Found a way to reopen growth plates (2 Viewers)

[DoorHandle5]

Dexter PrettyBoyMaxxing

For the proliferating zone, I sent this to my boy cuz I have no retort honestly, he said this:







the proliferating zone, once resuscitated, will build a gap between the osteoblasts and the resting zone's stem cells. once the gap is created by these columnar chondrocytes stacking one atop the other, the PTHrP gradient will naturally become great enough that prehypertrophic and hypertrophic zones can develop. these zones develop organically without the need for us to act. the key is the proliferating zone. if that is resuscitated, all bets are off. the gradients that are vital develop naturally by virtue of spacing. hormones need to be managed (AI's), but the zones themselves will otherwise provide the signals they all need to maintain themselves.



that written, there's a plethora of research done examining what transpires when SOX, PTHrP, and SMO agonists (or other Hedgehog pathway activators or enhancers) are applied to the growth plates of animal models, and from these studies, we can paint a picture of how plastic and flexible the system is, and how readily progenitors in the resting zone (mesenchymal stem cells) operate to generate chondrocytes if given the right circumstances. hell, in rabbits, they've even studied dissection of the growth plate and aberrant reinsertion (perpendicular to the original direction) and found that the growth plate would add length along the width of the bone. it demonstrates that the stem cells in the resting zone are polarized, and they will generate columns even if oriented in aberrant directions. they've studied constitutive Hedgehog activation (constantly active Hedgehog signaling) in murine models, done via PTCH1 knockout, and found that cartilaginous "islands" (ectopic cartilage) can be produced off the resting zone's chondroprogenitors. these studies elucidate that influencers like PTHrP, SOX, and even Hedgehog molecules can whip up a proliferative response dedicated to endochrondral ossification in theory. the trick is now seeing if we can harness that in vivo, which is admittedly extremely challenging to do! I will never take away from how difficult this is when local application of these agents is not possible. that is the crux of the problem to me. give me a way to ensure that the stem cell niche is constantly and specifically inundated with PTHrP & SOX proteins, and I will be much more optimistic. currently, no recourse therein. systemic circulation is the only hope.



I’m trying to recreate resting & proliferating zones. That’s the fundamental mission, and if there are remnant stem cells present, enough stimulation with PTHrP & SOX could potentially inhibit osteogenic pressures and induce the chondrogenesis necessary to recreate a proliferating zone that can build space between the resting zone and the osteoblast-containing front.



if I'm not mistaken, I think there might actually be research currently ongoing in which the researchers are seeking to cause transdifferentiation (from osteoblast to chondrocyte) of the cells of the fused epiphysis. my fixation is on a parallel strategy that focuses instead on multipotent stem cells that may already be present. these cells obviously have the potential to differentiate chondrogenically if inundated with the right factors.



the premise is that a sliver of cartilage would need to be generated first. this will be the resting zone. if that resting zone can survive with continuous PTHrP & SOX pressure, the proliferating zone ensues. with continuing chondrogenic pressure, the proliferating zone expands enough to buy the resting zone enough of a buffer to no longer require the inundation of PTHrP & SOX proteins. at this point, exogenous PTHrP supply is abrogated, and a natural PTHrP gradient develops that allows for prehypertrophic and hypertrophic zones to develop distal to the resting zone.



and just to reiterate becuz we seem to continuously come circling back to the fact that a functional growth plate has prehypertrophic and hypertrophic zones, as well as the proliferating & resting zones that I've chosen to fixate on. the point is that these former zones will develop organically once PTHrP provision is ceased because of the AMPLE osteogenic pressure provided by the cells of the trabecular bone below the growth plate. PTHrP & SOX generated by chondroprogenitors of the resting zone will not diffuse far enough away from the resting zone, and the consequent gradient will allow for chondrocyte hypertrophy to begin. there's no need for us to manipulate anything to facilitate the development of prehypertrophic and hypertrophic zones; the bone will ensure that that happens, anyway.



the bone WILL NOT allow for a proliferating zone to develop sans heavy SOX pressure, though. that is the part we have to play God on. hence, inundation with abaloparatide that can induce SOX activity. this ensures MSC renewal (PTHrP) and chondrogenesis at the expense of osteogenesis (SOX)

You haven’t responded to this either Synapse

Ur all talk bro

 

[DoorHandle5]

that's what I Initially thought but it was pretty clear he was using some form of ai (dexter)
View attachment 40597

Ai detectors aren’t accurate I believe but who knows

 

[Synapse]

took me a while to realize that as well, just at about 2022

all the issue with heightmaxxing come from something as simple as body homeostasis lol, thats the funniest part, hgh can help aid to reach your genetic potential but def will not make you taller than, if you are a manlet and have manlet genes no ammount of hgh will change that.

 

[Telmisartan]

ngl i kinda get him, not even worth putting that much effort into debunking something that stupid.

Same level of stupidity as humming for bone mass ngl

"Just open your growth plates again"

Nigga feeling like a YouTube influencer

View: https://m.youtube.com/watch?v=QnN7MWHs068

 

[Synapse]

You haven’t responded to this either Synapse

Ur all talk bro

im not gonna waste my time babbling cause i would make the same arguments as them, even funnier, if your theory worked trust me big pharma would've already taken advantage of it to make as much money from it as possible.

