骨愈合
医学
兰克尔
软骨内骨化
肿瘤坏死因子α
骨重建
骨吸收
免疫学
白细胞介素
炎症
免疫系统
癌症研究
细胞生物学
细胞因子
内科学
生物
软骨
解剖
受体
激活剂(遗传学)
作者
Tae-Joon Cho,Louis C. Gerstenfeld,George L. Barnes,Thomas A. Einhorn
出处
期刊:Current Opinion in Orthopaedics
[Ovid Technologies (Wolters Kluwer)]
日期:2001-10-01
卷期号:12 (5): 403-408
被引量:13
标识
DOI:10.1097/00001433-200110000-00007
摘要
Fracture healing has been speculated to recapitulate the processes of skeletal embryogenesis; however, the occurrence of an early inflammatory response and associated up-regulated expression of pro-inflammatory cytokines makes fracture healing distinct. The pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6) have been shown not only to coordinate the hematopoietic and immune systems, but also to contribute to bone repair by regulating osteoclastogenesis and the early recruitment and differentiation of osteoblastic lineage cells. Novel members of TNF/TNFR superfamily—RANKL, RANK, and OPG— were identified as the crucial factors in osteoclastogenesis and directly involved in the endochondral resorption and the remodeling phase of fracture healing. Further investigation into the roles and interactions of each of these cytokines is necessary for a better understanding of the normal and pathologic fracture healing and for the development of treatment tools to enhance it.
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