Can Apical Periodontitis Exacerbate Covid-19 Damage?

Introduction: The microorganisms own different resistance mechanisms that allow them to resist the chemo-mechanical cleanliness of root canal and antibiotic therapies causing the persistence of apical lesions. Methods: This clinical case describes a male patient diagnosed with pulp necrosis in the right lower central incisor due to trauma, which developed apical periodontitis manifesting itself extra orally. Root canal treatment along with antibiotic therapy was performed, but because the infectious process persisted, endodontic retreatment and a new antibiotic therapy were carried out, however, the clinical evolution was not favorable. For this reason, the intentional replantation was chosen as the outright treatment, performing apicectomy and curettage of the periapical lesion, from which the isolation and taxonomic study of microorganisms were carried out, with the respective antibiogram. Results: In the 10-day clinical follow-up, the extraoral infectious process disappeared almost completely and 6 months later, a complete repair of the bone tissue was observed on the tomography. Conclusion: A better understanding of the persistence of apical periodontitis was achieved by taxonomic identification of bacteria and the intentional replantation allowed to remove the apical biofilm gaining an excellent wound healing.

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Association between Systemic Diseases and Apical Periodontitis―A Review

Indian Journal of Public Health Research & Development ◽

10.37506/v10/i12/2019/ijphrd/192323 ◽

2019 ◽

Vol 10 (12) ◽

pp. 2177

Author(s):

Wesly Sophreniaa ◽

Arumugam Karthick ◽

Nagarajan Geethapriya ◽

Arunajatesan Subbiya

Keyword(s):

Apical Periodontitis ◽

Systemic Diseases

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Does the Endodontic Education Level Affect Decision-Making for Endodontically Treated Teeth With Apical Periodontitis? A Web-Based Survey

International Dental Journal ◽

10.1016/j.identj.2021.01.003 ◽

2021 ◽

Author(s):

Betul Aycan Alim-Uysal ◽

Asiye Nur Dincer ◽

Berkan Yurtgezen ◽

Mehmet Burak Guneser

Keyword(s):

Decision Making ◽

Education Level ◽

Apical Periodontitis ◽

Endodontically Treated Teeth ◽

Web Based

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An experimental intraradicular biofilm model in the pig for evaluating irrigation techniques

BMC Oral Health ◽

10.1186/s12903-021-01536-w ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Toshinori Tanaka ◽

Yoshio Yahata ◽

Keisuke Handa ◽

Suresh V. Venkataiah ◽

Mary M. Njuguna ◽

...

Keyword(s):

16S Rrna ◽

Root Canal ◽

Apical Periodontitis ◽

Exposure Model ◽

Rrna Gene ◽

16S Rrna Sequence ◽

Bacterial Phyla ◽

Biofilm Model ◽

Biofilm Removal

Abstract Background We established an in vivo intraradicular biofilm model of apical periodontitis in pigs in which we compared the efficacy of different irrigant activation techniques for biofilm removal. Methods Twenty roots from the deciduous mandibular second premolar of 5 male pigs were used. After pulpectomy, canals were left open for 2 weeks and then sealed for 4 weeks to enable the development of an intracanal biofilm. The intraradicular biofilms was evaluated using SEM and bacterial 16S rRNA gene-sequencing. To investigate the efficacy of biofilm removal, root canal irrigations were performed using conventional needle, passive ultrasonic, subsonic, or laser-activated irrigation. Real-time PCR was conducted to quantitate the remaining biofilm components. Statistical analysis was performed using ANOVA followed by a Tukey kramer post-hoc test with α = 0.05. Results The pulp exposure model was effective in inducing apical periodontitis and SEM analysis revealed a multi-layer biofilm formation inside the root canal. 16S rRNA sequence analysis identified Firmicutes, Bacteroidetes, and Fusobacteria as the predominant bacterial phyla components, which is similar to the microbiome profile seen in humans. None of the tested irrigation techniques completely eradicated the biofilm components from the root canal, but the subsonic and laser-activated irrigation methods produced the lowest bacterial counts (p < 0.05). Conclusions An experimental intraradicular biofilm model has been successfully established in pigs. Within the limitations of the study, subsonic or laser-activated irrigation demonstrated the best biofilm removal results in the pig system.

