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Guide Mechanisms behind bonesmashing proving its validity (NOT WATER) (3 Viewers)

Guide Mechanisms behind bonesmashing proving its validity (NOT WATER)

gandeism

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Mechanisms which will be included:

1. Mechanosensing and mechanotransduction
2. Actomyosin cytoskeleton response
3. FAK activation

We'll start going over what these mechanisms actually are and how bonesmashing activates them in order to remodel bone.

Mechanosensing and mechanotransduction


Mechanosensing is the initial detection of physical forces by bone cells, including osteoblasts. Mechanotransduction is the process that converts these mechanical stimuli into biochemical signals inside the cell.

So you're probably wondering what these biochemical signals will do in aiding bone growth... Well, they upregulate key osteogenic transcription factors.

Pathways increase the activity of Runx2 and Osterix (Sp7), which regulate bone formation and osteoblast differentiation. Upregulation in factors like Runx2 and Osterix (Sp7) promotes bone matrix production and mineralization.

Why does that happen? Well, Runx2 upregulates genes like FGFR2 and FGFR3, which increase progenitor cells that Osterix will then mature. (The cycle is so well put together it makes me cum.)

Let's summarise ts: Runx2 makes small progenitor cells and Osterix matures them (ts is for the iqlets who will reply with dnr).

Key mechanosensing pathways in osteoblasts

These pathways are directly triggered or amplified by mechanical force and contribute to the anabolic (bone-building) side of remodeling:

Ion channels and calcium signaling: Mechanosensitive channels like Piezo1 open in response to shear stress or tension, causing rapid Ca²⁺ influx. This activates downstream effectors such as calmodulin, mTOR, calcineurin/NFATc1, and YAP1, leading to increased osteoprotegerin (OPG) production (which inhibits osteoclasts) and osteoblast activity.


membranes-13-00167-g001.png


-Downstream effectors are the genes, proteins, or molecules whose expression or activity is directly or indirectly regulated/activated by an upstream factor (in this case, calmodulin, mTOR, calcineurin/NFATc1, and YAP1).
In short the Calcium ion influx increases osteoblast activity and decreases osteoclast activity

Wnt/β-catenin pathway: Mechanical strain or fluid flow stabilizes β-catenin, which translocates to the nucleus and upregulates genes for bone matrix proteins (e.g., collagen I) and osteoblast proliferation/differentiation. This is a key anabolic signal in Wolff’s law adaptation.


β-catenin: dual function protein, involved in regulation and coordination of cell–cell adhesion and gene transcription
2bct_murinebcat.jpg


Thats it for mechanosensing and mechanotransduction, There is a lot more to uncover but its tooo machh :(

Actomyosin cytoskeleton response

The actomyosin cytoskeleton is the contractile network inside the cell formed by actin filaments (F-actin) and myosin II motor proteins. It provides structural support, generates intracellular tension (contractility), and plays a central role in mechanotransduction in osteoblasts. (yep, we are back to mechanotransduction)

What it is and how it responds to mechanical force:


Actin filaments polymerize and bundle into stress fibers.
Myosin II binds to these filaments and uses ATP to generate pulling force, creating prestress (internal tension) in the cell.
Under mechanical loading (strain, fluid shear stress, or impact), the actomyosin network reorganizes: actin filaments align parallel to the direction of force, become thicker/more stable, and increase overall contractility.

Polymerises is the third-person singular present tense verb for the chemical process where small molecules, called monomers, react together to form long, chain-like, or three-dimensional networks known as polymers.
Osteocytes convert mechanical signals into biochemical signals:

Release signaling molecules (e.g., prostaglandins, nitric oxide)
Modulate pathways like Wnt/β-catenin signaling


All those factors result in the activation of osteoblast cells and the down regulation in the activation of osteoclasts

FAK activation (Focal Adhesion Kinase)
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase with key roles in the regulation of cell adhesion migration, proliferation and survival
41580_2005_Article_BFnrm1549_Fig1_HTML.jpg

How its applied to bonesmashing
FAK acts as a signaling hub controlling:


Cell behavior​

Cell adhesion and spreading
Migration (important in wound healing, cancer)

Survival and growth​

Activates pathways like: PI3K/Akt, MAPK/ERK

Mechanotransduction​

Converts mechanical force → biochemical signals

(It all comes down to mechanotransduction)

Thats it for todays guide, If you want me to elaborate or expand this topic to its full extent make sure to ask me.

