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B*nesmashing: Cope or Hope?
Welcome to the Loop
The self-improvement space by FaceIQ Labs. Share your journey, get advice from experts, and connect with others on the same path.
In this thread we will look into the age-old debate of whether 'B*nesmashing' is a viable method for mimicking or providing an increase in bone mass, this is divided into multiple threads. Obviously this is not endorsed by FaceIQ Labs, nor is it medical advice, follow at your own risk.
*as always TLDR at the bottom if you are too lazy to read.
B*nesmashing is mainly used to refer to the action of hitting areas of your face, most commonly the Cheekbones & Chin to mimick an increase in facial bone mass, which would increase Angularity & improve facial attractiveness for males.
There are dozens of different scientific theories aimed at explaining this method, however, for the sake of relevance and saving your time by not going through them all, I will cover the most plausible and coherent theory, which is the Scar tissue Fibrosis theory, as other theories that involve Wolff's Law, which aims to create fractures/microfractures in bone so that the bones grow back thicker, or Subperiostal Hematoma Ossification, which aims to form SPHs (Subperiostal Hematomas) under the skin until they eventually ossify and mimic bone, have many holes in both theory and application, and are very refutable.
Scar tissue fibrosis:
The main mechanism in this theory is Fibroproliferative Response to Repeated Trauma, which occurs as follows:
Phase 1: Immediate Trauma Response (0-24 hours post-hit)
When you hit:
1. Mechanical disruption
∙ Microtrauma to periosteum
∙ Capillary rupture (micro-bleeding)
∙ Cell membrane damage
∙ Tissue strain/deformation
2. Danger signal release
∙ DAMPs (damage-associated molecular patterns) released from damaged cells
∙ ATP, HMGB1, heat shock proteins leak out
∙ These are “alarm signals” to immune system
3. Immediate inflammatory cascade
∙ Mast cells degranulate (release histamine)
∙ Platelets aggregate at micro-injury sites
∙ Platelet activation releases:
∙ PDGF (platelet-derived growth factor)
∙ TGF-β1 (transforming growth factor beta-1)
∙ VEGF (vascular endothelial growth factor)
Phase 2: Acute Inflammation (Hours 6-48)
4. Neutrophil invasion
∙ First responder immune cells
∙ Clear debris and damaged tissue
∙ Release more cytokines (IL-1β, TNF-α, IL-6)
5. Macrophage recruitment (peaks 24-72hr)
∙ M1 macrophages (pro-inflammatory) arrive first
∙ Later shift to M2 macrophages (pro-fibrotic)
∙ M2 macrophages are KEY - they secrete massive amounts of TGF-β
Phase 3: Fibroblast Activation (Days 2-7)
6. The TGF-β cascade (THIS IS THE CRITICAL PART)
TGF-β binds to fibroblast receptors → activates SMAD2/3 signaling → nucleus → gene transcription changes:
∙ COL1A1/COL1A2 genes turn on → Type I collagen production ↑↑↑
∙ α-SMA gene activated → fibroblasts become myofibroblasts (contractile, aggressive collagen-producers)
∙ TIMP (tissue inhibitor of metalloproteases) ↑ → prevents collagen breakdown
∙ Fibronectin production ↑ → creates scaffold for collagen deposition
7. Fibroblast proliferation
∙ PDGF drives fibroblast division
∙ Population expansion at injury site
∙ These cells are now “primed” for collagen synthesis
Phase 4: Collagen Deposition (Days 3-21+)
8. Active collagen synthesis
∙ Fibroblasts pump out collagen Type I
∙ Initial deposition is disorganized (provisional matrix)
∙ Peak collagen production: days 7-14
9. Cross-linking (Days 14-60+)
∙ Lysyl oxidase enzyme creates covalent bonds between collagen fibers
∙ Tissue becomes progressively stiffer
∙ This is irreversible without enzymatic degradation
So now that we've established the main mechanism, we will move on to how the frequency of hits per day aids this mechanism.
Why 2-3x Daily is used to maintain inflammation
Single session , then rest for days:
Day 1: Hit → inflammation peaks at 24-48hr
Day 2-3: TGF-β levels high, fibroblasts activate
Day 4-5: Inflammation begins resolving
Day 6-7: Anti-inflammatory signals (IL-10, TGF-β decreases)
Day 7+: Tissue enters resolution phase
Result: One small pulse of fibroblast activity, then tissue homeostasis returns. (thus, any protocols involving one hard session per day, with rest days after are flawed, this is one of the reasons influencer 'Clavicular' could not yield permanent results with the method.)