 

[Telmisartan]

Dexter PrettyBoyMaxxing

For the proliferating zone, I sent this to my boy cuz I have no retort honestly, he said this:







the proliferating zone, once resuscitated, will build a gap between the osteoblasts and the resting zone's stem cells. once the gap is created by these columnar chondrocytes stacking one atop the other, the PTHrP gradient will naturally become great enough that prehypertrophic and hypertrophic zones can develop. these zones develop organically without the need for us to act. the key is the proliferating zone. if that is resuscitated, all bets are off. the gradients that are vital develop naturally by virtue of spacing. hormones need to be managed (AI's), but the zones themselves will otherwise provide the signals they all need to maintain themselves.



that written, there's a plethora of research done examining what transpires when SOX, PTHrP, and SMO agonists (or other Hedgehog pathway activators or enhancers) are applied to the growth plates of animal models, and from these studies, we can paint a picture of how plastic and flexible the system is, and how readily progenitors in the resting zone (mesenchymal stem cells) operate to generate chondrocytes if given the right circumstances. hell, in rabbits, they've even studied dissection of the growth plate and aberrant reinsertion (perpendicular to the original direction) and found that the growth plate would add length along the width of the bone. it demonstrates that the stem cells in the resting zone are polarized, and they will generate columns even if oriented in aberrant directions. they've studied constitutive Hedgehog activation (constantly active Hedgehog signaling) in murine models, done via PTCH1 knockout, and found that cartilaginous "islands" (ectopic cartilage) can be produced off the resting zone's chondroprogenitors. these studies elucidate that influencers like PTHrP, SOX, and even Hedgehog molecules can whip up a proliferative response dedicated to endochrondral ossification in theory. the trick is now seeing if we can harness that in vivo, which is admittedly extremely challenging to do! I will never take away from how difficult this is when local application of these agents is not possible. that is the crux of the problem to me. give me a way to ensure that the stem cell niche is constantly and specifically inundated with PTHrP & SOX proteins, and I will be much more optimistic. currently, no recourse therein. systemic circulation is the only hope.



I’m trying to recreate resting & proliferating zones. That’s the fundamental mission, and if there are remnant stem cells present, enough stimulation with PTHrP & SOX could potentially inhibit osteogenic pressures and induce the chondrogenesis necessary to recreate a proliferating zone that can build space between the resting zone and the osteoblast-containing front.



if I'm not mistaken, I think there might actually be research currently ongoing in which the researchers are seeking to cause transdifferentiation (from osteoblast to chondrocyte) of the cells of the fused epiphysis. my fixation is on a parallel strategy that focuses instead on multipotent stem cells that may already be present. these cells obviously have the potential to differentiate chondrogenically if inundated with the right factors.



the premise is that a sliver of cartilage would need to be generated first. this will be the resting zone. if that resting zone can survive with continuous PTHrP & SOX pressure, the proliferating zone ensues. with continuing chondrogenic pressure, the proliferating zone expands enough to buy the resting zone enough of a buffer to no longer require the inundation of PTHrP & SOX proteins. at this point, exogenous PTHrP supply is abrogated, and a natural PTHrP gradient develops that allows for prehypertrophic and hypertrophic zones to develop distal to the resting zone.



and just to reiterate becuz we seem to continuously come circling back to the fact that a functional growth plate has prehypertrophic and hypertrophic zones, as well as the proliferating & resting zones that I've chosen to fixate on. the point is that these former zones will develop organically once PTHrP provision is ceased because of the AMPLE osteogenic pressure provided by the cells of the trabecular bone below the growth plate. PTHrP & SOX generated by chondroprogenitors of the resting zone will not diffuse far enough away from the resting zone, and the consequent gradient will allow for chondrocyte hypertrophy to begin. there's no need for us to manipulate anything to facilitate the development of prehypertrophic and hypertrophic zones; the bone will ensure that that happens, anyway.



the bone WILL NOT allow for a proliferating zone to develop sans heavy SOX pressure, though. that is the part we have to play God on. hence, inundation with abaloparatide that can induce SOX activity. this ensures MSC renewal (PTHrP) and chondrogenesis at the expense of osteogenesis (SOX)

Nigga typed allat and seriously expected someone to read holy

 

[PrettyBoyMaxxing]

That’s just a fallacy. Simply put they aren’t measuring for GP opening so they won’t see it. Plus this specific theory was not put into place

When a drug like abalo is in clinical trials, patients DO regular x-rays and dexa's to monitor bone density, a gp reopening would clearly be shown ON these, you are simply adding more conditions to cope with the fact your a clueless moron, and radiologists are specifically trained to see and find changes.

"This specific theory was not put into place."
This is like saying, "Nobody has tried to fly by jumping off a building while wearing a specific mix of blue and red socks, so you can't say it doesn't work. Fucking kill yourself.

fyi the law of gravity doesn't give 2 fucks about the color of your socks.
now in comparison, the law of terminal differentiation doesn't care about which specific compounds you are using, drill that into your head.

you do if ur gonna say I should be the only one replying

you’re making a logical claim, In any debate, the person making the fucking claim has the burden of proof

 

[Michael1295]

I'm very skeptical of this.