Credits to pubmed for giving me a 100% of the information i needed, and for grok.ai improving my grammar


Incel credits go to: EqBeliever EqBeliever and birthdefect birthdefect for investing in me
 

gandeism

Im a greycel, be patient
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short ver:
mechanisms

  1. Mechanosensing → signals → activates Runx2 & Osterix → bone growth
  2. Actomyosin → adapts to force → boosts osteoblasts
  3. FAK → converts force → growth signals
core: mechanical force → mechanotransduction → bone formation
It would be growth signals after runx2 and osterix. But you must mention the difference between those 2 factors because osterix primarily without runx2 wont result in growth
 

EqBeliever

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Mechanisms which will be included:

1. Mechanosensing and mechanotransduction
2. Actomyosin cytoskeleton response
3. FAK activation

We'll start going over what these mechanisms actually are and how bonesmashing activates them in order to remodel bone.


Mechanosensing and mechanotransduction

Mechanosensing is the initial detection of physical forces by bone cells, including osteoblasts. Mechanotransduction is the process that converts these mechanical stimuli into biochemical signals inside the cell.

So you're probably wondering what these biochemical signals will do in aiding bone growth... Well, they upregulate key osteogenic transcription factors.

Pathways increase the activity of Runx2 and Osterix (Sp7), which regulate bone formation and osteoblast differentiation. Upregulation in factors like Runx2 and Osterix (Sp7) promotes bone matrix production and mineralization.

Why does that happen? Well, Runx2 upregulates genes like FGFR2 and FGFR3, which increase progenitor cells that Osterix will then mature. (The cycle is so well put together it makes me cum.)

Let's summarise ts: Runx2 makes small progenitor cells and Osterix matures them (ts is for the iqlets who will reply with dnr).

Key mechanosensing pathways in osteoblasts

These pathways are directly triggered or amplified by mechanical force and contribute to the anabolic (bone-building) side of remodeling:

Ion channels and calcium signaling: Mechanosensitive channels like Piezo1 open in response to shear stress or tension, causing rapid Ca²⁺ influx. This activates downstream effectors such as calmodulin, mTOR, calcineurin/NFATc1, and YAP1, leading to increased osteoprotegerin (OPG) production (which inhibits osteoclasts) and osteoblast activity.


View attachment 41181

-Downstream effectors are the genes, proteins, or molecules whose expression or activity is directly or indirectly regulated/activated by an upstream factor (in this case, calmodulin, mTOR, calcineurin/NFATc1, and YAP1).
In short the Calcium ion influx increases osteoblast activity and decreases osteoclast activity

Wnt/β-catenin pathway: Mechanical strain or fluid flow stabilizes β-catenin, which translocates to the nucleus and upregulates genes for bone matrix proteins (e.g., collagen I) and osteoblast proliferation/differentiation. This is a key anabolic signal in Wolff’s law adaptation.


β-catenin: dual function protein, involved in regulation and coordination of cell–cell adhesion and gene transcription
View attachment 41182


Thats it for mechanosensing and mechanotransduction, There is a lot more to uncover but its tooo machh :(

Actomyosin cytoskeleton response

The actomyosin cytoskeleton is the contractile network inside the cell formed by actin filaments (F-actin) and myosin II motor proteins. It provides structural support, generates intracellular tension (contractility), and plays a central role in mechanotransduction in osteoblasts. (yep, we are back to mechanotransduction)

What it is and how it responds to mechanical force:


Actin filaments polymerize and bundle into stress fibers.
Myosin II binds to these filaments and uses ATP to generate pulling force, creating prestress (internal tension) in the cell.
Under mechanical loading (strain, fluid shear stress, or impact), the actomyosin network reorganizes: actin filaments align parallel to the direction of force, become thicker/more stable, and increase overall contractility.

Polymerises is the third-person singular present tense verb for the chemical process where small molecules, called monomers, react together to form long, chain-like, or three-dimensional networks known as polymers.
Osteocytes convert mechanical signals into biochemical signals:

Release signaling molecules (e.g., prostaglandins, nitric oxide)
Modulate pathways like Wnt/β-catenin signaling


All those factors result in the activation of osteoblast cells and the down regulation in the activation of osteoclasts

FAK activation (Focal Adhesion Kinase)
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase with key roles in the regulation of cell adhesion migration, proliferation and survival
View attachment 41186

How its applied to bonesmashing
FAK acts as a signaling hub controlling:


Cell behavior​

Cell adhesion and spreading
Migration (important in wound healing, cancer)

Survival and growth​

Activates pathways like: PI3K/Akt, MAPK/ERK

Mechanotransduction​

Converts mechanical force → biochemical signals

(It all comes down to mechanotransduction)

Thats it for todays guide, If you want me to elaborate or expand this topic to its full extent make sure to ask me.