Multiple hits same day (2-3x):
Morning: Hit → inflammation cascade starts
Afternoon: Hit again → "boosts" existing inflammation
- Adds more DAMPs
- Re-recruits macrophages
- Sustains TGF-β elevation
Evening: Hit again → further amplifies signal
Next day: Inflammation doesn't drop back to baseline
- Sustained high TGF-β
- Fibroblasts stay activated longer
- More collagen synthesis time
Result: Chronic elevated inflammatory state, continuous fibroblast activation.
Research Backing High Frequency:
Study parallel: Hypertrophic scar formation
Research on keloids and hypertrophic scars shows:
∙ Repeated mechanical tension on healing wounds → chronic TGF-β elevation
∙ Sustained TGF-β (>7 days) → myofibroblast persistence → excessive collagen
∙ Single injury heals normally; repeated stress = fibrotic overgrowth
Study parallel: Dupuytren’s contracture
∙ Repeated palmar microtrauma (manual labor, gripping)
∙ Chronic fascial inflammation → TGF-β-driven fibrosis
∙ Creates permanent collagen nodules in palm
∙ Mechanism: repetitive mechanical stress maintaining inflammation
Study parallel: Achilles tendinopathy
∙ Repeated loading without adequate recovery
∙ Chronic low-grade inflammation
∙ Failed healing response → disorganized collagen deposition
∙ Tendon becomes thickened (fibrotic)
The pattern:
Acute injury + rest = normal healing
Chronic repeated injury = persistent inflammation = fibrotic tissue accumulation.
The high frequency (about 2-3 sessions per day) aims to create the second scenario intentionally.
The Inflammatory Dose-Response:
Finding derived from wound healing research:
TGF-β signaling is dose-dependent AND duration-dependent:
∙ Low TGF-β (short duration) → normal healing
∙ Moderate TGF-β (sustained) → fibrosis
∙ Very high TGF-β (chronic) → pathological fibrosis (keloid)
The goal for this method is the middle zone:
∙ Enough TGF-β to drive fibrosis
∙ Not so much you get disorganized scar (like keloid)
2-3x daily hits keeps you in optimal range as it:
∙ Sustains moderate TGF-β elevation
∙ Maintains M2 macrophage presence
∙ Keeps fibroblasts active
∙ Doesn’t cause overwhelming tissue damage.
To think constantly keeping an area swollen for MONTHS would NOT result in an inflammation response, i.e the collagen matrix deposition mass of some sort, which provides the mass we are chasing, is ignorant.
-SpectrumAesthetics3, A very helpful and reputable tester of this method, credit goes to him for the theorization and testing.
TLDR: B*nesmashing, while providing good temporary gains in the form of swelling of the facial bones, which mimics and provides the effect of increased percieved bone mass, also has the ability to yield permanent gains in the form of permanent accumulated scar tissue in areas that were kept swollen throughout the day and over the period of months
In the next thread I will discuss protocols, areas where hitting would be implemented, the limitations and downsides of b*nesmashing, and alot of different transformations caused by using this method.
-Skypsl
Bro put his own watermark on it when he didn't actually do anything other than paste an AI prompt
Absolutely cope just hardmaxx and forget about breaking your bones without any reason
my bro said son when i alredy look beter than him
Bonesmashing only works if done correctly, as it creates microfractures that the body automatically perceives as a stimulus for improvement and automatically increases bone density. It must be done correctly.
I'm not that educated in Bonesmashing but i know if done corrrectly wouldn't it increase only the bonemass but that wouldn't give any asthetic changes ?(it's just a question pls done't be mad)
im not going to be mad , It will make your bones thicker; your body will see it as a failure and will automatically try to remodel it. Imagine hitting your cheekbones; the other parts will also be affected, even if you don't hit them, due to the stimuli the body receives.
ok ty
im wrong in some things here but who cares
would you reccomend Bsmashing for asthetic benefit and are you going to do it?
im not doing it and you shouldnt do it , its a waste of time , do hardmewing , and hard thumpulling
im not that dumb
moai11dcope
Melodie is my queen SkyPSL where have you BEEN😭🥀
I have a question, is this tissue permanent if so when does it become permanent and when it does do you just stop bone smashing?