 

[DoorHandle5]

im not gonna waste my time babbling cause i would make the same arguments as them, even funnier, if your theory worked trust me big pharma would've already taken advantage of it to make as much money from it as possible.

You wouldn’t make the same argument as them because you don’t know anything.

Nigga typed allat and seriously expected someone to read holy

That’s on me

When a drug like abalo is in clinical trials, patients DO regular x-rays and dexa's to monitor bone density, a gp reopening would clearly be shown ON these, you are simply adding more conditions to cope with the fact your a clueless moron, and radiologists are specifically trained to see and find changes.

they monitor bone density but do they monitor the gp’s specifically? Measuring for open growth played is an entirely Different matter and one can also chalk it up to error such as not paying attention to it, although you are right this does raise major concern. I don’t see the need for the insults though. Can you show me some studies of them doing specific x rays around the gp please?

"This specific theory was not put into place."
This is like saying, "Nobody has tried to fly by jumping off a building while wearing a specific mix of blue and red socks, so you can't say it doesn't work. Fucking kill yourself.

fyi the law of gravity doesn't give 2 fucks about the color of your socks.
now in comparison, the law of terminal differentiation doesn't care about which specific compounds you are using, drill that into your head.

Yeah no that’s how science works. A specific theory has to be tested in order for it to be proven true/false; either that or you must use inductive thinking / logical deduction to prove that it can/cannot work which is what we are trying to do but not sure why you’re telling me to kms. Is this really the thanks I get for tryna share a helpful theory? I don’t see how any of this could lead to insults / you getting mad? Is it because you had no counterpoint to the response I provided from my boy?

you’re making a logical claim, In any debate, the person making the fucking claim has the burden of proof

Again according to what moral framework? Who said I specifically have to do it? The point is that I brought the information, sure my friend typed the response but I still gave it. This isn’t some official debate bro, this is Looksmax.gg. Who cares who it comes from. Take it easy

 

[DoorHandle5]

When a drug like abalo is in clinical trials, patients DO regular x-rays and dexa's to monitor bone density, a gp reopening would clearly be shown ON these, you are simply adding more conditions to cope with the fact your a clueless moron, and radiologists are specifically trained to see and find changes.

"This specific theory was not put into place."
This is like saying, "Nobody has tried to fly by jumping off a building while wearing a specific mix of blue and red socks, so you can't say it doesn't work. Fucking kill yourself.

fyi the law of gravity doesn't give 2 fucks about the color of your socks.
now in comparison, the law of terminal differentiation doesn't care about which specific compounds you are using, drill that into your head.

you’re making a logical claim, In any debate, the person making the fucking claim has the burden of proof

Genuinely just chill out bro , it’s not that serious

Be happy

 

[Synapse]

Same level of stupidity as humming for bone mass ngl

"Just open your growth plates again"

Nigga feeling like a YouTube influencer

View: https://m.youtube.com/watch?v=QnN7MWHs068

Nigga is trying to apply mouse biology to human biology, its stupid af, it's useless if you signal something that is already dead and closed, even more stupid to extrapolate info from animal studies and think that human biology makes a perfect conversion from it, even more to think you can alter the state of solid bone, you cant reverse the cartilage ossification at all, once its ossified there is no way back, also you can't even make this function localized, and also the biggest fallacy of this is the fact that if people grew because of PTH analogs women would grow after using them for osteporosis.

There is no niche or any functional cartilage left for chondrocytes to work on whatsoever, so the PTH proliferation theory is so bs, the studies and theory also only demonstrates plasticity and not the power to reverse the ossification, also what he mentioned of the "PTCH1 knockout" even tho this can expand the columns it can also create joint deformities, exostoses, growth retardation, and tumors not the controlled longitudinal growth that he is thinking about, also another fallacy, what he mentioned of the "PTHrP/SOX9" only shows that they can help maintain the proliferation and inhibit hypertrophy, and aid the repair of the physeal injuries, but not reopen fused growth plates, no way to revive fused bone, also the insane risk of an osteosarcoma, also no way to organize cell in a 3d controlled way as a columnar structure resting with proliferating columns (prehypertrophic and hypertrophic), polarized stem cells, and with real balanced paracrine gradients (which are the PTHrP from the resting zone vs. Ihh from the hypertrophic zone),again after ossification it's just bone with no real cartilage niche. Also all the clinical trials is just studies performed on animals with open growth plates, all of this is use to treat physeal injuries not reverse it.
PrettyBoyMaxxing

 

[Synapse]

When a drug like abalo is in clinical trials, patients DO regular x-rays and dexa's to monitor bone density, a gp reopening would clearly be shown ON these, you are simply adding more conditions to cope with the fact your a clueless moron, and radiologists are specifically trained to see and find changes.

"This specific theory was not put into place."
This is like saying, "Nobody has tried to fly by jumping off a building while wearing a specific mix of blue and red socks, so you can't say it doesn't work. Fucking kill yourself.

fyi the law of gravity doesn't give 2 fucks about the color of your socks.
now in comparison, the law of terminal differentiation doesn't care about which specific compounds you are using, drill that into your head.

you’re making a logical claim, In any debate, the person making the fucking claim has the burden of proof

same retarded fallacy of "muh hgh for bones" you cant controll how bone growth works, the fact you use something doesnt mean it will cause longitudinal growth or will add more layers to it, same bs as people who expect to blast pharma to grow localized their zygos or browridge. People expect pharma to give them exactly 10mm of projection exactly where they want.

