ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
FGF9-FGFR2 Signaling via Osteocytes-Preosteoblasts Crosstalks to Mediate Mechanotransduction-Driven Intramembranous Osteogenesis in the Underdeveloped Maxilla.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Signalling Pathways and Mechanical Forces Interact in Craniofacial Development and Homeostasis.International dental journal · 2026Review
- Cellular and Molecular Neuro-Bone Cell Interactions Drive Alveolar Bone Remodeling During Orthodontic Mechanical Loading.International journal of biological sciences · 2026Review
- FGF9-FGFR2 Signaling via Osteocytes-Preosteoblasts Crosstalks to Mediate Mechanotransduction-Driven Intramembranous Osteogenesis in the Underdeveloped Maxilla.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
Maxillary underdevelopment is a critical component of skeletal Class III malocclusion, closely linked to altered biomechanical signaling. Mechanical stimulation through early facemask protraction can effectively promote maxillary growth, yet the underlying mechanotransduction mechanisms remain unclear. In this study, fibroblast growth factor 9 (FGF9) is identified as a key biomechanical responder in maxillary development. Secreted predominantly by osteocytes, FGF9 interacts with fibroblast growth factor receptor 2 (FGFR2) on preosteoblasts to inhibit osteogenic differentiation. Mechanical stress reduces FGF9 secretion from osteocytes, thereby relieving its inhibitory effect and enhancing osteogenesis. Mechanistically, FGF9 promotes nuclear translocation of FGFR2 in preosteoblasts, which modulates transcription factors ATF5 and NR2F1 to suppress bone formation. In vivo, targeted overexpression of FGF9 in bone tissue led to significant maxillary growth impairment, underlying the pathological impact of disrupted mechanical signaling. These findings reveal a novel osteocyte-preosteoblast axis regulated by FGF9-FGFR2 signaling in response to mechanical stimulation and provide mechanistic insight into how biomechanical forces shape craniofacial development. This pathway offers new mechanistic insights and potential therapeutic targets for correcting craniofacial skeletal abnormalities.
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Registered trials
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