• Users Online: 234
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
GUEST EDITORIAL
Year : 2022  |  Volume : 34  |  Issue : 2  |  Page : 71-72

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


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

Date of Submission15-Jun-2022
Date of Decision17-Jun-2022
Date of Acceptance21-Jun-2022
Date of Web Publication01-Jul-2022

Correspondence Address:
Prof. Anil Kishen
Faculty of Dentistry, University of Toronto, Toronto, ON
Canada
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/endo.endo_159_22

Rights and Permissions

How to cite this article:
Kishen A. Endodontic therapy: Stop ringing the alarm; it is time to get out of the building!. Endodontology 2022;34:71-2

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 Aug 17];34:71-2. Available from: https://www.endodontologyonweb.org/text.asp?2022/34/2/71/349569



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.



 
  References Top

1.
Mariani E, Lisignoli G, Borzì RM, Pulsatelli L. Biomaterials: Foreign bodies or tuners for the immune response? Int J Mol Sci 2019;20:636.  Back to cited text no. 1
    
2.
Arango Duque G, Descoteaux A. Macrophage cytokines: Involvement in immunity and infectious diseases. Front Immunol 2014;5:491.  Back to cited text no. 2
    
3.
Meirow Y, Baniyash M. Immune biomarkers for chronic inflammation related complications in non-cancerous and cancerous diseases. Cancer Immunol Immunother 2017;66:1089-101.  Back to cited text no. 3
    
4.
Sasaki H, Hirai K, Martins CM, Furusho H, Battaglino R, Hashimoto K. Interrelationship between periapical lesion and systemic metabolic disorders. Curr Pharm Des 2016;22:2204-15.  Back to cited text no. 4
    
5.
Gazivoda D, Dzopalic T, Bozic B, Tatomirovic Z, Brkic Z, Colic M. Production of proinflammatory and immunoregulatory cytokines by inflammatory cells from periapical lesions in culture. J Oral Pathol Med 2009;38:605-11.  Back to cited text no. 5
    
6.
Jakovljevic A, Knezevic A, Karalic D, Soldatovic I, Popovic B, Milasin J, et al. Pro-inflammatory cytokine levels in human apical periodontitis: Correlation with clinical and histological findings. Aust Endod J 2015;41:72-7.  Back to cited text no. 6
    
7.
Graves DT, Oates T, Garlet GP. Review of osteoimmunology and the host response in endodontic and periodontal lesions. J Oral Microbiol 2011;3:10.3402/jom.v3i0.5304.  Back to cited text no. 7
    
8.
Matsuo T, Ebisu S, Nakanishi T, Yonemura K, Harada Y, Okada H. Interleukin-1 alpha and interleukin-1 beta periapical exudates of infected root canals: Correlations with the clinical findings of the involved teeth. J Endod 1994;20:432-5.  Back to cited text no. 8
    
9.
Lim GC, Torabinejad M, Kettering J, Linkhardt TA, Finkelman RD. Interleukin 1-beta in symptomatic and asymptomatic human periradicular lesions. J Endod 1994;20:225-7.  Back to cited text no. 9
    
10.
Letra A, Ghaneh G, Zhao M, Ray H Jr, Francisconi CF, Garlet GP, et al. MMP-7 and TIMP-1, new targets in predicting poor wound healing in apical periodontitis. J Endod 2013;39:1141-6.  Back to cited text no. 10
    
11.
Jakovljevic A, Nikolic N, Jacimovic J, Pavlovic O, Milicic B, Beljic-Ivanovic K, et al. Prevalence of apical periodontitis and conventional nonsurgical root canal treatment in general adult population: An updated systematic review and meta-analysis of cross-sectional studies published between 2012 and 2020. J Endod 2020;46:1371-86.e8.  Back to cited text no. 11
    
12.
Ruh C, Banjade R, Mandadi S, Marr C, Sumon Z, Crane JK. Immunomodulatory effects of antimicrobial drugs. Immunol Invest 2017;46:847-63.  Back to cited text no. 12
    
13.
Liu Y, Segura T. Biomaterials-mediated regulation of macrophage cell fate. Front Bioeng Biotechnol 2020;8:609297.  Back to cited text no. 13
    
14.
Zolnik BS, González-Fernández A, Sadrieh N, Dobrovolskaia MA. Nanoparticles and the immune system. Endocrinology 2010;151:458-65.  Back to cited text no. 14
    
15.
Hussein H, Kishen A. Proteomic profiling reveals engineered chitosan nanoparticles mediated cellular crosstalk and immunomodulation for therapeutic application in apical periodontitis. Bioact Mater 2022;11:77-89.  Back to cited text no. 15
    
16.
Hussein H, Kishen A. Local immunomodulatory effects of intracanal medications in apical periodontitis. J Endod 2022;48:430-56.  Back to cited text no. 16
    




 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
References

 Article Access Statistics
    Viewed865    
    Printed18    
    Emailed0    
    PDF Downloaded241    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]