 

[Synapse]

You wouldn’t make the same argument as them because you don’t know anything.

That’s on me

they monitor bone density but do they monitor the gp’s specifically? Measuring for open growth played is an entirely Different matter and one can also chalk it up to error such as not paying attention to it, although you are right this does raise major concern. I don’t see the need for the insults though. Can you show me some studies of them doing specific x rays around the gp please?

Yeah no that’s how science works. A specific theory has to be tested in order for it to be proven true/false; either that or you must use inductive thinking / logical deduction to prove that it can/cannot work which is what we are trying to do but not sure why you’re telling me to kms. Is this really the thanks I get for tryna share a helpful theory? I don’t see how any of this could lead to insults / you getting mad? Is it because you had no counterpoint to the response I provided from my boy?

Again according to what moral framework? Who said I specifically have to do it? The point is that I brought the information, sure my friend typed the response but I still gave it. This isn’t some official debate bro, this is Looksmax.gg. Who cares who it comes from. Take it easy

you can see it with any fucking xray moron, they dont have to scan for it specifically, if such a thing occured it would def be noticed.

 

[Synapse]

When a drug like abalo is in clinical trials, patients DO regular x-rays and dexa's to monitor bone density, a gp reopening would clearly be shown ON these, you are simply adding more conditions to cope with the fact your a clueless moron, and radiologists are specifically trained to see and find changes.

"This specific theory was not put into place."
This is like saying, "Nobody has tried to fly by jumping off a building while wearing a specific mix of blue and red socks, so you can't say it doesn't work. Fucking kill yourself.

fyi the law of gravity doesn't give 2 fucks about the color of your socks.
now in comparison, the law of terminal differentiation doesn't care about which specific compounds you are using, drill that into your head.

you’re making a logical claim, In any debate, the person making the fucking claim has the burden of proof

It's just wishful thinking at it's finest with this type of theories.

 

[Synapse]

You wouldn’t make the same argument as them because you don’t know anything.

That’s on me

they monitor bone density but do they monitor the gp’s specifically? Measuring for open growth played is an entirely Different matter and one can also chalk it up to error such as not paying attention to it, although you are right this does raise major concern. I don’t see the need for the insults though. Can you show me some studies of them doing specific x rays around the gp please?

Yeah no that’s how science works. A specific theory has to be tested in order for it to be proven true/false; either that or you must use inductive thinking / logical deduction to prove that it can/cannot work which is what we are trying to do but not sure why you’re telling me to kms. Is this really the thanks I get for tryna share a helpful theory? I don’t see how any of this could lead to insults / you getting mad? Is it because you had no counterpoint to the response I provided from my boy?

Again according to what moral framework? Who said I specifically have to do it? The point is that I brought the information, sure my friend typed the response but I still gave it. This isn’t some official debate bro, this is Looksmax.gg. Who cares who it comes from. Take it easy

He already clearly debunked your bs slop, keep back peddling.

 

[DoorHandle5]

Nigga is trying to apply mouse biology to human biology, its stupid af, it's useless if you signal something that is already dead and closed, even more stupid to extrapolate info from animal studies and think that human biology makes a perfect conversion from it, even more to think you can alter the state of solid bone, you cant reverse the cartilage ossification at all, once its ossified there is no way back, also you can't even make this function localized, and also the biggest fallacy of this is the fact that if people grew because of PTH analogs women would grow after using them for osteporosis.

Copium. I already explained the theory and how it’s possible. Rather than refuting it, you just restated your premise (“it’s not possible”)

And animals/human biology are pretty similar. It’s not really fallacious to use one to try and justify the other. But anyway that’s why this is just a theory.

you can see it with any fucking xray moron, they dont have to scan for it specifically, if such a thing occured it would def be noticed.

Prove it

There is no niche or any functional cartilage left for chondrocytes to work on whatsoever, so the PTH proliferation theory is so bs, the studies and theory also only demonstrates plasticity and not the power to reverse the ossification, also what he mentioned of the "PTCH1 knockout" even tho this can expand the columns it can also create joint deformities, exostoses, growth retardation, and tumors not the controlled longitudinal growth that he is thinking about, also another fallacy, what he mentioned of the "PTHrP/SOX9" only shows that they can help maintain the proliferation and inhibit hypertrophy, and aid the repair of the physeal injuries, but not reopen fused growth plates, no way to revive fused bone, also the insane risk of an osteosarcoma, also no way to organize cell in a 3d controlled way as a columnar structure resting with proliferating columns (prehypertrophic and hypertrophic), polarized stem cells, and with real balanced paracrine gradients (which are the PTHrP from the resting zone vs. Ihh from the hypertrophic zone),again after ossification it's just bone with no real cartilage niche. Also all the clinical trials is just studies performed on animals with open growth plates, all of this is use to treat physeal injuries not reverse it.
@ /data/avatars/s/0/737.jpg?1774733564 PrettyBoyMaxxing

this niche does remain, https://pmc.ncbi.nlm.nih.gov/articl...tic stem,to cancer initiation and progression.

