L Wang1, Z Sun, L Liu, B Peng. 1. Department of Operative Dentistry and Endodontics, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
Abstract
AIM: To investigate the expression of CX3CL1 and its receptor, CX3CR1, in the development of periapical lesions induced in rats and explore the possible role of these substances in the pathogenesis of periapical lesions. METHODOLOGY: Periapical lesions in mandibular first molar teeth were established in 30 rats following pulp exposure to the oral environment. The animals were killed 0, 7, 14, 21, 28 and 42 days after lesion induction. The development of periapical lesions was investigated by histological and enzyme histochemical examination. The distributions of CX3CL1 and CX3CR1 in the periapical tissue were examined by immunohistochemistry and immunofluorescence staining. Osteoclasts and CX3CL1-positive cells were counted in each specimen. The data were then analysed by one-way anova using the SPSS 13.0 statistical package. RESULTS: The lesions expanded from days 0 to 14 and stabilized thereafter. Where expansion of the periapical lesion was most evident, numerous CX3CL1-positive cells were observed around the apical foramen and adjacent periapical areas. From days 21 to 42, subjacent connective tissues presented intense CX3CL1 immunostaining in inflammatory cells with different morphologies, such as round, oval and fibroblastic. The number of CX3CL1-positive cells increased from days 7 to 28, but decreased on day 42 post-operation. Double immunofluorescence staining showed CX3CL1- and CX3CR1-positive cells around periapical lesions surrounding the apical foramen. Most CX3CL1-positive cells were mononuclear in nature, which suggests the presence of macrophages, infiltrating neutrophils and lymphocytes, and overlapped with CX3CR1-positive cells. CONCLUSIONS: CX3CL1 and CX3CR1 are related to the development of periapical lesions. The chemokine and its receptor may be involved in the progression of tissue destruction, including bone resorption, during periapical inflammation.
AIM: To investigate the expression of CX3CL1 and its receptor, CX3CR1, in the development of periapical lesions induced in rats and explore the possible role of these substances in the pathogenesis of periapical lesions. METHODOLOGY: Periapical lesions in mandibular first molar teeth were established in 30 rats following pulp exposure to the oral environment. The animals were killed 0, 7, 14, 21, 28 and 42 days after lesion induction. The development of periapical lesions was investigated by histological and enzyme histochemical examination. The distributions of CX3CL1 and CX3CR1 in the periapical tissue were examined by immunohistochemistry and immunofluorescence staining. Osteoclasts and CX3CL1-positive cells were counted in each specimen. The data were then analysed by one-way anova using the SPSS 13.0 statistical package. RESULTS: The lesions expanded from days 0 to 14 and stabilized thereafter. Where expansion of the periapical lesion was most evident, numerous CX3CL1-positive cells were observed around the apical foramen and adjacent periapical areas. From days 21 to 42, subjacent connective tissues presented intense CX3CL1 immunostaining in inflammatory cells with different morphologies, such as round, oval and fibroblastic. The number of CX3CL1-positive cells increased from days 7 to 28, but decreased on day 42 post-operation. Double immunofluorescence staining showed CX3CL1- and CX3CR1-positive cells around periapical lesions surrounding the apical foramen. Most CX3CL1-positive cells were mononuclear in nature, which suggests the presence of macrophages, infiltrating neutrophils and lymphocytes, and overlapped with CX3CR1-positive cells. CONCLUSIONS:CX3CL1 and CX3CR1 are related to the development of periapical lesions. The chemokine and its receptor may be involved in the progression of tissue destruction, including bone resorption, during periapical inflammation.