Immunohistochemical analysis of FoxP3+ cells in periapical granulomas and radicular cysts

• Published in: Archives of oral biology 2012-09, Vol.57 (9), p.1159-1164
• Main Authors: Peixoto, Raniel Fernandes, Pereira, Joabe dos Santos, Nonaka, Cassiano Francisco Weege, da Silveira, Éricka Janine Dantas, Miguel, Márcia Cristina da Costa
• Format: Article
• Language: English
• Subjects: Advanced Basic Science; Antibodies; Atrophy; Cell Count; Cysts; Dentistry; Epithelium - pathology; Forkhead box P3; Forkhead Transcription Factors - analysis; Foxp3 protein; Granuloma; Humans; Hyperplasia; Immunohistochemistry; Immunoregulation; Inflammation; Inflammation - pathology; Inflammation Mediators - analysis; Lymphocytes T; Microscopes; Periapical granuloma; Periapical Granuloma - pathology; Radicular cyst; Radicular Cyst - pathology; Regulatory T cells; Statistical analysis; T-Lymphocytes, Regulatory - pathology
• ISSN: 0003-9969; 1879-1506
• DOI: 10.1016/j.archoralbio.2012.02.005

Abstract Objectives To compare the number of FoxP3+ cells between periapical granulomas (PGs) and radicular cysts (RCs), and to correlate this number with the intensity of the inflammatory infiltrate in these lesions and with epithelial thickness of RCs. Study design Thirty PGs and 30 RCs were submitted to immunohistochemical analysis using an anti-FoxP3 polyclonal antibody. FoxP3+ cells were counted under a light microscope (×400 magnification) in five fields and the mean value was calculated for each specimen. Statistical tests were used to evaluate differences in the number of FoxP3+ cells according to type of lesion (PG vs. RC), intensity of the inflammatory infiltrate (grade I/II vs. grade III), and epithelial thickness of RCs (atrophic vs. hyperplastic). Results FoxP3+ cells were detected in most PGs (93.3%) and RCs (93.3%). The median number of FoxP3+ cells was 2.40 in PGs and 1.00 in RCs, with this difference being statistically significant ( P = 0.005). No significant differences in the number of FoxP3+ cells were observed in terms of the intensity of the inflammatory infiltrate ( P = 0.465) or epithelial thickness of RCs ( P = 0.737). Conclusions The present results suggest a greater participation of regulatory T cells in the modulation of the inflammatory response in PGs. In addition, the presence of a less effective regulatory environment in RCs, together with the high levels of inflammatory mediators as reported in the literature, may contribute to the greater growth potential of these lesions.