I’ve come from part 2bonesmashing and I’ve seeen spectrum asthetic,s videos but like I know like his jaw was uneven and he filled one part and all that stuff but I saw his before and after and it really looked like a double jaw surgery (I’m not educated in this topic) Ty for making this high iq post🥹
OverApr 4@skypsl “I see exactly what you’re doing—you’re tightening the model and removing weak objections. That’s a solid way to think. But even if we grant your best-case assumptions (low-grade, site-specific, repeated stimulus near bone), the mechanism still runs into a few hard biological constraints that your version doesn’t fully solve. I’ll go point-by-point, but focus only on what still breaks und…
OverApr 4I get what you’re doing here—you’re stress-testing the counterarguments, not just accepting them. That’s fair. But the part that still doesn’t hold up isn’t about whether inflammation biology exists—it’s about what kind of tissue you actually end up with and how it presents on a face. Let’s go directly at the gaps you pointed out. ⸻ 1. “Controlled low-grade, site-specific inflammation” This is…
skypslApr 4Sure, let's go through each point in full detail: --- **1. "Cytokines diffuse, so you can't localize the response"** Their argument assumes that because TGF-β and other cytokines diffuse, the entire inflammatory response becomes spatially uncontrollable. This is an oversimplification. - Diffusion is governed by **concentration gradients and tissue density** — in areas with dense connective tis…
OverApr 4I see exactly what you’re doing—you’re tightening the model and removing weak objections. That’s a solid way to think. But even if we grant your best-case assumptions (low-grade, site-specific, repeated stimulus near bone), the mechanism still runs into a few hard biological constraints that your version doesn’t fully solve. I’ll go point-by-point, but focus only on what still breaks under your s…
OverApr 4I put said theory into chat gpt this is the outcome's, “I’m going to be straight with you—this is one of those ideas that sounds scientific because it uses real biology terms, but the conclusion it reaches doesn’t match how facial tissue actually behaves in real life. ⸻ The core flaw in the theory Everything you wrote about inflammation, TGF-β, fibroblasts, collagen, etc. is real biology. But…
skypslApr 4jfl at your iq if you think AI is good at debating points, since this low effort copy & paste took no effort i will also put it into another chatbot and ask it to refute that point ChatGPT makes valid points but several of its rebuttals are **weaker than they appear:** **Where ChatGPT is right:** - Collagen organization is disorderly — fair point - You can't precisely control the inflammator…
OverApr 4lol the irony, I guess we’re just going AI for AI then. I get what you’re doing here—you’re stress-testing the counterarguments, not just accepting them. That’s fair. But the part that still doesn’t hold up isn’t about whether inflammation biology exists—it’s about what kind of tissue you actually end up with and how it presents on a face. Let’s go directly at the gaps you pointed out. ⸻ 1. “Co…
skypslApr 4so either provide points yourself or you're getting AI responses back
OverApr 4lol the irony, welp I guess we’re going AI for AI then.“I get what you’re doing here—you’re stress-testing the counterarguments, not just accepting them. That’s fair. But the part that still doesn’t hold up isn’t about whether inflammation biology exists—it’s about what kind of tissue you actually end up with and how it presents on a face. Let’s go directly at the gaps you pointed out. ⸻ 1. “Co…
OverApr 4I’m literally replying to your comment are you taking it down? lol
OverApr 4I get what you’re doing here—you’re stress-testing the counterarguments, not just accepting them. That’s fair. But the part that still doesn’t hold up isn’t about whether inflammation biology exists—it’s about what kind of tissue you actually end up with and how it presents on a face. Let’s go directly at the gaps you pointed out. ⸻ 1. “Controlled low-grade, site-specific inflammation” This is…
Thorbjorn_ScheuerApr 4Have you seen any results from bondsmashing yourself
skypslApr 4temporary results as i am yet to fully be consistent due to using knuckles instead of hammer which will wreck your skin
Nice post and actually very plausible mechanisms, unlike the wolff's law hypothesis, which sounds intuitive but is falls apart when examined closer. I have researched this before and I think with the right combination of retinoids or topical peptides and even microneedling to promote collagen synthesis, it could lead to noticeable improvements in facial angularity and contours.
Sounds really interesting i will have to research this further, my main concerns initially though would be with retinoids drying the skin, which would make it more prone to bruising, and if microneedling would also "weaken" the skin also making it bruise more. But yeah topical peptide injections have been tested and tried already and they've well provided faster results, so i fully agree there. M…
high iq thread, proved its cope tho
pack your bags guys user25637458 said it was cope
user25637458Apr 2keep doing your 3x12 bone smashes bro thats def a great way to ruin your skin and health indicators
whole lotta yap + cope
bonesmashing is not fawnd in neytsher
High effort thread
Yes, No. looks at MMA fighters stronger facial structure but its genetics you can too a certain degree the rest is peptides and surgery
Correlation not causation
skypslMar 27No, MMA fighters look angular because theyre on severe weight cuts & are very lean, its not a case that helps bonesmashing whatsoever. Also i disagree, i dont think theres a genetic ceiling for scar tissue accumulation, but i do agree that injecting peptides that would stimulate collagen deposition and scar tissue accumulation into the areas you bonesmash would boost results.
I'm not reading all that btw it works just do it everyday and maintain inflammation that will make sure scar tissue diposit
skypslMar 26mfw TLDR
Interesting article, keep it up!
bro censored bonesmashing