S Liu1, Q Li, Y Liu. 1. Department of Conservative Dentistry and Endodontics, School and Hospital of Stomatology, Wuhan University, Wuhan, Hubei, China.
Abstract
AIM: To explore the role of NALP3 inflammasome [NALP3, its effector molecule apoptosis associated speck-like protein (ASC), caspase-1, interleukin (IL)-1β and IL-18] in the development of periapical lesions in rats. METHODOLOGY: Periapical lesions were developed within 21 days after mandibular first molar pulp exposure in Sprague-Dawley rats. The animals were randomly sacrificed at 0, 1, 3, 7, 10, 14 and 21 days after pulpal exposure. The bilateral mandibles were extracted for histological processing, then they were haematoxylin-eosin (HE) stained to examine inflammation infiltration in the apical region and immunohistochemically examined for the NALP3 inflammasome signalling pathway. Data were analysed by one-way analysis of variance and the Pearson(') s correlation and linear tendency test. RESULTS: NALP3 was detected in the cytoplasm of fibroblasts, monocytes, neutrophils, macrophages and vascular endothelial cells in the periapical region. From day 1 to day 21, the number of NALP3-positive cells ascended and was significantly correlated with the intensity of inflammatory infiltration (r = 0.776, P < 0.01). ASC, caspase-1, IL-1β and IL-18 were all expressed in the inflammatory periapical tissues. The positive cell counts of IL-1β and IL-18 were significantly correlated with that of NALP3, and r = 0.718, P < 0.01; r = 0.688, P < 0.01, respectively. CONCLUSIONS: NALP3 inflammasome is expressed in the inflammatory periapical tissues. This cytokine-signalling pathway may therefore be crucial in the regulatory control of inflammatory responses in periapical tissues and the development of periapical lesions.
AIM: To explore the role of NALP3 inflammasome [NALP3, its effector molecule apoptosis associated speck-like protein (ASC), caspase-1, interleukin (IL)-1β and IL-18] in the development of periapical lesions in rats. METHODOLOGY: Periapical lesions were developed within 21 days after mandibular first molar pulp exposure in Sprague-Dawley rats. The animals were randomly sacrificed at 0, 1, 3, 7, 10, 14 and 21 days after pulpal exposure. The bilateral mandibles were extracted for histological processing, then they were haematoxylin-eosin (HE) stained to examine inflammation infiltration in the apical region and immunohistochemically examined for the NALP3 inflammasome signalling pathway. Data were analysed by one-way analysis of variance and the Pearson(') s correlation and linear tendency test. RESULTS: NALP3 was detected in the cytoplasm of fibroblasts, monocytes, neutrophils, macrophages and vascular endothelial cells in the periapical region. From day 1 to day 21, the number of NALP3-positive cells ascended and was significantly correlated with the intensity of inflammatory infiltration (r = 0.776, P < 0.01). ASC, caspase-1, IL-1β and IL-18 were all expressed in the inflammatory periapical tissues. The positive cell counts of IL-1β and IL-18 were significantly correlated with that of NALP3, and r = 0.718, P < 0.01; r = 0.688, P < 0.01, respectively. CONCLUSIONS: NALP3 inflammasome is expressed in the inflammatory periapical tissues. This cytokine-signalling pathway may therefore be crucial in the regulatory control of inflammatory responses in periapical tissues and the development of periapical lesions.