摘要
目的:观察大鼠根尖周病变过程中P-p38,RANKL和破骨细胞的表达及变化,探讨p38MAPK信号通路在根尖周炎症性骨吸收中的作用。方法:将24只SD大鼠开髓,分别于术后7,14,21,28d取下颌骨,制备组织切片,用免疫组织化学的方法测定P-p38和RANKL在大鼠根尖周炎中的表达,酶组织化学方法检测抗酒石酸酸性磷酸酶,观察破骨细胞。结果:在正常根尖周组织中偶见P-p38、RANKL阳性细胞和破骨细胞;术后7d根尖周有炎症细胞浸润,可见P-p38、RANKL阳性细胞和破骨细胞数量增多;术后14d,P-p38、RANKL阳性细胞和破骨细胞数量上升至最高值;术后21~28d,P-p38、RANKL阳性细胞和破骨细胞数量下降。从7d组到28d组,破骨细胞数量的变化与P-p38和RANKL阳性细胞数的变化呈现一致的趋势。结论:p38MAPK信号通路可能通过参与RANKL介导的信号转导途径,介导破骨细胞分化,参与根尖炎骨吸收的病理过程。
Objective: To investigate effects of p38 mitogen-activated protein kinase during the development of periapical lesions in rats. Methods: Periapical lesions were developed within 28 days following pulp exposure of the mandibular first molars in Wistar rats. The animals were sacrificed randomly at 0, 7, 14, 21, and 28 days after pulpal exposure. The jaws that contained the first molar were obtained and routinely prepared for immunohistochemistry and enzymehistochemistry. Results: A few phosphorylated p38 MAPK (P-p38), RANKL positive cells and osteoclasts could be observed on day 7, which all climaxed in number on day 14. In the 21- and 28-day samples, the P-p38 and RANKL expression decreased and fewer osteoclasts could be observed. Conclusion: These findings demonstrated that the activation of p38 MAPK might be associated with bone resorption in periapical lesions.
出处
《口腔医学研究》
CAS
CSCD
2013年第10期900-903,共4页
Journal of Oral Science Research
基金
湖北省自然科学基金资助项目(编号:2010CDB07003)