explain for each i cannot be asked to do research
Bro I’m ngl I was too lazy to write all that shit out just ask ChatGPT but it probably won’t give u a proper answer cuz these methods are considered “dangerous”
Yes bhai appreciate it
2. Synergistic Pathway Cross-Talk| Pathway | Effect | Cross-Link |
| Wnt/β-catenin (via sclerostin inhibition) | Promotes osteoblastogenesis | Enhances BMP-2 sensitivity |
| BMP-Smad pathway (via BMP-2) | Drives osteogenic differentiation | Upregulates Wnt pathway genes |
| Mechanotransduction (FAK–MAPK–YAP/TAZ) | Induces osteogenic gene expression and cytoskeletal adaptation | Increases both BMP and Wnt responsiveness |
3. Hypothetical Application Example
ChatGPT gives vague answers but u get the processI never understand why niggas buy courses when it’s a few researches away
Step 1: Baseline—Sclerostin Inhibition for Systemic Priming
- Mechanism: Administer an anti-sclerostin agent (e.g., romosozumab) to suppress osteocyte-mediated inhibition of the Wnt/β-catenin pathway.
- Effect: Systemic increase in osteoblast activity and bone formation potential.
- Purpose: Prepares the body’s overall bone metabolism to favor anabolic (bone-building) processes.
This establishes a pro-formation environment — osteoblasts are more active, and bone surfaces are primed to respond to further anabolic cues.
Step 2: Localized BMP-2 Delivery for Targeted Induction
- Mechanism: Apply recombinant human BMP-2 (rhBMP-2) locally via a scaffold, hydrogel, or collagen sponge at the site of desired bone formation (e.g., large defect, implant interface).
- Effect: BMP-2 recruits mesenchymal stem cells (MSCs) and drives their differentiation into osteoblasts and osteocytes.
- Purpose: Provides spatial control—ensures that the new bone formation occurs where it’s needed, not diffusely throughout the skeleton.
In this step, the environment set by sclerostin inhibition enhances responsiveness to BMP signaling, as both converge on osteogenic transcription factors like Runx2 and Osterix (SP7).
Step 3: Mechanotransductive Reinforcement
- Mechanism: Apply controlled mechanical loading (e.g., cyclic strain, vibration, or functional rehabilitation exercises).
- Effect: Activates cellular mechanosensors (e.g., integrins, Piezo1/2, focal adhesion kinase) and upregulates anabolic signaling (including Wnt and IGF-1 pathways).
- Purpose: Strengthens the microarchitecture of the forming bone, directing trabecular orientation and density for functional load-bearing.
Mechanical stimuli can also suppress sclerostin expression naturally, reinforcing the anti-sclerostin pharmacologic effect — forming a positive feedback loop.
Pathway Effect Cross-Link Wnt/β-catenin (via sclerostin inhibition) Promotes osteoblastogenesis Enhances BMP-2 sensitivity BMP-Smad pathway (via BMP-2) Drives osteogenic differentiation Upregulates Wnt pathway genes Mechanotransduction (FAK–MAPK–YAP/TAZ) Induces osteogenic gene expression and cytoskeletal adaptation Increases both BMP and Wnt responsiveness
Scenario: A patient with a large femoral defect post-trauma.
- Pre-treatment (systemic): Anti-sclerostin antibody for 2–4 weeks → primes bone metabolism.
- Surgical step (local): BMP-2-loaded collagen sponge or 3D scaffold implanted into defect.
- Rehabilitation (mechanical): Gradual weight-bearing and controlled mechanical loading → guides bone maturation and structural alignment.
Result: potentially faster, stronger, and more integrated bone regeneration.
@aibad
@Aryan Incel
@Orka
D as in DamianI never understand why niggas buy courses when it’s a few researches away
Step 1: Baseline—Sclerostin Inhibition for Systemic Priming
- Mechanism: Administer an anti-sclerostin agent (e.g., romosozumab) to suppress osteocyte-mediated inhibition of the Wnt/β-catenin pathway.
- Effect: Systemic increase in osteoblast activity and bone formation potential.
- Purpose: Prepares the body’s overall bone metabolism to favor anabolic (bone-building) processes.
This establishes a pro-formation environment — osteoblasts are more active, and bone surfaces are primed to respond to further anabolic cues.
Step 2: Localized BMP-2 Delivery for Targeted Induction
- Mechanism: Apply recombinant human BMP-2 (rhBMP-2) locally via a scaffold, hydrogel, or collagen sponge at the site of desired bone formation (e.g., large defect, implant interface).
- Effect: BMP-2 recruits mesenchymal stem cells (MSCs) and drives their differentiation into osteoblasts and osteocytes.
- Purpose: Provides spatial control—ensures that the new bone formation occurs where it’s needed, not diffusely throughout the skeleton.
In this step, the environment set by sclerostin inhibition enhances responsiveness to BMP signaling, as both converge on osteogenic transcription factors like Runx2 and Osterix (SP7).
Step 3: Mechanotransductive Reinforcement
- Mechanism: Apply controlled mechanical loading (e.g., cyclic strain, vibration, or functional rehabilitation exercises).
- Effect: Activates cellular mechanosensors (e.g., integrins, Piezo1/2, focal adhesion kinase) and upregulates anabolic signaling (including Wnt and IGF-1 pathways).
- Purpose: Strengthens the microarchitecture of the forming bone, directing trabecular orientation and density for functional load-bearing.
Mechanical stimuli can also suppress sclerostin expression naturally, reinforcing the anti-sclerostin pharmacologic effect — forming a positive feedback loop.
Pathway Effect Cross-Link Wnt/β-catenin (via sclerostin inhibition) Promotes osteoblastogenesis Enhances BMP-2 sensitivity BMP-Smad pathway (via BMP-2) Drives osteogenic differentiation Upregulates Wnt pathway genes Mechanotransduction (FAK–MAPK–YAP/TAZ) Induces osteogenic gene expression and cytoskeletal adaptation Increases both BMP and Wnt responsiveness
Scenario: A patient with a large femoral defect post-trauma.
- Pre-treatment (systemic): Anti-sclerostin antibody for 2–4 weeks → primes bone metabolism.
- Surgical step (local): BMP-2-loaded collagen sponge or 3D scaffold implanted into defect.
- Rehabilitation (mechanical): Gradual weight-bearing and controlled mechanical loading → guides bone maturation and structural alignment.
Result: potentially faster, stronger, and more integrated bone regeneration.
That sheit is 100% in androgenics course hehe
"Hypothetically" works
yeah and if you say something about “writing a research paper”
I do bonesmashing, and take sups bhai
I'll try to make smth about it bhai
Mechanotransduction is actually proven jfl, if u hug/kiss somone u love, your cells can detect impulses which stimulates cells to strengthen bones.
Mirin blue bhaiya
So original.
Only works with open plates so if youre poor and unc (18+) DNR
none of these methods rely on open growth plates. At all
It would be much more effective with open plates, but you’ll still see results with closed
Bmp 7 also known as relaxin? Mogs
it's bone mass not height.If thats the case im ascending
Watch me become 6'2 HTN buddy boyos
Very high IQ@Aress high iq post
