B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease
B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease
复制标题
DOI：
10.2353/ajpath.2006.060180
复制
发表时间：
2006-09-01
影响因子：
6
通讯作者：
Taubman, Martin A.
中科院分区：
文献类型：
--
作者：
Kawai, Toshihisa;Matsuyama, Takashi;Taubman, Martin A.
核因子 kappa B 受体激活剂 (RANKL) 介导的破骨细胞生成在炎症性骨吸收中发挥着关键作用。本研究的目的是确定牙周病骨吸收病变中 RANKL 的细胞来源。在患病组织匀浆中测量的可溶性 RANKL 浓度，但不是其诱饵受体骨保护素；患病牙龈组织中的含量显着高于健康组织。双色共聚焦显微镜分析表明，健康牙龈组织中表达 RANKL 的 B 细胞和 T 细胞均低于 20%。相比之下，在患病牙龈组织中由45% T细胞、50% B细胞和5%单核细胞组成的丰富单核细胞中，分别超过50%和90%以上的T细胞和B细胞表达RANKL。非淋巴细胞产生的 RANKL 尚未明确鉴定。从患者牙龈组织中分离的淋巴细胞在体外以 RANKL 依赖性方式诱导成熟破骨细胞的分化。然而，类似分离的外周血B和T细胞并不能诱导破骨细胞分化，除非它们在体外被激活以表达RANKL；强调牙周病组织中活化的表达 RANKL 的淋巴细胞的破骨潜力。这些结果表明，活化的 T 细胞和 B 细胞可以成为牙周病牙龈组织骨吸收的 RANKL 细胞来源。
Receptor activator of nuclear factor-kappa B (RANKL)-mediated osteoclastogenesis plays a pivotal role in inflammatory bone resorption. The aim of this study was to identify the cellular source of RANKL in the bone resorptive lesions of periodontal disease. The concentrations of soluble RANKL, but not its decoy receptor osteoprotegerin, measured in diseased tissue homogenates; were significantly higher in diseased gingival tissues than in healthy tissues. Double-color confocal microscopic analyses demonstrated less than 20% of both B cells and T cells expressing RANKL in healthy gingival tissues. By contrast, in the abundant mononuclear cells composed of 45% T cells, 50% B cells, and 5% monocytes in diseased gingival tissues, more than 50 and 90% of T cells and B cells, respectively, expressed RANKL. RANKL production by nonlymphoid cells was not distinctly identified. Lymphocytes isolated from gingival tissues of patients induced differentiation of mature osteoclast cells in a RANKL-dependent manner in vitro. However, similarly isolated peripheral blood B and T cells did not induce osteoclast differentiation, unless they were activated in vitro to express RANKL; emphasizing the osteoclastogenic potential of activated RANKL-expressing lymphocytes in periodontal disease tissue. These results suggest that activated T and B cells can be the cellular source of RANKL for bone resorption in periodontal diseased gingival tissue.