Periapical bone healing following endodontic treatment on the right lower premolar :Lydia Tadjudin, Juanita Gunawan, Dina Ratnasari, Scientific Dental Journal

CASE REPORT
Year : 2019 | Volume : 3 | Issue : 2 | Page : 66--69

Periapical bone healing following endodontic treatment on the right lower premolar

Lydia Tadjudin, Juanita Gunawan, Dina Ratnasari
Department of Conservative Dentistry, Faculty of Dentistry, Trisakti University, Jakarta, Indonesia

Correspondence Address:
Dr Dina Ratnasari
Department of Conservative Dentistry, Faculty of Dentistry, Trisakti University, Jakarta
Indonesia

Abstract

Background: Acute exacerbation represents a painful condition whereby the tooth becomes highly sensitive to percussion and bite testing, and it can be aggravated by traumatic occlusion. In general, it results from earlier acute apical periodontitis. Bone destruction can be detected via a radiographic examination, and it can be seen as a radiolucent area at the periapex. Bone resorption is caused by osteoclast activation, which results from pulp inflammation. Nonsurgical endodontic treatment is typically performed to resolve the condition. This study aimed to provide an overview of both the treatment protocol and the role of 2% chlorhexidine gluconate as an endodontic irrigant. Case Report: A 38-year-old woman presented with a major complaint regarding tenderness in her lower second right premolar. The patient reported having experienced similar pain approximately 8 months previously. Clinically, the tooth had lost 50% of its coronal structure, which indicated a Class II cavity. Radiographically, bone resorption was detected in the periapical area of the tooth. An analgesic had been consumed for approximately 3 days. The cavity was cleaned and opened, and working length measurements were performed using an electronic apex locator and conventional radiography. Biomechanical preparation was done using ProTaper NEXTTM files, until size X3. Irrigation was performed using 5.25% sodium hypochlorite at each file change and continued with 17% ethylenediaminetetraacetic acid and 2% chlorhexidine for final irrigation. Sterile Aqua Dest was used for each irrigation change to avoid interaction between irrigants. Obturation was performed by means of warm vertical compaction with an epoxy resin-based sealer. An endocrown composite was recommended for permanent restoration. Four months of follow-up revealed bone regeneration and healing. Conclusion: Bone resorption is a common finding in a diseased tooth, and it stems from the persistent inflammatory process. Osteoclasts are responsible for both bone demineralization and activated pro-inflammatory cytokines. The correct endodontic treatment protocol plays an essential role in periapical bone healing.

How to cite this article:
Tadjudin L, Gunawan J, Ratnasari D. Periapical bone healing following endodontic treatment on the right lower premolar.Sci Dent J 2019;3:66-69

How to cite this URL:
Tadjudin L, Gunawan J, Ratnasari D. Periapical bone healing following endodontic treatment on the right lower premolar. Sci Dent J [serial online] 2019 [cited 2023 Jun 9 ];3:66-69
Available from: https://www.scidentj.com/text.asp?2019/3/2/66/260563

Full Text

Background

Apical periodontitis is an inflammatory condition that affects the apical area of the tooth. It typically manifests radiographically as a radiolucent area in the apical third of the tooth. Patients with acute apical periodontitis complain severe pain when biting, with or without apical radiolucency in the radiograph. If patient has no complaints of pain, but there is an apical radiolucency in the radiograph, it is called chronic apical periodontitis. The etiology of the condition could be an endodontic infection (an acute apical abscess) or a periodontal infection (a periodontal abscess and pericoronitis).[1]

Bacteria can access the apical area of the tooth through various portal entries, including the apical foramen, lateral foramen, or root perforation. Once bacteria reach the periapex, they begin to induce inflammation. This inflammatory process can destroy both healthy and nonhealthy tissues. Acute exacerbation is a painful condition whereby the tooth is highly sensitive to percussion and bite testing, and it can be aggravated by traumatic occlusion. Enterococcus faecalis lipoteichoic acid (EfLTA) plays a major immunostimulatory role in the immune system. Lipoteichoic acid can also bind to dentinal hydroxyapatite at depths of up to 400 μm.[2],[3]

Chlorhexidine has a wide range of antimicrobial activity. Chlorhexidine cannot replace sodium hypochlorite as the main irrigation solution; however, with substantivity effect, it has longer antibacterial properties. It can bind dentine to a depth of 200 μm, and it can remain in dentinal tubules for 7 days. Therefore, the application of 2% chlorhexidine gluconate in root canals may exert a detrimental effect on the EfLTA.[4],[5]

Case Report

A 38-year-old woman presented with a major complaint of tenderness in her lower second right premolar. She had experienced similar pain some 8 months previously. Her prior medical history was not useful. The tooth did not respond to either thermal (cold) testing or the electric pulp testing. Clinically, the tooth had lost 50% of its coronal structure, which indicated a Class II cavity. Radiographically, bone resorption was detected in the periapical area of the tooth. Nonsteroidal anti-inflammatory drugs had been consumed for approximately 3 days. The carious cavity was cleaned, and the endodontic access cavity was opened. One orifice was found. Due to the loss of the coronal structure, an artificial wall was built using nanohybrid composite resin. A rubber dam was placed, and the glide path was secured using K-file number #10 (Dentsply Maifeller, Switzerland). Working length measurements were taken using an electronic apex locator (Root ZX, Morita, Japan) and then confirmed by means of radiography. The canal preparation was performed using the ProTaper Next™ Rotary System (Dentsply Maillefer) until size X3. Adequate preparation is evidenced when healthy dentin, which is usually white in color, is observed in the file flutes. The canal patency was determined after each instrumentation, and apical measurements were taken to re-confirm the apical size of the canal. Irrigation was performed using 5.25% sodium hypochlorite at each file change, with agitation using EndoActivator® (Dentsply) for 1 min. Final irrigation was done using 5.25% NaOCl, 17% ethylenediaminetetraacetic acid (EDTA) with surfactant, and 2% chlorhexidine gluconate. Sterile Aqua Dest was used for each irrigation change to avoid interaction between irrigants. Obturation was performed by means of warm vertical compaction with an epoxy resin-based sealer (AH Plus, Dentsply). An indirect composite endocrown (SR Adoro, Ivoclar Vivadent, Liechtenstein) was recommended for permanent restoration. Four months of follow-up revealed bone regeneration and healing [Figure 1].{Figure 1}

