Stop being such a narcy retard and reply straight up you fucking utter faggot. How the fuck are you getting asymmetries if bonesmashing does nuffin?+Most asymetries come from postural issues like jaw drift, bone asymmetries, unless they are in the deformity tier, practically do not affect aesthetics.
Would you or would you not. Would you or would you not bonesmash after seeing the proof.
Yes i would but your "proof" are either misunderstandings of human biology or mental gymnastic whom i disproved so you had to attack me (Ad hominem)
My proof is years of research done by top scientists in their own respected area.
Nigga just making shit up
1: this is what I'm talking about (since you're unfamiliar? "bonesmashing" will give you Heterotopic ossification)
This gotta be ragebait
Ad hominem are you stupid or are you ragebaiting?Did nigga just personify a cell
1. Not true, mitosis of osteoblast cells wont result in ho since it is slight growth on the subperiostal part of the bone, in order for it to induce ho it would have to become a severe fracture scattered all around in the local area for it to regrow into soft tissue
Don't care. What do you think repeated craniofacial trauma will do?
Yes, that makes it worse
If you believe bonesmashing is a valid LM you're already retarded
just say ad hominem when you cant make an counterargument, also call it ragebait
this is just BS i wont entertain, if you negate the research, there is nothing we can talk about
Literally disproved the first few lines of your thread before you started to ramble about some bs either disprove my arguments or your thread is worthless
No you didnt, and if godveil was actually going to do that, it would just show how retarded the lm community really is
This nigga cant read never post again
Not only did i reply and disprove this but tabula did too. Are you blind or ignorant i cant tell
Nice disproving
?? I know. Are you acting like a retard or you are one i cant tell
This nigga cant be real
This is just fantasy, the body doesnt treat it as anything, its not like the body has a mind and decides how the area is acted upon but instead there are signaling molecules and pathways etc which indicate the body what its supposed to send/do to the area. And those pathways do get stimulated, its not an if they most likely will because of the way bone has adapted thru years, the pathways ARE SUPPOSED TO get stimulated its what they are made for. There is no such mechanism that makes particles in the bone matrix come together as some kind of force but instead the matrix develops.
First of yes the body has a "mind" its called dna
what is truly remarkable is the way youre ignorant, there is no such thing as a mind to the body, cells have dna which is used to do various complex tasks/processes, not the body, cells decide what happens to them, not the body.
prepare your anus
sure, you started typing like 9 mins ago and gave up, do your research first
Im going to school to do my exam and as soon as i come back im raping you
sure sure you micro dick faggot
Bump my 2 rep shitMechanisms 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 and
birthdefect for investing in me
2 reps because it's shit
bs was made as a meme and is a memeMechanisms 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:
DNR stopped after reading bonesmashingMechanisms 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:
i still dont understand this mechanotransduction theoryMechanisms 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:
mechanotransduction wont do such thing, the mechanism you mean is ossification. The amount of stress "damage" that needs to be done is in ranges, the more stress the more pathways are opened
