LAUSR

AIM To evaluate the specific role of ICAM-1 in host responses against endodontic infection. METHODS Apical periodontitis was experimentally induced in the mandibular first molars of ICAM-1 knockout and wild-type (WT) mice by pulp exposure to the oral environment. At 7, 21 and 42 days following pulp infection, the animals were euthanized and the jaws were prepared for analysis under conventional and fluorescence microscopy (histopathologic and morphometric analysis), immunohistochemistry (polymorphonuclear leukocytes), enzyme histochemistry (osteoclasts and cementoclasts) and RT-PCR (IL-1 α, TNF-α, INF-γ, IL-10, RANK, RANKL and OPG). A generalized linear model with glimmix procedure with Satterthwaite approximation method of degrees of freedom, Tukey-Kramer, pseudo-ranking nonparametric, Bonferroni-Holm multiple testing adjustment, analysis of variance (ANOVA) and the Tukey's multiple comparisons tests were used to evaluate the statistical differences between the groups, by the SAS 9.4 and the Graphpad Prism 5.0 softwares (α = 0.05). RESULTS Compared to WT mice, ICAM-1 knockout mice had significantly greater bone resorption (p˂0.05), reduced recruitment of neutrophils to periapical inflammatory tissues (p˂0.05) and an increased number of fibroblasts (p˂0.05) at all experimental periods. The osteoclast number was significantly higher in ICAM-1 KO than that of WT animals at 42 days (p˂0.05), while there was no significant difference between the groups regarding cementoclasts. At day 21, the level of IL-1α, RANK, RANKL and IL-10 had increased significantly in tissues from ICAM-1 KO versus WT mice (p˂0.05), while no significant difference was observed in TNF-α and OPG levels (p˃0.05). Tissue levels of INF-γ were significantly lower in ICAM-1 KO than those in WT mice (p˂0.05). CONCLUSION ICAM-1 deficiency impaired the host response against endodontic infection, resulting in increased tissue destruction.