Discussion

Periapical tissues undergo several changes during the development of dental caries. Extensive bacterial invasion involving the pulp can reach the periapex through the apical foramen and its ramification. The build-up of necrotic tissue within the pulp chamber and canals provides the nutrients necessary for pathogenic bacteria to grow and form a periapical lesion. Apical periodontitis is typically the host response to a localized bacterial invasion.[6] In response to the injury, chemotaxis occurs and initiates inflammation. Immune cells, such as macrophages, leukocytes, and lymphocytes, enter the inflammation site, and the phagocytosis of bacteria and foreign bodies occurs.[7] Inflammation also causes the release of pro-inflammatory cytokines, including interleukin (IL) IL1, IL6, IL7, and tumor necrosis factor-alpha (TNF-α). IL6 and TNF-α represent the major cytokines that cause bone resorption by means of osteoclast activation. Bone resorption manifests as a radiolucent area upon radiographic examination. Furthermore, as a result of these inflammation sequelae, a persistent bacterial infection may contribute to acute exacerbation. This chronic bacterial infection may trigger the host's immune system, and once the host's immunity decreases, the virulence of the bacteria increases, which induces pain.[3],[6]

Endodontic treatment is intended to clean and shape the root canal system. Adequate cleaning and shaping can be performed through good irrigation and instrumentation. The chemomechanical preparation should result in a root canal system that is completely clean and disinfected, thereby leaving the root canal at the minimal bacterial stage.[7] To achieve endodontic success, the debridement of the root canal system is essential. One of the many obstacles encountered during endodontic instrumentation is the smear layer, which consists of organic and inorganic substances, fragments of odontoblastic processes, microorganisms, and necrotic materials stemming from root canal formation. The smear layer prevents the penetration of both intracanal irrigation solutions and sealers into the dentinal tubules, which may result in compromised seals following root filling.[8] NaOCl is considered to be the “gold standard” irrigation solution in the field of endodontics due to its ability to dissolve organic components and its antibacterial effect. EDTA and a calcium-chelating agent are commonly used for the removal of smear layer.[9] In this case, it was considered mandatory to use 2% chlorhexidine gluconate solution due to its dentinal substantivity and its broad spectrum of antibacterial properties. Prior studies have revealed that chlorhexidine acts as a slow-release antibacterial agent in the root canal system. It continues to be released for 48–72 h following its introduction into the root canal, and it maintains an antibacterial effect for 7 days. The use of 2% chlorhexidine gluconate hence instills greater and long-lasting antimicrobial activity.[9]

Irrigation can be delivered and activated in various ways. Studies have shown that the EndoActivator performed significantly better than no activation of the irrigant at both 5 mm and 8 mm from the apex, while there was a significant increase in smear layer removal when compared to passive ultrasonic irrigation at 3 mm from the apex. Further, the study showed significantly greater smear layer removal when the EndoActivator was used instead of ultrasonic agitation and a canal brush.[8],[10]

Bone healing begins as soon as inflammation starts. When irritants and bacteria have been successfully removed from the canal system by means of endodontic therapy, inflammatory mediators are no longer produced in the periapical tissues. Initially, bone healing follows the same general principle as the healing of connective tissues elsewhere in the body, including the formation of fibrovascular granulation tissue and the removal of necrotic tissue and dead bacteria by activated macrophages.[11] In addition, during periapical healing, the cells of the viable periodontal ligament stemming from the adjacent root surfaces proliferate to cover the root surfaces on which the periodontal ligament was damaged by apical periodontitis and then removed by macrophages. Proteins from Hertwig's epithelial root sheath are required for cementoblast differentiation. Moreover, the osteoblasts or mesenchymal cells lining the surfaces of the endosteum are stimulated by the transforming growth factor beta (TGF-β), bone morphogenetic proteins (BMPs), insulin-like growth factor (IFGs), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and cytokines released by the stromal cells, osteoblasts, platelets, and bone matrix following bone resorption. This can lead to bone matrix production. When one of the cortical bone plates (buccal or lingual/palatal) is destroyed, the mesenchymal cells in the inner periosteal layer of the periosteum under the oral mucosa are stimulated by the TGF-β, BMPs, IGFs, PDGF, and VEGF.[12] The healing time varies, and it can range from 3 months to 4 years. The assessment of periapical healing is performed using plain radiographs or cone-beam computed tomography.[13]

The prognosis of the patient's tooth is good. Adequate coronal and apical sealing are required to ensure that there is no bacterial reinfection. Coronal sealing can be performed by means of fabrication of an indirect composite endocrown. An endocrown was chosen due to its minimally invasive preparation and its ability to provide full cuspal coverage.[14]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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