“even tho this can expand the columns it can also create joint deformities, exostoses, growth retardation, and tumors”
Has this been found in studies regarding abaloparatide? Furthermore nobody is saying risk doesn’t exist. I just don’t care. Risk doesn’t negate the validity of the theory.

 

[DoorHandle5]

He already clearly debunked your bs slop, keep back peddling.

So how can we effectively rescusitate the growth plate? Do u have any theories of ur own?

 

[PrettyBoyMaxxing]

Copium. I already explained the theory and how it’s possible. Rather than refuting it, you just restated your premise (“it’s not possible”)

And animals/human biology are pretty similar. It’s not really fallacious to use one to try and justify the other. But anyway that’s why this is just a theory.

Mice have indeterminate growth and we have determinate growth with estrogen induced terminal fusion, using a 14 day old mouse study to justify this stupid protocol is funny

 

[PrettyBoyMaxxing]

Prove it

If a 40 year old suddenly developed a 2mm non calcified gap, they would believe it's lytic lesion which would then bring more attention to the matter until they've found out your supposed theory

this niche does remain, https://pmc.ncbi.nlm.nih.gov/articles/PMC6204189/#:~:text=Adult tissues retain somatic stem,to cancer initiation and progression.

“even tho this can expand the columns it can also create joint deformities, exostoses, growth retardation, and tumors”
Has this been found in studies regarding abaloparatide? Furthermore nobody is saying risk doesn’t exist. I just don’t care. Risk doesn’t negate the validity of the theory.

Risk actually does negate the validity if the 'growth' isn't longitudinal. If your theory produces exostoses and chondroid lesions instead of a polarized growth plate, you haven't 'reopened' anything you just triggered pathology imo, validity requires the intended outcome not just random cell growth, go ahead and try your theory

 

[Synapse]

Copium. I already explained the theory and how it’s possible. Rather than refuting it, you just restated your premise (“it’s not possible”)

And animals/human biology are pretty similar. It’s not really fallacious to use one to try and justify the other. But anyway that’s why this is just a theory.

Prove it

this niche does remain, https://pmc.ncbi.nlm.nih.gov/articles/PMC6204189/#:~:text=Adult tissues retain somatic stem,to cancer initiation and progression.

“even tho this can expand the columns it can also create joint deformities, exostoses, growth retardation, and tumors”
Has this been found in studies regarding abaloparatide? Furthermore nobody is saying risk doesn’t exist. I just don’t care. Risk doesn’t negate the validity of the theory.

Completely wrong with the take that animal biology is the same as human biology, it's actually pretty fucking diff on every single level, keep backpeddling with the claims "thats why this is just a theory" but you were affirming this would work, all the lab rat studies you mentioned, the xrays and scans only showed increase of BMD not elongation of the bones or the revival of cells and chondrocytes, when you are conducting a scientific research anomalies need to be mentioned and noted, guess what? none of the studies mentioned showed or noted any of that, this studies are conducted by real scientists not people like you, also the entire growth plate cartilage undergoes programmed senescence, the entire plates is replaced by bone and the left chondrocytes are disorganized and not on any sort of structure that could be re used for longitudinal

If a 40 year old suddenly developed a 2mm non calcified gap, they would believe it's lytic lesion which would then bring more attention to the matter until they've found out your supposed theory

Risk actually does negate the validity if the 'growth' isn't longitudinal. If your theory produces exostoses and chondroid lesions instead of a polarized growth plate, you haven't 'reopened' anything you just triggered pathology imo, validity requires the intended outcome not just random cell growth, go ahead and try your theory

bone growth, also PTH analogs promote bone formation that's why they are use to increase BMD, but they don't keep the cartilage alive which is what i needed for it to then ossify, basically because when you have closed growth plates THERE IS NOT CARTILAGE LEFT, also the cartilage niche goes to shit once the plate is already ossified, also there is no way to control the highly osteogenic environment, if we ignore all what i said before and this magically works it would ossify super fast, not the span of time needed for proper cartilage growth and then ossification, all the animal studies conducted also don't show any evidence that could proof this at all whatsoever,

 

[Synapse]

If a 40 year old suddenly developed a 2mm non calcified gap, they would believe it's lytic lesion which would then bring more attention to the matter until they've found out your supposed theory

Risk actually does negate the validity if the 'growth' isn't longitudinal. If your theory produces exostoses and chondroid lesions instead of a polarized growth plate, you haven't 'reopened' anything you just triggered pathology imo, validity requires the intended outcome not just random cell growth, go ahead and try your theory

Bone growth comes in a ton of diff ways, not just elongation, this is why all the pharma for increasing bones with this and that is retarded af, you can't control where the growth is gonna occur and certainly not localized.

 

[PrettyBoyMaxxing]

they monitor bone density but do they monitor the gp’s specifically? Measuring for open growth played is an entirely Different matter and one can also chalk it up to error such as not paying attention to it, although you are right this does raise major concern. I don’t see the need for the insults though. Can you show me some studies of them doing specific x rays around the gp please?

