- Key is first trimester diagnosis risk: The FGFR pathway has been implicated in the formation of craniosynostosis. In vitro and in vivo mouse studies have focused on potential drugs that affect it. Pharmacological agents include tyrosine inhibitors, NOGGIN protein, and anti- TGFβ2 antibody injected or placed locally onto the suture. There is promising information that suggests that sutural fusion may be inhibited (67). However, these drugs must be given in the first trimester of gestation, applied to the suture before closure, and may have detrimental effects on normal metabolic pathways. Genetic studies will continue to elucidate the molecular cause of craniosynostosis and may lead to nonsurgical, noninvasive therapy for this disorder (54).
- Bone substitutes: Studies are beginning to appear about bone generators and scaffolding material in animal models. While not currently applicable to single suture craniosymostosis, they do bear watching (72).
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