IADR Abstract Archives
Role of Tumor Necrosis Factor-Alpha Dependent Signaling in Apical Periodontitis
Objectives: The goal of this research was to investigate the role of tumor necrosis factor-α (TNF-α) in the development of apical periodontitis.
Methods: To evaluate the periapical bone response, an animal model was used (Ethics approval protocol # 2019.1.139.58.0), in which the pulp tissue was removed and the root canals exposed to the buccal environment for microbial contamination. The right upper and lower first molars were submited to contamination while the left homologous teeth were kept healthy (control). Genetically deficient mice to TNF-α receptor-1 (p55; 6-Tnfrsf1atm1|mx) response was compared to response in wild type animals (C57Bl6). After 42 days, the animals were euthanized and the blocks containing tooth and bone were frozen for evaluation of real-time RT-PCR gene expression (n = 8 teeth per group) or processed for histologic analysis with hematoxylin-eosin staining (n = 8 teeth per group). Data were analyzed using one way ANOVA and Tukey tests (α = 0.05).
Results: Contamination of dental root canals resulted in apical periodontitis formation in mice, characterized by inflammatory cells recruitment and periapical bone loss. During the development of apical periodontitis, the synthesis of the gene that encodes TNF-α was higher in exposed teeth compared to healthy teeth (p < 0.05). When both models were compared regarding to expression of osteoclastogenic and osteogenic genes, it was observed that Acp5, Bglap3, Crcp, Cstk, Dcstamp, Mmp9, Nfatc1, Tnfrsf11b and Tnfsf11 gene expression was not different in TNF-α deficient compared to wild type animals (p > 0.05).
Conclusions: Although TNF-α synthesis was induced during apical periodontitis development, the absence of TNF-α receptor-1 did not impaired osteoclastogenic and osteogenic signaling.
Methods: To evaluate the periapical bone response, an animal model was used (Ethics approval protocol # 2019.1.139.58.0), in which the pulp tissue was removed and the root canals exposed to the buccal environment for microbial contamination. The right upper and lower first molars were submited to contamination while the left homologous teeth were kept healthy (control). Genetically deficient mice to TNF-α receptor-1 (p55; 6-Tnfrsf1atm1|mx) response was compared to response in wild type animals (C57Bl6). After 42 days, the animals were euthanized and the blocks containing tooth and bone were frozen for evaluation of real-time RT-PCR gene expression (n = 8 teeth per group) or processed for histologic analysis with hematoxylin-eosin staining (n = 8 teeth per group). Data were analyzed using one way ANOVA and Tukey tests (α = 0.05).
Results: Contamination of dental root canals resulted in apical periodontitis formation in mice, characterized by inflammatory cells recruitment and periapical bone loss. During the development of apical periodontitis, the synthesis of the gene that encodes TNF-α was higher in exposed teeth compared to healthy teeth (p < 0.05). When both models were compared regarding to expression of osteoclastogenic and osteogenic genes, it was observed that Acp5, Bglap3, Crcp, Cstk, Dcstamp, Mmp9, Nfatc1, Tnfrsf11b and Tnfsf11 gene expression was not different in TNF-α deficient compared to wild type animals (p > 0.05).
Conclusions: Although TNF-α synthesis was induced during apical periodontitis development, the absence of TNF-α receptor-1 did not impaired osteoclastogenic and osteogenic signaling.