A radiologist’s entire job is pattern recognition. An adult femur is supposed to be a continuous, solid white structure on an x-ray. If a growth plate reappeared, it would show up as a black gap in the bone, do you not understand that?

Yeah no that’s how science works. A specific theory has to be tested in order for it to be proven true/false; either that or you must use inductive thinking / logical deduction to prove that it can/cannot work which is what we are trying to do but not sure why you’re telling me to kms. Is this really the thanks I get for tryna share a helpful theory? I don’t see how any of this could lead to insults / you getting mad? Is it because you had no counterpoint to the response I provided from my boy?

We don't need to test every theory if it violates a biological law. We don't test if jumping off a building while wearing blue socks makes you fly, because we understand gravity. if you want me to explain that compparison, think of terminal differentiation as gravity, once a cell's dna is methylated and locked into osteocyte, it loses chromatin access to even become a growth plate again... you can't inudate a cell with signals if the cell has already thrown away the receiver for those signals.

Again according to what moral framework? Who said I specifically have to do it? The point is that I brought the information, sure my friend typed the response but I still gave it. This isn’t some official debate bro, this is Looksmax.gg. Who cares who it comes from. Take it easy

well nope, it'd be like tucking your tail under your legs and pussying out due to your lack of education, he should be the one presenting it if he's replying to us, I don't like middle mans.

 

[PrettyBoyMaxxing]

So how can we effectively rescusitate the growth plate? Do u have any theories of ur own?

Bone growth comes in a ton of diff ways, not just elongation, this is why all the pharma for increasing bones with this and that is retarded af, you can't control where the growth is gonna occur and certainly not localized.

niggas will quite literally do anything but accept reality and get LL/filler

 

[Synapse]

niggas will quite literally do anything but accept reality and get LL/filler

Completely wrong with the take that animal biology is the same as human biology, it's actually pretty fucking diff on every single level, keep backpeddling with the claims "thats why this is just a theory" but you were affirming this would work, all the lab rat studies you mentioned, the xrays and scans only showed increase of BMD not elongation of the bones or the revival of cells and chondrocytes, when you are conducting a scientific research anomalies need to be mentioned and noted, guess what? none of the studies mentioned showed or noted any of that, this studies are conducted by real scientists not people like you, also the entire growth plate cartilage undergoes programmed senescence, the entire plates is replaced by bone and the left chondrocytes are disorganized and not on any sort of structure that could be re used for longitudinal


bone growth, also PTH analogs promote bone formation that's why they are use to increase BMD, but they don't keep the cartilage alive which is what i needed for it to then ossify, basically because when you have closed growth plates THERE IS NOT CARTILAGE LEFT, also the cartilage niche goes to shit once the plate is already ossified, also there is no way to control the highly osteogenic environment, if we ignore all what i said before and this magically works it would ossify super fast, not the span of time needed for proper cartilage growth and then ossification, all the animal studies conducted also don't show any evidence that could proof this at all whatsoever,

true, also this, every single pathway wrong as well for what i explained here.

 

[Synapse]

niggas will quite literally do anything but accept reality and get LL/filler

Basically, 1: growth plates senescence prohibits this as this is a genetic biological process 2: once it's solid bone there is not cartilage matrix left, all bone, 3: even if there is is the cell and cartilage structure is completely disorganized which would not cause any longitudinal organized growth, 4 the gene once methylated is not usable at all, 5: you cant signal it to work again cause its already fused, 6: there needs to be something taking care of the cartilage to create for it not to instantly ossify cause of the highly osteogenic environment (explained in more words: "PTCH1 knockout" even tho this can expand the columns it can also create joint deformities, exostoses, growth retardation, and tumors not the controlled longitudinal growth that he is thinking about, also another fallacy, what he mentioned of the "PTHrP/SOX9" only shows that they can help maintain the proliferation and inhibit hypertrophy, and aid the repair of the physeal injuries, but not reopen fused growth plates, no way to revive fused bone, also the insane risk of an osteosarcoma, also no way to organize cell in a 3d controlled way as a columnar structure resting with proliferating columns (prehypertrophic and hypertrophic), polarized stem cells, and with real balanced paracrine gradients (which are the PTHrP from the resting zone vs. Ihh from the hypertrophic zone),again after ossification it's just bone with no real cartilage niche).

 

[Synapse]

A radiologist’s entire job is pattern recognition. An adult femur is supposed to be a continuous, solid white structure on an x-ray. If a growth plate reappeared, it would show up as a black gap in the bone, do you not understand that?

We don't need to test every theory if it violates a biological law. We don't test if jumping off a building while wearing blue socks makes you fly, because we understand gravity. if you want me to explain that compparison, think of terminal differentiation as gravity, once a cell's dna is methylated and locked into osteocyte, it loses chromatin access to even become a growth plate again... you can't inudate a cell with signals if the cell has already thrown away the receiver for those signals.

well nope, it'd be like tucking your tail under your legs and pussying out due to your lack of education, he should be the one presenting it if he's replying to us, I don't like middle mans.

funny how op is not willing to test this, at the end of the day who doesnt wanna be taller?

 

[FoidSlayer]

funny how op is not willing to test this, at the end of the day who doesnt wanna be taller?

