 2.5% sodium hypochlorite. The access was made with a high speed carbide ball bur 4 and 6; once the access was made, 2 drops of 10% Carbamide Peroxide were placed in the cavity. The canal was deobturated with Peeso #2 and #3 drills, irrigated with 2.5% sodium hypochlorite (1.8ml) and used Root ZXII apical locator (Morita). The instrumentation was carried out with “crown-apical” technique and Protaper rotary system (Dentsply Maillefer) of 25mm at 350 rpm. The instrumentation started with S1-S2 and Sx, passively irrigated with 2.5% sodium hypochlorite (1.8ml) and corroborated working length with RootZx II apical locator (Morita). Instrumentation was continued with F1,F2 with Protaper (Dentsply Maillefer) at 350rpm and passively irrigated with 2.5% Sodium Hypochlorite (1.8ml) and corroborated working length with a K-File no. 10 file (Dentsply Maillefer). 10 (Dentsply Maillefer) and RootZx II apical locator (Morita), completed instrumentation with F3,F4 with Protaper rotary system (Dentsply Maillefer) at 350rpm and passively irrigated with Sodium Hypochlorite 2.5% (3.6ml) and corroborated working length with RootZx II apical locator (Morita) and K-File no. 10 (Dentsply Maillefer).
When the instrumentation was completed, 3.6ml of physiological solution was irrigated, the canal was dried with paper tips (Hygenic) and the working length was corroborated with a master apical file and RootZx II (Morita). EDTA 17% (Roth International LTD) was placed in the cavity for one minute and the apical foramen was patented with K-File no. 10 (Dentsply Maillefer) and irrigated with Sodium Hypochlorite 2.5% (3.6ml) and the canal was dried with paper tips (Hygenic). The obturation was performed with gutta percha tips (Hygenic), zinc oxide and eugenol based sealer cement (Silco) and lateral condensation technique. The cement was taken to the canal with lentulus (Dentsply Maillefer) at 200rpm, gutta-percha tip (Hygenic) was adjusted to working length and obturated with MA57 spacer (Hu- Friedy), the excess gutta- percha was cut (Figure 2).
1st Control Appointment
July 29, 2005 (8 months).
Clinical Evaluation
Patient is asymptomatic, absence of signs of inflammation, absence of sinus tract and optimal sealing.
Radiographic Evaluation
Reduction of the apical and lateral lesion is observed. Reduction of the cementum of the apical PUFF is observed (Figure 3).
Second Follow-Up Appointment
September 2, 2020 (15 years).
Clinical Evaluation
Patient is asymptomatic, absence of signs of inflammation, absence of sinus tract and optimal seal.
Radiographic Evaluation
Healthy periodontal ligament is observed on the entire surface of the DO, resorption of the cementum of the apical PUFF (Figure 4).
3rd Follow-up Appointment
March 24, 2023 (18 years).
Clinical Evaluation
Patient is asymptomatic,absence of signs of inflammation, absence of sinus tract and optimal seal.
Radiographic Evaluation
Healthy periodontal ligament is observed on the apical surface of the root canal, resorption of the cementum of the apical PUFF. Restoration of the root canal with fiberglass post and crown is observed, the fiberglass post ends at the level of the lateral canal. Recurrence of periradicular lesion is observed at the level of the lateral canal in the mesial zone of the root canal caused by bacterial filtration via coronal (red circle) (Figure 5).
Apical cement extrusion has long been a source of controversy in endodontics [20]. Biological principles of obturation dictate that overfilling can lead to chronic inflammation, as cementum is a foreign material that is often cytotoxic before setting [21].Goldberg et al. found that unintentional overfilling of the canal by lateral condensation and various epoxy and zinc oxide sealants with an evolution time of 4.86 years did not have a statistically significant impact on the results [22]. Similarly, Ricucci et al. also concluded that in cases where cement was extruded apically by lateral condensation with epoxy and zinc oxide cements after four years of evolution did not produce statistically significant differences in the results, even when the extruded cement was still present radiographically. They concluded that the main determinant of outcome was the presence of a preoperative periapical lesion, which is consistent with most of the accepted endodontic evidence [23].
Ricucci mentions that histopathological and histobacteriological observations of untreated teeth revealed that the tissue conditions within the lateral canals reflect the conditions of the pulp in the main canal. In turn, observations of treated teeth allowed some practical conclusions to be drawn: such as that the material that appears radiographically in the lateral canals and apical branches was forced into these areas, but this in no way indicates that the branch is sealed or disinfected; and that because bacteria located in large branches could reach sufficient numbers to cause or maintain disease, strategies other than finding a technique that best penetrates the sealer or gutta-percha into the branches and lateral canals to optimize the treatment outcome [19]. Weine, in the chapter The lateral canal enigma in North American clinics, published in 1984, mentions that the only condition for a lateral canal to generate an endodontic failure is to leave an empty space for a post that is associated with the presence at that level of a lateral canal, that is, an empty space of gutta-percha from the obturation of the main canal [24]. Even if there are lateral canals, if the main canal is well obturated, the evidence shows that without these lateral canals being occupied with gutta-percha and even if there are periradicular lesions associated with them, these repair when the main canal is properly instrumented and obturated. The authors believe that even if there is no gutta percha void, but the main canal is occupied by an intraradicular post, which has been sealed with self-curing resin, there is a high risk of endodontic failure in the sense that coronal microleakage reaches the lateral canal [25,26].
The main etiology of apical periodontitis and endodontic failure associated with periapical pathology is the presence of bacteria in the root canal system. There has always been controversy about the impact on the prognosis of endodontic treatment of lateral canals, so in the present case it can be demonstrated, thanks to the evidence of clinical controls, that obturation of the main canal leads to a resolution of periapical and periradicular pathology at the level of the middle third of the root canal associated with the lateral canal, This can be interpreted as one of the possible reasons for the failure of the first treatment, since when retreatment of the canal was performed, remission of the lesion was achieved, showing great changes after 8 months, having periodontal health at the 15-year control, however, when the main canal was obturated for prosthetic reasons, periradicular periodontitis at the level of the lateral canal returned.