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      A comprehensive in vitro comparison of the biological and physicochemical properties of bioactive root canal sealers

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          Abstract

          Objectives

          To evaluate the biological and physicochemical features of bioactive root canal sealers.

          Materials and methods

          Human periodontal ligament fibroblasts (hPDLF) and human osteoblasts (hOB) were exposed to eluates of three bioactive root canal sealers, GuttaFlow® bioseal (GF), BioRoot™ RCS (BR), and TotalFill® BC Sealer (TF), and the epoxy resin–based sealer AH plus® (AH). Cytotoxicity and cellular inflammatory response were evaluated. The osteogenic potential was examined using human mesenchymal stem cells (hMSC). Film thickness, flowability, and pH were assessed. Root canal treatment was performed on human extracted teeth to evaluate the sealers’ tightness towards bacterial penetration. The antibacterial activity against common pathogens in primary root canal infections was tested.

          Results

          AH was severely cytotoxic to hPDLF and hOB ( p < 0.001). The bioactive sealers were generally less cytotoxic. IL-6 levels in hPDLF were elevated in the presence of AH ( p < 0.05). AH and GF suppressed IL-6 production in hOB ( p < 0.05). AH and BR stimulated the PGE 2 production in hPDLF and hOB ( p < 0.05). BR was the only sealer that led to calcium deposits in hMSC ( p < 0.05). TF and AH showed the lowest film thickness and the highest flowability. Bacterial tightness was best in teeth filled with AH and BR. All sealers showed similar antimicrobial activity, but the overall antimicrobial efficacy was moderate as the bacteria were reduced by just one log scale ( p < 0.05).

          Conclusions

          This study revealed favorable in vitro results regarding the biocompatibility of the bioactive root canal sealers.

          Clinical relevance

          Bioactive root canal sealers may be a useful alternative to epoxy resin–based sealers.

          Supplementary Information

          The online version contains supplementary material available at 10.1007/s00784-022-04570-2.

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          Most cited references51

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          Apoptosis: a review of programmed cell death.

          Susan A. Elmore (2007)
          The process of programmed cell death, or apoptosis, is generally characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms. Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death. Inappropriate apoptosis (either too little or too much) is a factor in many human conditions including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types of cancer. The ability to modulate the life or death of a cell is recognized for its immense therapeutic potential. Therefore, research continues to focus on the elucidation and analysis of the cell cycle machinery and signaling pathways that control cell cycle arrest and apoptosis. To that end, the field of apoptosis research has been moving forward at an alarmingly rapid rate. Although many of the key apoptotic proteins have been identified, the molecular mechanisms of action or inaction of these proteins remain to be elucidated. The goal of this review is to provide a general overview of current knowledge on the process of apoptosis including morphology, biochemistry, the role of apoptosis in health and disease, detection methods, as well as a discussion of potential alternative forms of apoptosis.
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            IL-6 in inflammation, immunity, and disease.

            Toshio Tanaka, Masashi Narazaki, Tadamitsu Kishimoto (2014)
            Interleukin 6 (IL-6), promptly and transiently produced in response to infections and tissue injuries, contributes to host defense through the stimulation of acute phase responses, hematopoiesis, and immune reactions. Although its expression is strictly controlled by transcriptional and posttranscriptional mechanisms, dysregulated continual synthesis of IL-6 plays a pathological effect on chronic inflammation and autoimmunity. For this reason, tocilizumab, a humanized anti-IL-6 receptor antibody was developed. Various clinical trials have since shown the exceptional efficacy of tocilizumab, which resulted in its approval for the treatment of rheumatoid arthritis and juvenile idiopathic arthritis. Moreover, tocilizumab is expected to be effective for other intractable immune-mediated diseases. In this context, the mechanism for the continual synthesis of IL-6 needs to be elucidated to facilitate the development of more specific therapeutic approaches and analysis of the pathogenesis of specific diseases.
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              Regulation of immune responses by prostaglandin E2.

              Pawel Kalinski (2012)
              PGE(2), an essential homeostatic factor, is also a key mediator of immunopathology in chronic infections and cancer. The impact of PGE(2) reflects the balance between its cyclooxygenase 2-regulated synthesis and 15-hydroxyprostaglandin dehydrogenase-driven degradation and the pattern of expression of PGE(2) receptors. PGE(2) enhances its own production but suppresses acute inflammatory mediators, resulting in its predominance at late/chronic stages of immunity. PGE(2) supports activation of dendritic cells but suppresses their ability to attract naive, memory, and effector T cells. PGE(2) selectively suppresses effector functions of macrophages and neutrophils and the Th1-, CTL-, and NK cell-mediated type 1 immunity, but it promotes Th2, Th17, and regulatory T cell responses. PGE(2) modulates chemokine production, inhibiting the attraction of proinflammatory cells while enhancing local accumulation of regulatory T cells cells and myeloid-derived suppressor cells. Targeting the production, degradation, and responsiveness to PGE(2) provides tools to modulate the patterns of immunity in a wide range of diseases, from autoimmunity to cancer.
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                Author and article information

                Contributors
                Sabina Noreen Wuersching:
                ORCID: http://orcid.org/0000-0001-6565-7255
                sabina.wuersching@med.uni-muenchen.de
                Journal
                Journal ID (nlm-ta): Clin Oral Investig
                Journal ID (iso-abbrev): Clin Oral Investig
                Title: Clinical Oral Investigations
                Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )
                ISSN (Print): 1432-6981
                ISSN (Electronic): 1436-3771
                Publication date (Electronic): 3 June 2022
                Publication date PMC-release: 3 June 2022
                Publication date (Print): 2022
                Volume: 26
                Issue: 10
                Pages: 6209-6222
                Affiliations
                GRID grid.5252.0, ISNI 0000 0004 1936 973X, Department of Conservative Dentistry and Periodontology, , University Hospital, LMU Munich, ; Goethestrasse 70, 80336 Munich, Germany
                Author information
                http://orcid.org/0000-0001-6565-7255
                Article
                Publisher ID: 4570
                DOI: 10.1007/s00784-022-04570-2
                PMC ID: 9525420
                PubMed ID: 35660956
                SO-VID: 2fd3434f-898b-4216-b898-e5cc0f8851b7
                Copyright © © The Author(s) 2022
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 28 February 2022
                Date accepted : 29 May 2022
                Funding
                Funded by: Verein zur Förderung der wissenschaftlichen Zahnheilkunde in Bayern e.V.
                Award ID: Annual research grant 2020
                Award Recipient :
                Funded by: Universitätsklinik München (6933)
                Open Access :

                Open Access funding enabled and organized by Projekt DEAL.

                Categories
                Subject: Original Article
                Custom metadata
                issue-copyright-statement © Springer-Verlag GmbH Germany, part of Springer Nature 2022

                ScienceOpen disciplines: Dentistry
                Keywords: antimicrobial properties,apical periodontitis,bioactivity,cytotoxicity,physicochemical properties,root canal sealer
                Data availability:
                ScienceOpen disciplines: Dentistry
                Keywords: antimicrobial properties, apical periodontitis, bioactivity, cytotoxicity, physicochemical properties, root canal sealer

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