I dnrd, this is about stem cells isn't it?

 

[Synapse]

I dnrd, this is about stem cells isn't it?

just schizo bs theories of cherry picked info with no real argument basis about that and pth analogs.

 

[DoorHandle5]

funny how op is not willing to test this, at the end of the day who doesnt wanna be taller?

Nope it’s gonna get tested. The original guy who gave me this theory said he finna try in 3 months

Ur saying I should avoid it?

 

[rapist]

 

[birthdefect]

I find that I have no retort.

its ok WE have made a mistake like this before
conflating mice plates with human plates when mice one just never fully fuse like humans do

 

[Dexter]

Dexter PrettyBoyMaxxing

For the proliferating zone, I sent this to my boy cuz I have no retort honestly, he said this:







the proliferating zone, once resuscitated, will build a gap between the osteoblasts and the resting zone's stem cells. once the gap is created by these columnar chondrocytes stacking one atop the other, the PTHrP gradient will naturally become great enough that prehypertrophic and hypertrophic zones can develop. these zones develop organically without the need for us to act. the key is the proliferating zone. if that is resuscitated, all bets are off. the gradients that are vital develop naturally by virtue of spacing. hormones need to be managed (AI's), but the zones themselves will otherwise provide the signals they all need to maintain themselves.



that written, there's a plethora of research done examining what transpires when SOX, PTHrP, and SMO agonists (or other Hedgehog pathway activators or enhancers) are applied to the growth plates of animal models, and from these studies, we can paint a picture of how plastic and flexible the system is, and how readily progenitors in the resting zone (mesenchymal stem cells) operate to generate chondrocytes if given the right circumstances. hell, in rabbits, they've even studied dissection of the growth plate and aberrant reinsertion (perpendicular to the original direction) and found that the growth plate would add length along the width of the bone. it demonstrates that the stem cells in the resting zone are polarized, and they will generate columns even if oriented in aberrant directions. they've studied constitutive Hedgehog activation (constantly active Hedgehog signaling) in murine models, done via PTCH1 knockout, and found that cartilaginous "islands" (ectopic cartilage) can be produced off the resting zone's chondroprogenitors. these studies elucidate that influencers like PTHrP, SOX, and even Hedgehog molecules can whip up a proliferative response dedicated to endochrondral ossification in theory. the trick is now seeing if we can harness that in vivo, which is admittedly extremely challenging to do! I will never take away from how difficult this is when local application of these agents is not possible. that is the crux of the problem to me. give me a way to ensure that the stem cell niche is constantly and specifically inundated with PTHrP & SOX proteins, and I will be much more optimistic. currently, no recourse therein. systemic circulation is the only hope.



I’m trying to recreate resting & proliferating zones. That’s the fundamental mission, and if there are remnant stem cells present, enough stimulation with PTHrP & SOX could potentially inhibit osteogenic pressures and induce the chondrogenesis necessary to recreate a proliferating zone that can build space between the resting zone and the osteoblast-containing front.



if I'm not mistaken, I think there might actually be research currently ongoing in which the researchers are seeking to cause transdifferentiation (from osteoblast to chondrocyte) of the cells of the fused epiphysis. my fixation is on a parallel strategy that focuses instead on multipotent stem cells that may already be present. these cells obviously have the potential to differentiate chondrogenically if inundated with the right factors.



the premise is that a sliver of cartilage would need to be generated first. this will be the resting zone. if that resting zone can survive with continuous PTHrP & SOX pressure, the proliferating zone ensues. with continuing chondrogenic pressure, the proliferating zone expands enough to buy the resting zone enough of a buffer to no longer require the inundation of PTHrP & SOX proteins. at this point, exogenous PTHrP supply is abrogated, and a natural PTHrP gradient develops that allows for prehypertrophic and hypertrophic zones to develop distal to the resting zone.



and just to reiterate becuz we seem to continuously come circling back to the fact that a functional growth plate has prehypertrophic and hypertrophic zones, as well as the proliferating & resting zones that I've chosen to fixate on. the point is that these former zones will develop organically once PTHrP provision is ceased because of the AMPLE osteogenic pressure provided by the cells of the trabecular bone below the growth plate. PTHrP & SOX generated by chondroprogenitors of the resting zone will not diffuse far enough away from the resting zone, and the consequent gradient will allow for chondrocyte hypertrophy to begin. there's no need for us to manipulate anything to facilitate the development of prehypertrophic and hypertrophic zones; the bone will ensure that that happens, anyway.



the bone WILL NOT allow for a proliferating zone to develop sans heavy SOX pressure, though. that is the part we have to play God on. hence, inundation with abaloparatide that can induce SOX activity. this ensures MSC renewal (PTHrP) and chondrogenesis at the expense of osteogenesis (SOX)

neither am i reading this, nor am i replying to this with an argument

there is literally NOTHING you can say that will even come close to the accuracy in my post; because i know whatever i stated is 100% correct and there is no other way to say it

 

[DoorHandle5]

neither am i reading this, nor am i replying to this with an argument

there is literally NOTHING you can say that will even come close to the accuracy in my post; because i know whatever i stated is 100% correct and there is no other way to say it

Please read it just for me

 

[DoorHandle5]

neither am i reading this, nor am i replying to this with an argument

there is literally NOTHING you can say that will even come close to the accuracy in my post; because i know whatever i stated is 100% correct and there is no other way to say it

So ur running away

 

[Telmisartan]

So ur running away

 

[Dexter]

So ur running away

from misinformation, yes

 

[DanishLoser]

How Abaloparatide for 3 weeks daily then hgh + AI

Explanation later in comments

W engagement lmao. Never mentioned a dosage for either abalo hgh and AI. And dont mention how AI increases E2 which makes u retarded. Is this ur personal cycle that made u retarded?

