: 2022  |  Volume : 34  |  Issue : 2  |  Page : 71--72

Endodontic therapy: Stop ringing the alarm; it is time to get out of the building!

Anil Kishen 
 Professor, Endodontics Program, Faculty of Dentistry, University of Toronto; Principal Investigator, Dental Research Institute; Associate Scientist, Mount Sinai Hospital, Toronto, ON, Canada

Correspondence Address:
Prof. Anil Kishen
Faculty of Dentistry, University of Toronto, Toronto, ON

How to cite this article:
Kishen A. Endodontic therapy: Stop ringing the alarm; it is time to get out of the building!.Endodontology 2022;34:71-72

How to cite this URL:
Kishen A. Endodontic therapy: Stop ringing the alarm; it is time to get out of the building!. Endodontology [serial online] 2022 [cited 2022 Oct 6 ];34:71-72
Available from: https://www.endodontologyonweb.org/text.asp?2022/34/2/71/349569

Full Text

The immune response is a biological network responsible for protecting the host tissue from external irritants and maintaining homeostasis.[1] The process of inflammation comprises of various cells from the innate and adaptive arms of the immune system, collectively orchestrating a host response to irritants. In apical periodontitis, the presence of intraradicular microbes stimulates immune cells to secrete proinflammatory mediators and cytokines into the inflamed tissue.[2] If the inflammatory stimulant lingers, the persistent recruitment of innate and adaptive immune cells and production of proinflammatory mediators results in undesirable tissue damage.[3] The pattern of posttreatment periapical host response will be influenced by local tissue-related factors and residual microbial burden in proximity to the apical foramen. Such cytokine-mediated immune regulation may result in low-grade systemic inflammation, which is considered the fundamental mechanism linking periapical lesions with metabolic disorders as well as their complications.[4]

Symptomatic apical periodontitis has been suggested to be an immunologically active disease state resulting from upregulated proinflammatory cytokines such as tumor necrosis factor-α and interleukin-1 β.[5],[6] These proinflammatory cytokines affect RANKL/OPG balance, resulting in bone resorption characteristic of apical periodontitis.[7] Studies have also reported that the levels of proinflammatory cytokines are not significantly different between symptomatic and asymptomatic apical periodontitis.[8],[9] Immune cells also secrete tissue-degrading factors, such as MMPs, which dominant in active lesions, whereas the expression of tissue inhibitors of MMPs dominates in asymptomatic lesions.[10] The interplay between eliminating microbial biofilm and limiting damage to periapical tissues is an immunological conundrum in apical periodontitis.

The principles of endodontic therapy are based on eliminating intraradicular microbial biofilms to a feasible level, followed by blocking off major portals of communication between the canal lumen and periodontal tissue. Periapical radiographs are the commonly employed method to assess the treatment effectiveness. However, the practice of judging endodontic treatment outcomes on the basis of periapical radiographs may be inadequate to provide the answers to some of the following questions: Are bacteria still persisting in the apical root canal? What is the posttreatment cellular response at the tissue level? What is the predicted posttreatment healing time for the case? Furthermore, if apical periodontitis is a significant disease in terms of local and systemic risks – are patient-based outcomes such as tooth survival adequate? These questions cannot be ignored since the prevalence of posttreatment apical periodontitis has been increasing in spite of the considerable progress in endodontic treatment techniques.[11]

The nature of the posttreatment immune response is regulated by the signaling cues and microenvironment in the periapical region. Therefore, it is logical for the specialty to focus on modulating the immune, or the healing response over newer strategies to agitate sodium hypochlorite within the root canal. The advantage of using newer antimicrobials should also be carefully gauged. The future objectives should be to develop local immune modulators that up-regulate or down-regulate immune pathways and to achieve predictable and rapid periapical healing.[12] The main goal of immune modulation is to regulate the immune system to recruit principal players to secrete pro-regenerative cytokines and growth factors, while depositing a pro-reparative matrix, thus creating a microenvironment conducive to healing.[13] Moreover, sequential delivery of proinflammatory and anti-inflammatory molecules to exert more comprehensive control over tissue healing will also be beneficial. In nanoparticle-enabled immunomodulation, manipulating the particles' size and physicochemical characteristics can influence their interaction with the immune cells to induce desired therapeutic benefits.[14],[15]

The current endodontic treatment procedures are considered safe, effective, and evidence-based to prevent and heal apical periodontitis and manage its associated risks. However, the clinical specialty of endodontics focussing on maintaining healthy and functional natural dentition in patients must not be complacent in this era of scientific rigor and molecular immunology. In the context of managing microbial-mediated inflammation, immunomodulation is a key approach to achieving predictable, rapid, and stable form of post-treatment healing.[16] This strategy warrants more investigations for clinical translation in endodontic therapy.


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