Effect of intercellular adhesion molecule 1 deficiency on the development of apical periodontitis

Abstract

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 leucocytes), 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 using SAS 9.4 and the GraphPad Prism 5.0 software (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 all times (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.

Diagnostic biomarker candidates for pulpitis revealed by bioinformatics analysis of merged microarray gene expression datasets

“…Miyuki Azuma et al studied the immune responses in mouse dental pulp, and founded that expression of CD86 were enhanced in dental pulp after cusp trimming, but disappeared within 2 h and migrated into regional lymph nodes at 24 h after acid treatment [30]. As chemokines launch and boost the process of inflammation, an increased expression of CCL2 was observed in chronic periapical lesions, indicating the association between chemokines and dental pulp inflammation [31,32] In addition, IL6, TLR8, CXCL8, MMP9, and ICAM1 are also associated with immunity and inflammation in dental pulp as reported [1,[33][34][35][36][37]…”

Diagnostic biomarker candidates for pulpitis revealed by bioinformatics analysis of merged microarray gene expression datasets

“…Accordingly, increased expression of CCL2 has been observed in chronic periapical lesions, indicating an association between chemokines and dental pulp in ammation [45,46]. In addition, IL6, MMP9, TLR8, CXCL8, and ICAM1 have been reported to be associated with immunity and in ammation in dental pulp [1,17,[47][48][49][50]. The above hub genes may play critical roles in pulp in ammation and therefore be potential biomarkers for use in pulpitis diagnosis.…”

Diagnostic biomarker candidates for pulpitis revealed by bioinformatics analysis of merged microarray gene expression datasets

“…Accordingly, increased expression of CCL2 has been observed in chronic periapical lesions, indicating an association between chemokines and dental pulp inflammation [ 46 , 47 ]. In addition, IL6, MMP9, TLR8, CXCL8, and ICAM1 have been reported to be associated with immunity and inflammation in dental pulp [ 1 , 17 , 48 – 51 ]. The above hub genes may play critical roles in pulp inflammation and therefore be potential biomarkers for use in pulpitis diagnosis.…”