 

[DoorHandle5]

from misinformation, yes

I’m confused how it’s misinformation though

 

[DoorHandle5]

from misinformation, yes

Why’re you running away bro?

 

[Telmisartan]

Why’re you running away bro?

Because you're a retard

 

[DoorHandle5]

Because you're a retard

Prove it

 

[DoorHandle5]

Dexter Synapse PrettyBoyMaxxing You three didn’t address this right here which is why I’m confused:

the proliferating zone, once resuscitated, will build a gap between the osteoblasts and the resting zone's stem cells. once the gap is created by these columnar chondrocytes stacking one atop the other, the PTHrP gradient will naturally become great enough that prehypertrophic and hypertrophic zones can develop. these zones develop organically without the need for us to act. the key is the proliferating zone. if that is resuscitated, all bets are off. the gradients that are vital develop naturally by virtue of spacing. hormones need to be managed (AI's), but the zones themselves will otherwise provide the signals they all need to maintain themselves.



that written, there's a plethora of research done examining what transpires when SOX, PTHrP, and SMO agonists (or other Hedgehog pathway activators or enhancers) are applied to the growth plates of animal models, and from these studies, we can paint a picture of how plastic and flexible the system is, and how readily progenitors in the resting zone (mesenchymal stem cells) operate to generate chondrocytes if given the right circumstances. hell, in rabbits, they've even studied dissection of the growth plate and aberrant reinsertion (perpendicular to the original direction) and found that the growth plate would add length along the width of the bone. it demonstrates that the stem cells in the resting zone are polarized, and they will generate columns even if oriented in aberrant directions. they've studied constitutive Hedgehog activation (constantly active Hedgehog signaling) in murine models, done via PTCH1 knockout, and found that cartilaginous "islands" (ectopic cartilage) can be produced off the resting zone's chondroprogenitors. these studies elucidate that influencers like PTHrP, SOX, and even Hedgehog molecules can whip up a proliferative response dedicated to endochrondral ossification in theory. the trick is now seeing if we can harness that in vivo, which is admittedly extremely challenging to do! I will never take away from how difficult this is when local application of these agents is not possible. that is the crux of the problem to me. give me a way to ensure that the stem cell niche is constantly and specifically inundated with PTHrP & SOX proteins, and I will be much more optimistic. currently, no recourse therein. systemic circulation is the only hope.



I’m trying to recreate resting & proliferating zones. That’s the fundamental mission, and if there are remnant stem cells present, enough stimulation with PTHrP & SOX could potentially inhibit osteogenic pressures and induce the chondrogenesis necessary to recreate a proliferating zone that can build space between the resting zone and the osteoblast-containing front.



if I'm not mistaken, I think there might actually be research currently ongoing in which the researchers are seeking to cause transdifferentiation (from osteoblast to chondrocyte) of the cells of the fused epiphysis. my fixation is on a parallel strategy that focuses instead on multipotent stem cells that may already be present. these cells obviously have the potential to differentiate chondrogenically if inundated with the right factors.



the premise is that a sliver of cartilage would need to be generated first. this will be the resting zone. if that resting zone can survive with continuous PTHrP & SOX pressure, the proliferating zone ensues. with continuing chondrogenic pressure, the proliferating zone expands enough to buy the resting zone enough of a buffer to no longer require the inundation of PTHrP & SOX proteins. at this point, exogenous PTHrP supply is abrogated, and a natural PTHrP gradient develops that allows for prehypertrophic and hypertrophic zones to develop distal to the resting zone.



and just to reiterate becuz we seem to continuously come circling back to the fact that a functional growth plate has prehypertrophic and hypertrophic zones, as well as the proliferating & resting zones that I've chosen to fixate on. the point is that these former zones will develop organically once PTHrP provision is ceased because of the AMPLE osteogenic pressure provided by the cells of the trabecular bone below the growth plate. PTHrP & SOX generated by chondroprogenitors of the resting zone will not diffuse far enough away from the resting zone, and the consequent gradient will allow for chondrocyte hypertrophy to begin. there's no need for us to manipulate anything to facilitate the development of prehypertrophic and hypertrophic zones; the bone will ensure that that happens, anyway.



the bone WILL NOT allow for a proliferating zone to develop sans heavy SOX pressure, though. that is the part we have to play God on. hence, inundation with abaloparatide that can induce SOX activity. this ensures MSC renewal (PTHrP) and chondrogenesis at the expense of osteogenesis (SOX)

 

[Catastrophicnoob]

Abaloparatide for 3 weeks daily then hgh + AI

Explanation later in comments

They can’t be reopened
Mark me as solution