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.

PART 1: DEFINITION AND THEORY

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.

AGAIN NONE OF THIS IS MEDICAL ADVICE, THIS IS NOT AN ADVISED METHOD, EXPERIMENT AT YOUR OWN RISK, YOU HAVE BEEN WARNED

-Skypsl