Credits to pubmed for giving me a 100% of the information i needed, and for grok.ai improving my grammar


Incel credits go to: EqBeliever EqBeliever and birthdefect birthdefect for investing in me
Glad that i have an high iq friends it was obvious that the first post was retardbait
 

Tabula Rasa

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Mechanisms which will be included:

1. Mechanosensing and mechanotransduction
2. Actomyosin cytoskeleton response
3. FAK activation

We'll start going over what these mechanisms actually are and how bonesmashing activates them in order to remodel bone.


Mechanosensing and mechanotransduction

Mechanosensing is the initial detection of physical forces by bone cells, including osteoblasts. Mechanotransduction is the process that converts these mechanical stimuli into biochemical signals inside the cell.

So you're probably wondering what these biochemical signals will do in aiding bone growth... Well, they upregulate key osteogenic transcription factors.

Pathways increase the activity of Runx2 and Osterix (Sp7), which regulate bone formation and osteoblast differentiation. Upregulation in factors like Runx2 and Osterix (Sp7) promotes bone matrix production and mineralization.

Why does that happen? Well, Runx2 upregulates genes like FGFR2 and FGFR3, which increase progenitor cells that Osterix will then mature. (The cycle is so well put together it makes me cum.)

Let's summarise ts: Runx2 makes small progenitor cells and Osterix matures them (ts is for the iqlets who will reply with dnr).

Key mechanosensing pathways in osteoblasts

These pathways are directly triggered or amplified by mechanical force and contribute to the anabolic (bone-building) side of remodeling:

Ion channels and calcium signaling: Mechanosensitive channels like Piezo1 open in response to shear stress or tension, causing rapid Ca²⁺ influx. This activates downstream effectors such as calmodulin, mTOR, calcineurin/NFATc1, and YAP1, leading to increased osteoprotegerin (OPG) production (which inhibits osteoclasts) and osteoblast activity.


View attachment 41181

-Downstream effectors are the genes, proteins, or molecules whose expression or activity is directly or indirectly regulated/activated by an upstream factor (in this case, calmodulin, mTOR, calcineurin/NFATc1, and YAP1).
In short the Calcium ion influx increases osteoblast activity and decreases osteoclast activity

Wnt/β-catenin pathway: Mechanical strain or fluid flow stabilizes β-catenin, which translocates to the nucleus and upregulates genes for bone matrix proteins (e.g., collagen I) and osteoblast proliferation/differentiation. This is a key anabolic signal in Wolff’s law adaptation.


β-catenin: dual function protein, involved in regulation and coordination of cell–cell adhesion and gene transcription
View attachment 41182


Thats it for mechanosensing and mechanotransduction, There is a lot more to uncover but its tooo machh :(

Actomyosin cytoskeleton response

The actomyosin cytoskeleton is the contractile network inside the cell formed by actin filaments (F-actin) and myosin II motor proteins. It provides structural support, generates intracellular tension (contractility), and plays a central role in mechanotransduction in osteoblasts. (yep, we are back to mechanotransduction)

What it is and how it responds to mechanical force:


Actin filaments polymerize and bundle into stress fibers.
Myosin II binds to these filaments and uses ATP to generate pulling force, creating prestress (internal tension) in the cell.
Under mechanical loading (strain, fluid shear stress, or impact), the actomyosin network reorganizes: actin filaments align parallel to the direction of force, become thicker/more stable, and increase overall contractility.

