Feng Wei, Guo Jie, Li Minqi
Department of Bone Metabolism, School of Stomatology Shandong University, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Wenhua West Road 44-1, Jinan 250012, China; Department of Endodontics, Jinan Stomatological Hospital, Jinan, China.
Department of Bone Metabolism, School of Stomatology Shandong University, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Wenhua West Road 44-1, Jinan 250012, China.
J Oral Biosci. 2019 Mar;61(1):16-21. doi: 10.1016/j.job.2019.01.001. Epub 2019 Jan 11.
Osteoclasts are functional cells required for bone resorption. They are derived from hematopoietic precursors and undergo a series of differentiation and fusion steps in response to various humoral factors. Depending on the importance in osteoclastogenesis, the pathways for the differentiation of hematopoietic precursors to mature osteoclasts can be divided into two categories: canonical and the non-canonical. Receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclast formation is considered as an important canonical pathway. Non-canonical pathways of osteoclastogenesis mainly involve several humoral factors that can substitute for RANKL to induce osteoclast formation. Among these factors, tumor necrosis factor (TNF)-α, interleukin (IL)-1, "homologous to lymphotoxins, exhibiting inducible expression, and competing with herpes simplex virus glycoprotein D for herpesvirus entry mediator, a receptor expressed by T lymphocytes" (LIGHT), a proliferation-inducing ligand (APRIL), and B cell-activating factor (BAFF) belong to the TNF superfamily. Other RANKL substitutes are primarily cytokines and growth factors including transforming growth factor β (TGFβ), IL-6, IL-11, nerve growth factor (NGF), insulin-like growth factor (IGF)-I, and IGF-II. In this review, we summarize the involvement of these factors in inducing osteoclastogenesis in vitro. Although these factors weakly induce osteoclast formation, they may play a major role in pathological bone resorption.
破骨细胞是骨吸收所必需的功能性细胞。它们来源于造血前体细胞，并在各种体液因子的作用下经历一系列分化和融合步骤。根据在破骨细胞生成中的重要性，造血前体细胞向成熟破骨细胞分化的途径可分为两类：经典途径和非经典途径。核因子κB受体激活剂配体（RANKL）诱导的破骨细胞形成被认为是一条重要的经典途径。破骨细胞生成的非经典途径主要涉及几种体液因子，它们可以替代RANKL来诱导破骨细胞形成。在这些因子中，肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1、“与淋巴毒素同源，表现出可诱导表达，并与单纯疱疹病毒糖蛋白D竞争疱疹病毒进入介质，一种由T淋巴细胞表达的受体”（LIGHT）、增殖诱导配体（APRIL）和B细胞激活因子（BAFF）属于TNF超家族。其他RANKL替代物主要是细胞因子和生长因子，包括转化生长因子β（TGFβ）、IL-6、IL-11、神经生长因子（NGF）、胰岛素样生长因子（IGF）-I和IGF-II。在本综述中，我们总结了这些因子在体外诱导破骨细胞生成中的作用。尽管这些因子诱导破骨细胞形成的作用较弱，但它们可能在病理性骨吸收中起主要作用。
