Imunoexpression of ING4, VEGF e NF-κB in inflamatory periapical lesions
Growth inhibitor; NF-kappa B; Vascular endothelial growth factor; Periapical granuloma; Radicular cyst.
IPLs are pathological conditions resulting from infections of odontogenic origin, being mainly represented by PGs and RCs. Its pathogenesis is associated with immunological and angiogenic mechanisms, characterized by the self-limitation of the inflammatory reaction. Therefore, this retrospective, semi-quantitative and comparative study aimed to analyze the immunohistochemical expression of ING4, VEGF and NF-κB in IPLs, and to correlate the pattern of expression of these proteins. The sample consisted of 62 IPLs, of which 41.9% were PGs, 27.4% RCs, 30.6% RRCs. Morphological analysis was performed, evaluating epithelial thickness and inflammatory infiltrate, and the correlation of these findings with the immunohistochemical expression pattern of ING4, VEGF and NF-κB proteins in IPLs. To perform the statistical analysis, the chi-square, Kruskal-Wallis, Mann-Whitney and Spearmen correlation tests were used. The intensity of the inflammatory infiltrate showed a significant association in the IPLs, showing greater intensity in the PG when compared to the cysts. Furthermore, the RCs showed a higher intensity of the inflammatory infiltrate when compared to the RRCs. By associating the expression of ING4 in inflammatory cells of the connective tissue or fibrous capsule, the PGs and RCs showed greater expression of this protein both at the nuclear and cytoplasmic levels. Immunoexpression of VEGF in the nucleus of inflammatory cells of the connective tissue or fibrous capsule shows a significant association with IPLs, with greater expression of this protein in the cysts than in the PG. There was a statistically significant association between NF-κB immunostaining and IPLs, in which PGs exhibited higher protein expression in relation to RCs and RRCs. When compared between the cysts, there was no statistically significant association, however the median of NF-κB expression was higher for the RCs. In the fibrous capsule, nuclear immunoexpression of NF-κB in inflammatory cells was higher in periapical lesions with intense inflammatory infiltrate. Similarly, the cytoplasmic immunoexpression of NF-κB in inflammatory cells was higher in cases of periapical lesions that presented intense inflammatory infiltrate. Therefore, it is suggested that ING4, VEGF and NF-κB participate in the etiopathogenesis of IPLs, and that there is a directly proportional relationship between the expression of these proteins.