Polymerises is the third-person singular present tense verb for the chemical process where small molecules, called monomers, react together to form long, chain-like, or three-dimensional networks known as polymers.
Osteocytes convert mechanical signals into biochemical signals:

Release signaling molecules (e.g., prostaglandins, nitric oxide)
Modulate pathways like Wnt/β-catenin signaling


All those factors result in the activation of osteoblast cells and the down regulation in the activation of osteoclasts

FAK activation (Focal Adhesion Kinase)
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase with key roles in the regulation of cell adhesion migration, proliferation and survival
View attachment 41186

How its applied to bonesmashing
FAK acts as a signaling hub controlling:


Cell behavior​

Cell adhesion and spreading
Migration (important in wound healing, cancer)

Survival and growth​

Activates pathways like: PI3K/Akt, MAPK/ERK

Mechanotransduction​

Converts mechanical force → biochemical signals

(It all comes down to mechanotransduction)

Thats it for todays guide, If you want me to elaborate or expand this topic to its full extent make sure to ask me.

Credits to pubmed for giving me a 100% of the information i needed, and for grok.ai improving my grammar


Incel credits go to: EqBeliever EqBeliever and birthdefect birthdefect for investing in me
Good thread, but I think you haven't quite grasped a few things. I'd also appreciate your sources.
 

gandeism

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Good thread, but I think you haven't quite grasped a few things. I'd also appreciate your sources.
Thank you for the review, as I said 100% of the information put into my thread is from pubmed. It may sound bad but they have done a lot of research on such subjects. Id love if you were to help me grasp what i havent yet to improve my thread and ill make sure to tag you.
 

Tabula Rasa

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Thank you for the review, as I said 100% of the information put into my thread is from pubmed. It may sound bad but they have done a lot of research on such subjects. Id love if you were to help me grasp what i havent yet to improve my thread and ill make sure to tag you.
Your description of the osteoblast-osteoclast balance is incorrect. These pathways do not inhibit osteoclasts, primarily because bone resorption is necessary for the release of growth factors in the bone remodeling process. These pathways increase osteoblasts independently of osteoclasts, resulting in a net anabolic effect. The rest is relatively correct but extremely simplified, you should elaborate on your points and cite the studies you're drawing from. For example, your explanation of the Wnt/β-catenin pathway isn't incorrect, but it's too simplistic, so much so that it misrepresents how it manifests itself.

https://looksmax.gg/threads/mechano...ng-full-science-breakdown-and-theories.25319/

In this thread i explain the whole Wnt/β-catenin pathway and axis.

Can you link me the studies tho?
 

gandeism

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Your description of the osteoblast-osteoclast balance is incorrect. These pathways do not inhibit osteoclasts, primarily because bone resorption is necessary for the release of growth factors in the bone remodeling process. These pathways increase osteoblasts independently of osteoclasts, resulting in a net anabolic effect. The rest is relatively correct but extremely simplified, you should elaborate on your points and cite the studies you're drawing from. For example, your explanation of the Wnt/β-catenin pathway isn't incorrect, but it's too simplistic, so much so that it misrepresents how it manifests itself.

https://looksmax.gg/threads/mechano...ng-full-science-breakdown-and-theories.25319/

In this thread i explain the whole Wnt/β-catenin pathway and axis.

Can you link me the studies tho?
Thank you for your feedback. I'll look into the pathway inhibition of osteoclasts and if you are correct ill tag you and fix my mistake. Also i do understand i oversimplified not just the beta catenin pathway but most of the processes because it would take me way to long and many people would'nt understand. Ill look into your thread, and if you give me a few minutes ill give you all of the pubmed studies i used, Ill dm them to you. Thanks!
 

gandeism

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dnr

what do you recommend is optimal then smashing hard with a hammer or some light tapping bs
A mixture of smashing with a dense object equally on both sides of the bone if there isnt a mono smashing point, then following it up by fast, mild repeated hits like from a massage gun or knuckles. That would equal to the most stress, and the most pathways opened. Make sure to put a wet cloth over the point of smashing to minimise the friction induced skin damage. Thanks!
 

EqBeliever

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A mixture of smashing with a dense object equally on both sides of the bone if there isnt a mono smashing point, then following it up by fast, mild repeated hits like from a massage gun or knuckles. That would equal to the most stress, and the most pathways opened. Make sure to put a wet cloth over the point of smashing to minimise the friction induced skin damage. Thanks!
Credit me nigga
 

