International endodontic journal · 2022
Interferon-gamma inducible protein 16 and type I interferon receptors expression in experimental apical periodontitis induced in wild-type mice.
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Pucinelli Carolina Maschietto, Lima Ricardo B, Almeida Lana K Y, Lucisano Marilia P, Córdoba Amily Z, Marchesan Julie T, da Silva Lea A B, da Silva Raquel A B
Аннотация
AIM: The aim of this study was to evaluate the IFI16 and IFN-α/β receptors expression during the genesis and development of experimental apical periodontitis (AP) in mice teeth.
METHODOLOGY: Apical periodontitis was induced in the lower first molars of 40 C57BL/6 mice. They were divided according to the experimental periods 2, 7, 14, 21 and 42 days (n = 8 per group). Five animals were used as a control group (without AP). Specimens were submitted to histological processing for description of the inflammatory process, immunostaining for the presence/absence and localization of IFI16 and IFN-α/β receptors (qualitative and semi-quantitative analysis) and tartrate-resistant acid phosphatase (TRAP) histoenzimology.
RESULTS: The results showed a gradual development of AP over the experimental times. The expression of IFI16 was noticeably more exacerbated in the experimental early period (day 2) whilst the lowest expression was observed in the control group (p = .02). For IFN-α/β receptors, a higher intensity staining was observed 42 days after AP induction, that was statistically different from the control group (p = .02). In addition, the number of TRAP-positive cells was higher on the later periods (days 21 and 42; p < .001).
CONCLUSION: IFI16 protein expression was highest during the early periods after AP induction in mice teeth, whilst IFN-α/β receptor expression was highest after AP became established.
METHODOLOGY: Apical periodontitis was induced in the lower first molars of 40 C57BL/6 mice. They were divided according to the experimental periods 2, 7, 14, 21 and 42 days (n = 8 per group). Five animals were used as a control group (without AP). Specimens were submitted to histological processing for description of the inflammatory process, immunostaining for the presence/absence and localization of IFI16 and IFN-α/β receptors (qualitative and semi-quantitative analysis) and tartrate-resistant acid phosphatase (TRAP) histoenzimology.
RESULTS: The results showed a gradual development of AP over the experimental times. The expression of IFI16 was noticeably more exacerbated in the experimental early period (day 2) whilst the lowest expression was observed in the control group (p = .02). For IFN-α/β receptors, a higher intensity staining was observed 42 days after AP induction, that was statistically different from the control group (p = .02). In addition, the number of TRAP-positive cells was higher on the later periods (days 21 and 42; p < .001).
CONCLUSION: IFI16 protein expression was highest during the early periods after AP induction in mice teeth, whilst IFN-α/β receptor expression was highest after AP became established.