IWILLASCENDD
Iron
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MARPE/FME are known for breaking open the midpalatal sutures and loosening all the surrounding sutures.
FGFR1-2 Inhibitors multiply the fibrous connective tissue in these sutures, keeping them open for longer for more forward growth in the maxilla.
Those with Crouzon syndrome have hyperactive FGFR2 levels and their craniofacial development stops very early because of the closing of those sutures.
MARPE/FME + facemask is comparable to a non-surgical lefort 3 in the hands of a good orthodontist. Plus, when you open your maxillary sutures, you can keep them open with FGFR1-2 inhibitors to maximize the forward growth without surgery.
Link to the forum
https://wholebodybreathing.com/comm...oving-the-maxilla-up-and-forwards/#post-24711
However, MARPE/FME + Facemask do give forward growth, but it is very minimal, and this is because of the limited time that your maxillary sutures remain open.
"Also keep in mind that if you want to achieve 18mm of forward displacement, you would need to find a way to keep the sutures open indefinitely, as those kind of gains will take a year or more to achieve."
This study shows that when inhibiting FGFR2 in Crouzon Syndrome mice, they were able to successfully prevent premature suture fusion without obvious adverse effects.
https://pmc.ncbi.nlm.nih.gov/articles/PMC1693709/
"We conclude that, when applied in a certain range of concentration, PLX052 is capable of attenuating the signal emanating from the activated Crouzon-like Fgfr2c mutant to prevent premature suture fusion, and that the attenuated signal transmitted from the normal Fgfr2c allele under these conditions still permits undisturbed suture growth and development."
The drug the study used was PLX052 which binds to the FGFR kinase domain and blocks its ability to transmit signals downstream.
This reduces downstream signaling pathways such as FRS2α phosphorylation and MAPK/ERK signaling, which are activated by FGFR2.
In the Crouzon mouse model, reducing this excessive FGFR2 signaling prevented premature coronal suture fusion in cultured skull tissue.
TLDR: If people can get their hands on a selective fgfr1-2, or something that works similarly to PLX052, then they can theoretically delay suture fusion during MARPE/FME to maximize forward growth and direct it upwards with facemask.
btw this is my first post
pls dont dnr
this is all just a theory btw hopefully someone tries something like this out during their expansion
FGFR1-2 Inhibitors multiply the fibrous connective tissue in these sutures, keeping them open for longer for more forward growth in the maxilla.
Those with Crouzon syndrome have hyperactive FGFR2 levels and their craniofacial development stops very early because of the closing of those sutures.
MARPE/FME + facemask is comparable to a non-surgical lefort 3 in the hands of a good orthodontist. Plus, when you open your maxillary sutures, you can keep them open with FGFR1-2 inhibitors to maximize the forward growth without surgery.
Link to the forum
https://wholebodybreathing.com/comm...oving-the-maxilla-up-and-forwards/#post-24711
However, MARPE/FME + Facemask do give forward growth, but it is very minimal, and this is because of the limited time that your maxillary sutures remain open.
"Also keep in mind that if you want to achieve 18mm of forward displacement, you would need to find a way to keep the sutures open indefinitely, as those kind of gains will take a year or more to achieve."
This study shows that when inhibiting FGFR2 in Crouzon Syndrome mice, they were able to successfully prevent premature suture fusion without obvious adverse effects.
https://pmc.ncbi.nlm.nih.gov/articles/PMC1693709/
"We conclude that, when applied in a certain range of concentration, PLX052 is capable of attenuating the signal emanating from the activated Crouzon-like Fgfr2c mutant to prevent premature suture fusion, and that the attenuated signal transmitted from the normal Fgfr2c allele under these conditions still permits undisturbed suture growth and development."
The drug the study used was PLX052 which binds to the FGFR kinase domain and blocks its ability to transmit signals downstream.
This reduces downstream signaling pathways such as FRS2α phosphorylation and MAPK/ERK signaling, which are activated by FGFR2.
In the Crouzon mouse model, reducing this excessive FGFR2 signaling prevented premature coronal suture fusion in cultured skull tissue.
TLDR: If people can get their hands on a selective fgfr1-2, or something that works similarly to PLX052, then they can theoretically delay suture fusion during MARPE/FME to maximize forward growth and direct it upwards with facemask.
btw this is my first post
pls dont dnr
this is all just a theory btw hopefully someone tries something like this out during their expansion
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