发育性髋关节发育不良不仅仅是髋臼与股骨头对应关系的异常，同时还包括髋臼和股骨头的发育异常。为了克服行走期发育性髋关节发育不良儿童髋关节复位后仍然存在的髋关节不稳定，尤其是髋臼前外侧的发育缺陷， Robert Salter 于1961年发明了 Salter 骨盆截骨术( salter innominate osteotomy，SIO )治疗发育性髋关节发育不良。SIO 以耻骨联合为铰链，可使髋臼向前、下、外恢复覆盖，骨盆截骨处可通过骨块和克氏针固定，从而得到一个稳定复位的髋关节。1962年SIO还用于治疗Perthes病。SIO 至今已经沿用了50余年，治疗了大量的发育性髋关节发育不良病例，结合对于截骨应力、截骨方式的改良、植骨材料以及内固定等多方面的研究，SIO 在全世界多个医学中心获得了良好的短期和长期效果[1]。

Fibroblast growth factor (FGF)/fibroblast growth factor receptor (FGFR) signaling plays essential roles in bone development and diseases. Missense mutations in FGFs and FGFRs in humans can cause various congenital bone diseases, including chondrodysplasia syndromes, craniosynostosis syndromes and syndromes with dysregulated phosphate metabolism. FGF/FGFR signaling is also an important pathway involved in the maintenance of adult bone homeostasis. Multiple kinds of mouse models, mimicking human skeleton diseases caused by missense mutations in FGFs and FGFRs, have been established by knock-in/out and transgenic technologies. These genetically modified mice provide good models for studying the role of FGF/FGFR signaling in skeleton development and homeostasis. In this review, we summarize the mouse models of FGF signaling-related skeleton diseases and recent progresses regarding the molecular mechanisms, underlying the role of FGFs/FGFRs in the regulation of bone development and homeostasis. This review also provides a perspective view on future works to explore the roles of FGF signaling in skeletal development and homeostasis.