Journal of endodontics · 2025
Effects of Systemic and Local Anti-tumor Necrosis Factor-α Receptor-1 Administration on Periapical Bone Loss in Mice.
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de Almeida-Junior Luciano Aparecido, de Lima Gonçalves Juliana, Arnez Maya Fernanda Manfrin, Rostrán Jimenez Nallery Steysi, Marañón-Vasquez Guido Artemio, Paula-Silva Francisco Wanderley Garcia de
Аннотация
INTRODUCTION: The aim of this study was to evaluate whether systemic or topical administration of a monoclonal antibody against tumor necrosis factor-α receptor-1 (TNFR1) could control periapical bone loss in mice.
METHODS: Thirty C57Bl6 mice were used for induction of periapical lesion through the exposure of the root canals to the oral environment. The root canals remained open to microbial contamination from the oral cavity for 28 days. Then, the animals were randomly assigned to 3 different experimental groups: G1: animals received no medication and periapical lesion followed its natural course up to 42 days; G2: systemic administration of the TNFR1 antibody; G3: intracanal topical administration of the TNFR1 antibody. Healthy teeth were used as controls. At 42 days following periapical lesion induction, the animals were anesthetized then euthanized, and tissues containing bone and teeth were collected for microtomographic, histomorphometry, and quantitative reverse transcriptase polymerase chain reaction analysis. Then groups were compared using one-way analysis of variance followed by Turkey tests (α = 5%).
RESULTS: Systemic and topical anti-TNFR1 administered in groups G2 and G3 did not have an impact on the area and volume of periapical lesions when compared to the untreated control group G1 (P > .05). Lower expression of RANKL mRNA was observed in G3 compared to G1 (P < .05) but no change on OPG, MMP-9 or CTSK was detected (P > .05).
CONCLUSIONS: Under the experimental conditions of this study, systemic or local administration of a TNFR1 antibody was not effective in limiting the expansion of periapical lesions.
METHODS: Thirty C57Bl6 mice were used for induction of periapical lesion through the exposure of the root canals to the oral environment. The root canals remained open to microbial contamination from the oral cavity for 28 days. Then, the animals were randomly assigned to 3 different experimental groups: G1: animals received no medication and periapical lesion followed its natural course up to 42 days; G2: systemic administration of the TNFR1 antibody; G3: intracanal topical administration of the TNFR1 antibody. Healthy teeth were used as controls. At 42 days following periapical lesion induction, the animals were anesthetized then euthanized, and tissues containing bone and teeth were collected for microtomographic, histomorphometry, and quantitative reverse transcriptase polymerase chain reaction analysis. Then groups were compared using one-way analysis of variance followed by Turkey tests (α = 5%).
RESULTS: Systemic and topical anti-TNFR1 administered in groups G2 and G3 did not have an impact on the area and volume of periapical lesions when compared to the untreated control group G1 (P > .05). Lower expression of RANKL mRNA was observed in G3 compared to G1 (P < .05) but no change on OPG, MMP-9 or CTSK was detected (P > .05).
CONCLUSIONS: Under the experimental conditions of this study, systemic or local administration of a TNFR1 antibody was not effective in limiting the expansion of periapical lesions.