Pâmella Recco Álvares1, José Alcides Almeida de Arruda2, Leni Verônica Oliveira Silva3, Leorik Pereira da Silva4, George João Ferreira do Nascimento5, Marcia Maria Fonseca da Silveira1, Ana Paula Veras Sobral1. 1. Department of Oral and Maxillofacial Pathology, School of Dentistry, Universidade de Pernambuco, Camaragibe, Pernambuco, Brazil. 2. Department of Oral Surgery and Pathology, School of Dentistry, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. Electronic address: alcides_almeida@hotmail.com. 3. Department of Oral Surgery and Pathology, School of Dentistry, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. 4. Postgraduate Program in Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Norte, Natal, Rio Grande do Norte, Brazil. 5. Biological Sciences Center, School of Dentistry, Universidade Federal de Campina Grande, Patos, Paraiba, Brazil.
Abstract
INTRODUCTION: The purpose of this study was to evaluate the expression of cyclooxygenase-2 (COX-2) and tumor necrosis factor alpha (TNF-α) in periapical granuloma (PG) and radicular cyst (RC) samples and to correlate it with the type of lesion, the intensity of the inflammatory infiltrate, and the thickness of the epithelial lining. METHODS: A total of 51 cases of periapical lesions (25 PGs and 26 RCs) were subjected to morphologic analysis and immunohistochemical study. The anti-COX-2 and anti-TNF-α antibodies were applied using the immunoperoxidase technique. Data were analyzed by the Mann-Whitney test, Pearson chi-square test, Fisher exact test, and Spearman correlation. RESULTS: Analysis of the inflammatory infiltrate revealed that 80% of PGs exhibited a grade III infiltrate as opposed to a 19% rate in RCs (P < .001). Morphologic evaluation of the epithelial thickness of RCs revealed the presence of atrophic epithelium in 73% of cases. The majority of PGs had a score of 1 for COX-2 immunoexpression (n = 14, 54%) and a score of 2 for TNF-α expression (n = 16, 64%), whereas in cases of RCs a score of 1 was more prevalent for COX-2 and TNF-α expression (n = 17, 65%). Significant differences in the expression scores of COX-2 and TNF-α were detected in periapical lesions (P < .001). CONCLUSIONS: Based on these findings, we emphasize that RCs and PGs have a similar expression of inflammatory mediators (COX-2 and TNF-α) although the secretion of TNF-α by macrophages and of COX-2 by several cells was higher in PGs, indicating a greater inflammatory response in these lesions.
INTRODUCTION: The purpose of this study was to evaluate the expression of cyclooxygenase-2 (COX-2) and tumor necrosis factor alpha (TNF-α) in periapical granuloma (PG) and radicular cyst (RC) samples and to correlate it with the type of lesion, the intensity of the inflammatory infiltrate, and the thickness of the epithelial lining. METHODS: A total of 51 cases of periapical lesions (25 PGs and 26 RCs) were subjected to morphologic analysis and immunohistochemical study. The anti-COX-2 and anti-TNF-α antibodies were applied using the immunoperoxidase technique. Data were analyzed by the Mann-Whitney test, Pearson chi-square test, Fisher exact test, and Spearman correlation. RESULTS: Analysis of the inflammatory infiltrate revealed that 80% of PGs exhibited a grade III infiltrate as opposed to a 19% rate in RCs (P < .001). Morphologic evaluation of the epithelial thickness of RCs revealed the presence of atrophic epithelium in 73% of cases. The majority of PGs had a score of 1 for COX-2 immunoexpression (n = 14, 54%) and a score of 2 for TNF-α expression (n = 16, 64%), whereas in cases of RCs a score of 1 was more prevalent for COX-2 and TNF-α expression (n = 17, 65%). Significant differences in the expression scores of COX-2 and TNF-α were detected in periapical lesions (P < .001). CONCLUSIONS: Based on these findings, we emphasize that RCs and PGs have a similar expression of inflammatory mediators (COX-2 and TNF-α) although the secretion of TNF-α by macrophages and of COX-2 by several cells was higher in PGs, indicating a greater inflammatory response in these lesions.