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Inhibition of the CXCL9-CXCR3 axis suppresses the progression of experimental apical periodontitis by blocking macrophage migration and activation

Scientific Reports ◽

10.1038/s41598-021-82167-7 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Tatsuya Hasegawa ◽

V. Venkata Suresh ◽

Yoshio Yahata ◽

Masato Nakano ◽

Shigeto Suzuki ◽

...

Keyword(s):

Peritoneal Macrophages ◽

Lesion Size ◽

Chronic Inflammatory Disease ◽

Apical Periodontitis ◽

Host Immune System ◽

Tissue Destruction ◽

Complex Interactions ◽

Infected Root ◽

Principal Factors ◽

Infected Root Canal

AbstractApical periodontitis (AP) is an acute or chronic inflammatory disease caused by complex interactions between infected root canal and host immune system. It results in the induction of inflammatory mediators such as chemokines and cytokines leading to periapical tissue destruction. To understand the molecular pathogenesis of AP, we have investigated inflammatory-related genes that regulate AP development. We found here that macrophage-derived CXCL9, which acts through CXCR3, is recruited by progressed AP. The inhibition of CXCL9 by a CXCR3 antagonist reduced the lesion size in a mouse AP model with decreasing IL-1β, IL-6 and TNFα expression. The treatment of peritoneal macrophages with CXCL9 and LPS induced the transmigration and upregulation of osteoclastogenic cytokines such as IL-1β, IL-6 and matrix metalloprotease 2, a marker of activated macrophages. This suggests that the CXCL9-CXCR3 axis plays a crucial role in the development of AP, mediated by the migration and activation of macrophages for periapical tissue destruction. Our data thus show that CXCL9 regulates the functions of macrophages which contribute to AP pathogenesis, and that blocking CXCL9 suppresses AP progression. Knowledge of the principal factors involved in the progression of AP, and the identification of related inflammatory markers, may help to establish new therapeutic strategies.

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Effect of Antibacterial Root Canal Sealer on Persistent Apical Periodontitis

Antibiotics ◽

10.3390/antibiotics10060741 ◽

2021 ◽

Vol 10 (6) ◽

pp. 741

Author(s):

Zheng Wang ◽

Ge Yang ◽

Biao Ren ◽

Yuan Gao ◽

Xian Peng ◽

...

Keyword(s):

Enterococcus Faecalis ◽

Therapeutic Effect ◽

Root Canal ◽

Apical Periodontitis ◽

Control Group ◽

Root Canal Sealer ◽

Root Canal Filling ◽

First Time ◽

Cone Beam Computer Tomography ◽

Better Than

The infection of Enterococcus faecalis and its interacting microorganisms in the root canal could cause persistent apical periodontitis (AP). Antibacterial root canal sealer has favorable prospects to inhibit biofilms. The purpose of this study was to investigated the antibacterial effect of root canal sealer containing dimethylaminododecyl methacrylate (DMADDM) on persistent AP in beagle dogs for the first time. Persistent AP was established by a two-step infection with Enterococcus faecalis and multi-bacteria (Enterococcus faecalis, Lactobacillus acidophilus, Actinomycesnaeslundii, Streptococcus gordonii). Root canal sealer containing DMADDM (0%, 1.25%, 2.5%) was used to complete root canal filling. The volume of lesions and inflammatory grade in the apical area were evaluated by cone beam computer tomography (CBCT) and hematoxylin-eosin staining. Both Enterococcus-faecalis- and multi-bacteria-induced persistent AP caused severe apical destruction, and there were no significant differences in pathogenicity between them. DMADDM-modified sealer significantly reduced the volume of periapical lesion and inflammatory grade compared with the control group, among them, the therapeutic effect of the 2.5% group was better than the 1.25% group. In addition, E.faecalis-induced reinfection was more sensitive to the 2.5% group than multi-bacteria reinfection. This study shows that root canal sealer containing DMADDM had a remarkable therapeutic effect on persistent AP, especially on E. faecalis-induced reinfection.

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