Taubman Martin A, Kawai Toshihisa, Han Xiaozhe
J Clin Periodontol. 2007 May;34(5):367-9. doi: 10.1111/j.1600-051X.2007.01065.x.
In this issue Bostanci et al. (2007) demonstrate that receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG) were oppositely regulated in gingival crevice fluid (GCF) from periodontitis patients. RANKL, RANK and OPG are key molecules that regulate osteoclast recruitment, differentiation and activation. New concepts of the pathogenesis of periodontitis have implicated inflammation triggered by host immune response to periodontal biofilm microorganisms(s) in disease. Host response to bacteria involves activation of T and B cells in the inflammatory infiltrate which bear abundant RANKL that promotes osteoclastic bone resorption. Periodontal tissue destruction can be ameliorated by immunobiological interference with immune cell RANKL expression or function. The new disease concepts provide a foundation to build biological approaches to target RANKL production in periodontal lesions.
在本期杂志中，博斯坦奇等人（2007年）证明，在牙周炎患者的龈沟液（GCF）中，核因子κB受体活化因子配体（RANKL）和骨保护素（OPG）受到相反的调节。RANKL、RANK和OPG是调节破骨细胞募集、分化和激活的关键分子。牙周炎发病机制的新概念表明，宿主对牙周生物膜微生物的免疫反应引发的炎症与疾病有关。宿主对细菌的反应涉及炎症浸润中T细胞和B细胞的激活，这些细胞带有丰富的RANKL，可促进破骨细胞性骨吸收。通过对免疫细胞RANKL表达或功能的免疫生物学干预，可以改善牙周组织破坏。这些新的疾病概念为构建针对牙周病变中RANKL产生的生物学方法提供了基础。
