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gazoro
Iron
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Facial fibrosis is the excessive buildup of thick connective tissue and collagen in the skin and underlying fascia caused by an overactive or prolonged healing response.
How It Works:
• The Trigger: Injury, surgery (like facelifts or liposuction/laser procedures), chronic inflammation, or repeated mechanical stress signals the body to repair the area.
• Overdrive of Myofibroblasts: Normally, the body produces collagen to fix a wound and then stops. With fibrosis, cells called fibroblasts turn into myofibroblasts and keep pumping out dense collagen continuously, even after healing should be finished.
• Tissue Stiffening: Normal, soft, and flexible facial tissue is replaced by rigid, dense sheets or small hard nodules.
How to increase amount of fibrosis in the face:
Chronic, Unresolved Mechanical Tension
• Physical Stress on Wounds: To have maximum results the most important thing is consistency. Keeping the skin under constant physical tension or stretch during a healing phase forces fibroblasts to continuously generate dense structural matrix proteins to resist the pulling forces.
• Immobilisation/Restricted Movement: Alternatively, completely restricting the natural movement or dynamic sliding of facial tissue layers (such as deep structural restrictions after aggressive trauma) prevents normal tissue remodeling and causes fibroblasts to bundle collagen fibers into rigid, unyielding networks.
Inhibiting Tissue Degradation
Bonesmashing can hypothetically create permanent bone:
Dermal Calcification or ossification:
When fibrotic tissue becomes so hard that it feels like bone, the tissue is likely experiencing a specific biological process called dermal calcification or ossification.
Under certain conditions, severely damaged soft tissue actually begins to transition into stone-hard, mineralized structures.
Hypothetically, repeated trauma or a single severe blunt force injury can cause bone tissue to form in the skin years after a hematoma (deep bruise) or chronic mechanical irritation occurs. Blunt force causes local tissue injury, cell death, and bleeding (hematoma) within the dermis or subcutaneous layer, triggering a long term inflammatory response. This causes the damaged environment to release an abundance of inflammatory cytokines and growth factors. Localized signaling molecules, osteoblastic metaplasia alter the genetic programming of nearby mesenchymal stem cells or dermal fibroblasts (the cells that normally make collagen and scar tissue). Instead of building a normal scar, they mistakenly differentiate into osteoblasts, creating bone.
Over time, these osteoblasts create mineralized matrixes, resulting in hard bone directly inside the skin.
How It Works:
• The Trigger: Injury, surgery (like facelifts or liposuction/laser procedures), chronic inflammation, or repeated mechanical stress signals the body to repair the area.
• Overdrive of Myofibroblasts: Normally, the body produces collagen to fix a wound and then stops. With fibrosis, cells called fibroblasts turn into myofibroblasts and keep pumping out dense collagen continuously, even after healing should be finished.
• Tissue Stiffening: Normal, soft, and flexible facial tissue is replaced by rigid, dense sheets or small hard nodules.
How to increase amount of fibrosis in the face:
Chronic, Unresolved Mechanical Tension
• Physical Stress on Wounds: To have maximum results the most important thing is consistency. Keeping the skin under constant physical tension or stretch during a healing phase forces fibroblasts to continuously generate dense structural matrix proteins to resist the pulling forces.
• Immobilisation/Restricted Movement: Alternatively, completely restricting the natural movement or dynamic sliding of facial tissue layers (such as deep structural restrictions after aggressive trauma) prevents normal tissue remodeling and causes fibroblasts to bundle collagen fibers into rigid, unyielding networks.
Inhibiting Tissue Degradation
- Blocking Matrix Metalloproteinases (MMPs): For fibrosis to accumulate, MMPs, which break down excess or old collagen, must be deactivated or overwhelmed by Tissue Inhibitors of Metalloproteinases (TIMPs). Suppressing these enzymes prevents the tissue from ever reabsorbing the dense, tough collagen sheets it deposits.
- Methods to block MMPs:
- Doxycycline hyclate: This antibiotic is currently the primary FDA-approved clinical medication used for its off-target MMP-inhibitory properties
- Dietary and Natural Compounds: Plant-derived flavonoids and polyphenols (such as quercetin, kaempferol, baicalein, and green tea catechins) can suppress MMP expression or directly chelate zinc ions.
Bonesmashing can hypothetically create permanent bone:
Dermal Calcification or ossification:
When fibrotic tissue becomes so hard that it feels like bone, the tissue is likely experiencing a specific biological process called dermal calcification or ossification.
Under certain conditions, severely damaged soft tissue actually begins to transition into stone-hard, mineralized structures.
Hypothetically, repeated trauma or a single severe blunt force injury can cause bone tissue to form in the skin years after a hematoma (deep bruise) or chronic mechanical irritation occurs. Blunt force causes local tissue injury, cell death, and bleeding (hematoma) within the dermis or subcutaneous layer, triggering a long term inflammatory response. This causes the damaged environment to release an abundance of inflammatory cytokines and growth factors. Localized signaling molecules, osteoblastic metaplasia alter the genetic programming of nearby mesenchymal stem cells or dermal fibroblasts (the cells that normally make collagen and scar tissue). Instead of building a normal scar, they mistakenly differentiate into osteoblasts, creating bone.
Over time, these osteoblasts create mineralized matrixes, resulting in hard bone directly inside the skin.