MedSlayer

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Pathways increase the activity of Runx2 and Osterix (Sp7), which regulate bone formation and osteoblast differentiation. Upregulation in factors like Runx2 and Osterix (Sp7) promotes bone matrix production and mineralization.
30 seconds in and i already see 2 problems
1. Those pathways respond to mechanical loading not random blunt trauma or hitting it over time
2. Those pathways mostly make bones more dense any expansion in bone volume via those pathways are too small to make a visible difference
Will problably dnr the rest
 

gandeism

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30 seconds in and i already see 2 problems
1. Those pathways respond to mechanical loading not random blunt trauma or hitting it over time
2. Those pathways mostly make bones more dense any expansion in bone volume via those pathways are too small to make a visible difference
Will problably dnr the rest
Mechanical loading, the definition:
Mechanical loading is
the physical stress, forces (such as gravity or muscle contraction), and strain applied to biological tissues (bone, muscle, tendon) or mechanical structures during activity

2. Is just BS, how can cellular mitosis make the bone only denser
 

Tabula Rasa

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1. Those pathways respond to mechanical loading not random blunt trauma or hitting it over time
I want to know your reasoning behind how you've managed to separate these two things as something exclusive.
2. Those pathways mostly make bones more dense any expansion in bone volume via those pathways are too small to make a visible difference
Will problably dnr the rest
???? :banderas:
 

MedSlayer

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Mechanical loading, the definition:
Mechanical loading is
the physical stress, forces (such as gravity or muscle contraction), and strain applied to biological tissues (bone, muscle, tendon) or mechanical structures during activity

2. Is just BS, how can cellular mitosis make the bone only denser
1.Technically yes but its so hard to stimulate bones this way most people who bonesmash either dont use enough force for it to be considered a stimulus or their body interpret it as an injury thus giving the inflammation
2.Wont go too much in detail but basically when cellular mitosis happens your body prefer to increase bone density rather than expanding thus making expansion minimal and not visible
 

gandeism

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1.Technically yes but its so hard to stimulate bones this way most people who bonesmash either dont use enough force for it to be considered a stimulus or their body interpret it as an injury thus giving the inflammation
2.Wont go too much in detail but basically when cellular mitosis happens your body prefer to increase bone density rather than expanding thus making expansion minimal and not visible
1. Thats your anecdote idgaf
2. Your body does not have such mechanism, it only regulates the mitosis
 

MedSlayer

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1. Thats your anecdote idgaf
2. Your body does not have such mechanism, it only regulates the mitosis
1.Not anecdote look throught the forums everybody who bonesmashed either saw no difference(no stimulus) or they just got inflammation (still doesnt stimulate those pathways)
2. 1.Genetic blueprint
2.Mechanical effiency
3.Energy cost
 

gandeism

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1.Not anecdote look throught the forums everybody who bonesmashed either saw no difference(no stimulus) or they just got inflammation (still doesnt stimulate those pathways)
2. 1.Genetic blueprint
2.Mechanical effiency
3.Energy cost
1. now i have your anecdote and the anecdote of the forum members which i do not know if they exist cause you could have made them up

2.thats litteraly just the regulation of cells
 

MedSlayer

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1. now i have your anecdote and the anecdote of the forum members which i do not know if they exist cause you could have made them up

2.thats litteraly just the regulation of cells
1.
I Guess GIF

2.Exactly and those cells prefer to improve bone density rather than expansion

stress i need a drink GIF
 

Circadex

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Mechanisms which will be included:

1. Mechanosensing and mechanotransduction
2. Actomyosin cytoskeleton response
3. FAK activation

We'll start going over what these mechanisms actually are and how bonesmashing activates them in order to remodel bone.


Mechanosensing and mechanotransduction

Mechanosensing is the initial detection of physical forces by bone cells, including osteoblasts. Mechanotransduction is the process that converts these mechanical stimuli into biochemical signals inside the cell.

So you're probably wondering what these biochemical signals will do in aiding bone growth... Well, they upregulate key osteogenic transcription factors.

Pathways increase the activity of Runx2 and Osterix (Sp7), which regulate bone formation and osteoblast differentiation. Upregulation in factors like Runx2 and Osterix (Sp7) promotes bone matrix production and mineralization.

Why does that happen? Well, Runx2 upregulates genes like FGFR2 and FGFR3, which increase progenitor cells that Osterix will then mature. (The cycle is so well put together it makes me cum.)

Let's summarise ts: Runx2 makes small progenitor cells and Osterix matures them (ts is for the iqlets who will reply with dnr).

Key mechanosensing pathways in osteoblasts

These pathways are directly triggered or amplified by mechanical force and contribute to the anabolic (bone-building) side of remodeling:

Ion channels and calcium signaling: Mechanosensitive channels like Piezo1 open in response to shear stress or tension, causing rapid Ca²⁺ influx. This activates downstream effectors such as calmodulin, mTOR, calcineurin/NFATc1, and YAP1, leading to increased osteoprotegerin (OPG) production (which inhibits osteoclasts) and osteoblast activity.


