The Expression Of JAK2/STAT3 In Human Chronic Apical Periodontitis

Objective JAK/STAT is a signal transduction pathway stimulated by cytokine.It has been found that this signal transduction pathway participates in many biological functions such as cell proliferation,differentiation and immune regulation.In the meanwhile,some studies have found that SOCS3 protein is an important negative regulator of JAK/STAT signal transduction pathway.Chronic apical periodontitis is a common stomatological disease in which pulp inflammation is caused mainly by bacteria,which causes destruction of the tissue around the root tip,and eventually leads to different degrees of destruction of the bone tissue around the root tip.After pulp necrosis,there is a lack of blood supply in the pulp cavity,the main source of nutrient supply is destroyed,the immune defense ability of the teeth is reduced,and the pulp cavity becomes a hotbed for anaerobic microorganisms to survive.Only thorough cleansing,shaping and root canal filling can eliminate the source of apical periodontitis and create an environment that remineralization the tissue around the root tip.At present,the main treatment for apical periodontitis is root canal therapy,but the success rate of root canal therapy is 31% to 96%.The teeth become easily broken due to lack of nutrient supply,and the chewing function will have a certain degree of influence after root canal therapy.Therefore,the prevention of the occurrence of apical periodontitis at the root can improve the survival life of the teeth and improve the chewing efficiency.A better understanding of the pathogenesis of periapical periodontitis can better guide the clinic and is especially important for the prevention and treatment of periapical periodontitis.Based on the above theoretical basis,this study proposes the following hypothesis: The JAK2/STAT3 signal transduction pathway has a higher expression in human chronic apical periodontitis than in the periodontal tissues of normal teeth.JAK2/STAT3 signal transduction pathway can be detected by PCR and western blot.This study can clarify the mechanism of inflammatory bone destruction mediated by JAK2/STAT3 signaling pathway and provide a theoretical basis for the prevention and treatment of periapical diseases and other oral inflammatory diseases.The expression of JAK2/STAT3 in human chronic apical periodontitis was detected by immunohistochemistry,PCR and Western Blot at the histological and molecular levels,and the effect of SOCS3 on JAK2/STAT3 was analyzed.Immunofluorescence double staining was used to detect the expression of JAK2 and STAT3 in periapical periodontitis,and the double staining of JAK2 and STAT3 in cells was observed.Methods From March 2017 to February 2018,in the Department of Stomatology,Affiliated Hospital of Qingdao University,100 cases of periapical tissue were collected from patients with severe chronic apical periodontitis and requiring removal of teeth or apical surgery.There were 50 cases of chronic apical periodontal cysts and 50 cases of chronic periapical granuloma,and 50 cases of healthy periodontal tissues extracted by wisdom teeth or orthodontics were used as controls.The expression levels of JAK2,STAT3,p-JAK2,p-STAT3 and SOCS3 were detected by immunohistochemistry in 30 cases of chronic apical periodontal cysts and 30 cases of chronic apical granuloma and 30 normal tissues.The expression levels of JAK2,STAT3 and SOCS3 were detected by PCR in 10 specimens.Ten specimens were selected for western blot analysis of JAK2,STAT3,p-JAK2 and p-STAT3 expression.Fluorescent double staining of JAK2 and STAT3 was detected by immunofluorescence.Results Immunohistochemistry showed that different degrees of expression of p/t JAK2,p/t STAT3 and SOCS3 were detected in normal periodontal soft tissues and periapical cysts and granulomatous specimens,But the expression levels of p/t JAK2,p/STAT3 and SOCS3 in the periapical periodontal cysts and granulomatous tissues were significantly higher than those in normal periodontal soft tissues(p<0.05,statistically significant),while the periapical granulomatous lower than periodontal cysts tissues(p>0.05,no statistical significance).The merge of JAK2 and STAT3 was observed by immunofluorescence double staining.The results of p/t JAK2 and p/t STAT3 obtained by PCR and Western Blot were consistent with the results of immunohistochemistry.The results of PCR showed that the expression of IL-6 was in the control group < periapical granuloma(p<0.01,statistically significant),and the control group was <peric periapical cyst(p<0.01,statistically significant),periapical granuloma <perical cysts(p < 0.05,statistically significant).The expression of SOCS3 was in the control group > periapical granuloma group(p<0.05,statistically significant),and the control group > periapical cyst group(p<0.05,statistically significant),periapical granuloma> pericardial cyst(p>0.05,no statistical significance).Conclusions The expression of JAK2/STAT3 is increased in chronic apical periodontitis,and JAK2/STAT3 signaling pathway may be involved in the development of inflammation in chronic periapical periodontitis.