Liu Lingshuang, Peng Bin
State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
J Endod. 2013 Aug;39(8):984-9. doi: 10.1016/j.joen.2013.03.001. Epub 2013 Apr 9.
Macrophage migration inhibitory factor (MIF) has been defined as a key cytokine in regulation of innate and adaptive immunity. The purpose of this study was to investigate the immunohistochemical localization of MIF and its relationship with receptor activator of nuclear factor kappa B ligand (RANKL) protein during the development of periapical lesions in rats.
Apical periodontitis was induced in Wistar rats by occlusal pulp exposure in mandibular first molar teeth. The animals were randomly killed at 0, 7, 14, 21, 28, and 35 days after pulp exposure. The jaws that contained the first molar were obtained and were prepared for histologic analysis, enzyme histochemistry, immunohistochemistry, and double immunofluorescence staining.
From day 0 to day 35, the areas of periapical bone loss increased and seemed to be stabilized on day 35. A few MIF-positive and RANKL-positive cells and osteoclasts could be observed on day 7, and all climaxed on day 14. From day 21 to day 35, the expression of MIF and RANKL protein decreased, and fewer osteoclasts could be observed.
These findings showed that MIF might be associated with the differentiation of osteoclasts in the periapical lesions. MIF contributes to the pathogenesis of the periapical lesions through the induction of RANKL protein.
巨噬细胞移动抑制因子（MIF）已被定义为调节先天性和适应性免疫的关键细胞因子。本研究旨在探讨大鼠根尖周病变发展过程中MIF的免疫组织化学定位及其与核因子κB受体活化因子配体（RANKL）蛋白的关系。
通过暴露下颌第一磨牙牙髓诱导Wistar大鼠根尖周炎。在牙髓暴露后0、7、14、21、28和35天随机处死动物。获取包含第一磨牙的颌骨，准备进行组织学分析、酶组织化学、免疫组织化学和双重免疫荧光染色。
从第0天到第35天，根尖周骨质吸收面积增加，在第35天似乎趋于稳定。在第7天可观察到少量MIF阳性和RANKL阳性细胞及破骨细胞，所有这些在第14天达到高峰。从第21天到第35天，MIF和RANKL蛋白表达下降，破骨细胞数量减少。
这些发现表明，MIF可能与根尖周病变中破骨细胞的分化有关。MIF通过诱导RANKL蛋白促进根尖周病变的发病机制。