View attachment 41181

-Downstream effectors are the genes, proteins, or molecules whose expression or activity is directly or indirectly regulated/activated by an upstream factor (in this case, calmodulin, mTOR, calcineurin/NFATc1, and YAP1).
In short the Calcium ion influx increases osteoblast activity and decreases osteoclast activity

Wnt/β-catenin pathway: Mechanical strain or fluid flow stabilizes β-catenin, which translocates to the nucleus and upregulates genes for bone matrix proteins (e.g., collagen I) and osteoblast proliferation/differentiation. This is a key anabolic signal in Wolff’s law adaptation.


β-catenin: dual function protein, involved in regulation and coordination of cell–cell adhesion and gene transcription
View attachment 41182


Thats it for mechanosensing and mechanotransduction, There is a lot more to uncover but its tooo machh :(

Actomyosin cytoskeleton response

The actomyosin cytoskeleton is the contractile network inside the cell formed by actin filaments (F-actin) and myosin II motor proteins. It provides structural support, generates intracellular tension (contractility), and plays a central role in mechanotransduction in osteoblasts. (yep, we are back to mechanotransduction)

What it is and how it responds to mechanical force:


Actin filaments polymerize and bundle into stress fibers.
Myosin II binds to these filaments and uses ATP to generate pulling force, creating prestress (internal tension) in the cell.
Under mechanical loading (strain, fluid shear stress, or impact), the actomyosin network reorganizes: actin filaments align parallel to the direction of force, become thicker/more stable, and increase overall contractility.

Polymerises is the third-person singular present tense verb for the chemical process where small molecules, called monomers, react together to form long, chain-like, or three-dimensional networks known as polymers.
Osteocytes convert mechanical signals into biochemical signals:

Release signaling molecules (e.g., prostaglandins, nitric oxide)
Modulate pathways like Wnt/β-catenin signaling


All those factors result in the activation of osteoblast cells and the down regulation in the activation of osteoclasts

FAK activation (Focal Adhesion Kinase)
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase with key roles in the regulation of cell adhesion migration, proliferation and survival
View attachment 41186

How its applied to bonesmashing
FAK acts as a signaling hub controlling:


Cell behavior​

Cell adhesion and spreading
Migration (important in wound healing, cancer)

Survival and growth​

Activates pathways like: PI3K/Akt, MAPK/ERK

Mechanotransduction​

Converts mechanical force → biochemical signals

(It all comes down to mechanotransduction)

Thats it for todays guide, If you want me to elaborate or expand this topic to its full extent make sure to ask me.

Credits to pubmed for giving me a 100% of the information i needed, and for grok.ai improving my grammar


Incel credits go to: EqBeliever EqBeliever and birthdefect birthdefect for investing in me
Just shut up about this bonesmashing cope it's ridiculous

it can't enhance your aesthetics, end of.
 

gandeism

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Just shut up about this bonesmashing cope it's ridiculous

it can't enhance your aesthetics, end of.
yes, it would be nice to shut up... THATS IF THE PROOF WASNT ON THE SIDE OF BONESMASHING. I truly appreciate normies like you denying it, it divides us from your kind.
 

gandeism

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Enjoy your asymmetry inducing heterotopic ossification & CTE :banderas:
first you overestimated bonesmashing by saying the gains will be so massive it will make you assymetrical then you do it again by saying CTE is guaranteed
 

Circadex

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first you overestimated bonesmashing by saying the gains will be so massive it will make you assymetrical then you do it again by saying CTE is guaranteed
So it works for bone augmentation?

What the fuck are you talking about? Are you both retarded?

do you know what I'm talking about
 

MedSlayer

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Sure sure, let chatgpt cook me up then ill fold your ass
Just prove your a low iq monkey i say one type of sophism and think muhhh chatgpt read some books and devellop your intellect instead of posting some ass threads and saying dumb shit like this
 

gandeism

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Just prove your a low iq monkey i say one type of sophism and think muhhh chatgpt read some books and devellop your intellect instead of posting some ass threads and saying dumb shit like this
Reject what you dont like, would you believe in god if you saw him in front of you with your own 2 human eyes
 

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