CD68 and F4/80 Markers Demonstrate Inflammatory Synergism Between Apical Periodontitis and Liver Fibrosis in Wistar Rats.
Source: PubMed, NCBI / U.S. National Library of Medicine
To evaluate CD68 and F4/80 glycoproteins in the worsening of apical periodontitis (AP) and liver fibrosis (LF) in Wistar rats. Thirty-two Wistar rats were distributed in the following groups (n = 8): C-control; AP-apical periodontitis; LF-liver fibrosis; APLF-AP and LF. LF was induced by carbon tetrachloride administration for 8 weeks and surgical bile duct ligation; AP was induced by the exposure of the dental pulp to the oral environment for 30 days. Mandibles and livers were removed after euthanasia. The histological and immunohistochemical analysis of CD68 and F4/80 glycoproteins were performed. Two-way ANOVA test was used for statistical analysis (p < 0.05). The livers of the LF and APLF groups showed generalised portal inflammatory infiltrate and collagen fibres, confirming the presence of LF. The immunohistochemical analysis in the liver revealed a greater number of CD68 and F4/80 in the APLF group when compared with AP (p < 0.05). Histopathological analysis in the mandibles of the AP and APLF groups showed areas of necrosis comprising the entire dental pulp and periapical tissue surrounded by inflammatory infiltrate. Immunohistochemical analysis showed greater immunolabelling for CD68 and F4/80 in the APLF group than in the AP group (p < 0.05). CD68 and F4/80 glycoproteins exhibit inflammatory synergy between apical periodontitis and liver fibrosis, increasing macrophage numbers in the inflammatory
Abstract
To evaluate CD68 and F4/80 glycoproteins in the worsening of apical periodontitis (AP) and liver fibrosis (LF) in Wistar rats. Thirty-two Wistar rats were distributed in the following groups (n = 8): C-control; AP-apical periodontitis; LF-liver fibrosis; APLF-AP and LF. LF was induced by carbon tetrachloride administration for 8 weeks and surgical bile duct ligation; AP was induced by the exposure of the dental pulp to the oral environment for 30 days. Mandibles and livers were removed after euthanasia. The histological and immunohistochemical analysis of CD68 and F4/80 glycoproteins were performed. Two-way ANOVA test was used for statistical analysis (p < 0.05). The livers of the LF and APLF groups showed generalised portal inflammatory infiltrate and collagen fibres, confirming the presence of LF. The immunohistochemical analysis in the liver revealed a greater number of CD68 and F4/80 in the APLF group when compared with AP (p < 0.05). Histopathological analysis in the mandibles of the AP and APLF groups showed areas of necrosis comprising the entire dental pulp and periapical tissue surrounded by inflammatory infiltrate. Immunohistochemical analysis showed greater immunolabelling for CD68 and F4/80 in the APLF group than in the AP group (p < 0.05). CD68 and F4/80 glycoproteins exhibit inflammatory synergy between apical periodontitis and liver fibrosis, increasing macrophage numbers in the inflammatory processes of both diseases.