Nanki Toshihiro
Tokyo Medical and Dental University, Department of Medicine and Rheumatology.
Clin Calcium. 2007 Apr;17(4):510-6.
Osteoclast in the synovium of rheumatoid arthritis (RA) plays an important role for bone destruction of the affected joints. The osteoclast is differentiated from macrophage-like synoviocyte, which is migrated from peripheral blood monocytes. In the RA synovium, receptor activator of NF-kappaB ligand (RANKL) which is expressed by T cells and fibroblast-like synoviocytes (FLS) and macrophage colony-stimulating factor (M-CSF) which is expressed by FLS induce the differentiation into osteoclast from macrophage-like synoviocyte. TNF-alpha, interleukin (IL) -1, IL-6, and IL-17 which are expressed by macrophages, FLS, and/or T cells in the synovium enhance the differentiation and activation of the osteoclast. Thus, such synovial cells contribute osteoclastgenesis and bone destruction.
类风湿关节炎（RA）滑膜中的破骨细胞在受累关节的骨质破坏中起重要作用。破骨细胞由巨噬细胞样滑膜细胞分化而来，巨噬细胞样滑膜细胞则源自外周血单核细胞。在RA滑膜中，T细胞和成纤维细胞样滑膜细胞（FLS）表达的核因子κB受体活化因子配体（RANKL）以及FLS表达的巨噬细胞集落刺激因子（M-CSF）可诱导巨噬细胞样滑膜细胞分化为破骨细胞。滑膜中的巨噬细胞、FLS和/或T细胞表达的肿瘤坏死因子-α、白细胞介素（IL）-1、IL-6和IL-17可增强破骨细胞的分化和活化。因此，这些滑膜细胞促成了破骨细胞生成和骨质破坏。
