Chen Zhang1,2, Jun Liu1, Changqing Yuan1, Qiuxia Ji1, Daiyun Chen3, Han Zhao4, Weijie Jiang1,2, Kangjie Ma1,2, Lingshuang Liu1. 1. Department of Stomatology, Affiliated Hospital of Qingdao University Qingdao, P. R. China. 2. Qingdao University Qingdao, P. R. China. 3. Department of Stomatology, Affiliated Hospital of Taishan University Taian, P. R. China. 4. Department of Pathology, Affiliated Hospital of Qingdao University Qingdao, P. R. China.
Abstract
OBJECTIVE: It has been shown that JAK2/STAT3 is involved in the occurrence of various inflammatory diseases. The purpose of this study was to associate the expression of Janus kinase 2 (JAK2) and its receptor signal transducer and activator of transcription 3 (STAT3) and suppressors of cytokine signaling 3 (SOCS3), to periapical granuloma. METHODS: Samples were collected from 40 patients who were divided into two groups, namely, healthy control (N=20) and periapical granuloma (N=20) groups in accordance with classified standards. The samples were prepared for histological analysis, immunohistochemistry, and double immunofluorescence staining. RESULTS: Only slight inflammatory cell infiltration was observed in the tissues from the healthy control group. Extensive infiltration of inflammatory cells was observed in patients with chronic periapical disease. The periapical granuloma group had higher levels of JAK2, STAT3, p-JAK2, p-STAT3 and SOCS3 (all P<0.05) than the control group. Double immunofluorescence staining results showed the presence of JAK2-positive and STAT3-positive cells in the periapical lesion areas. CONCLUSIONS: This study demonstrated that JAK2, STAT3, and SOCS3 can be observed and may be associated with the inflammatory process in periapical lesions. The results of this study will provide new insights into the pathological mechanisms of human periapical granuloma. IJCEP
OBJECTIVE: It has been shown that JAK2/STAT3 is involved in the occurrence of various inflammatory diseases. The purpose of this study was to associate the expression of Janus kinase 2 (JAK2) and its receptor signal transducer and activator of transcription 3 (STAT3) and suppressors of cytokine signaling 3 (SOCS3), to periapical granuloma. METHODS: Samples were collected from 40 patients who were divided into two groups, namely, healthy control (N=20) and periapical granuloma (N=20) groups in accordance with classified standards. The samples were prepared for histological analysis, immunohistochemistry, and double immunofluorescence staining. RESULTS: Only slight inflammatory cell infiltration was observed in the tissues from the healthy control group. Extensive infiltration of inflammatory cells was observed in patients with chronic periapical disease. The periapical granuloma group had higher levels of JAK2, STAT3, p-JAK2, p-STAT3 and SOCS3 (all P<0.05) than the control group. Double immunofluorescence staining results showed the presence of JAK2-positive and STAT3-positive cells in the periapical lesion areas. CONCLUSIONS: This study demonstrated that JAK2, STAT3, and SOCS3 can be observed and may be associated with the inflammatory process in periapical lesions. The results of this study will provide new insights into the pathological mechanisms of human periapical granuloma. IJCEP