🧬 The Science behind TECaR Therapy 🧬

Fibroblasts are central players in the healing and repair of tissue after injury. Their role is dynamic and changes throughout the phases of wound healing. They heal all human tissue, from bone/ muscle and the skin.

Muscle Tissue

Their role is a bit different because muscle has its own regenerative cells (satellite cells), but fibroblasts work alongside them. Here’s how it happens:

1. After Muscle Injury (Inflammatory Phase)

Fibroblasts are recruited to the injury site by inflammatory signals.

They start producing extracellular matrix (ECM) proteins, mainly collagen, to provide a temporary scaffold for muscle stem cells (satellite cells) and immune cells.

2. Repair & Regeneration Phase

Collaboration with satellite cells: Satellite cells are the main muscle-regenerating cells. Fibroblasts create the ECM “environment” that helps satellite cells proliferate and fuse into new muscle fibers.

Growth factors & signaling: Fibroblasts secrete growth factors (like FGF and TGF-β) that regulate how much muscle vs. scar tissue is formed.

3. Remodeling Phase

Fibroblasts produce collagen and elastin to restore tensile strength.

They help organize collagen fibers so the repaired tissue can withstand muscle contraction.

Summary: 

Fibroblasts heal muscle tissue by

building the ECM scaffold,

·      supporting satellite cell activity,

·      contracting and closing the injury, and

·      remodeling collagen into a functional structure.

Bone Tissue

Fibroblasts also play an important part in bone healing, though they’re not the main bone-building cells (that job belongs to osteoblasts). Instead, fibroblasts act as the early repair crew, setting the stage for new bone to form. Here’s how it works:

1. Inflammatory Phase (first few days)

After a fracture, blood clots form at the injury site (fracture hematoma).

Fibroblasts migrate into the area and start producing collagen fibers and other extracellular matrix (ECM) proteins.

This forms a fibrous scaffold that stabilizes the fracture and provides a framework for new tissue.

2. Soft Callus Formation (first few weeks)

Fibroblasts (and related stem-like cells called fibroblast-like mesenchymal stem cells) contribute to forming a fibrocartilaginous callus.

This “soft callus” bridges the broken bone ends, holding them together while new tissue grows.

Fibroblasts also release growth factors that attract osteoblasts and chondrocytes (cartilage cells).

3. Hard Callus Formation (weeks to months)

As healing progresses, the fibrocartilage callus is gradually replaced by woven bone, thanks to osteoblast activity.

Fibroblasts help remodel and align collagen fibers, ensuring the callus can support mineralization.

4. Remodeling Phase (months to years)

Fibroblasts continue contributing to the organization of collagen and ECM, helping shape the bone back to its original form.

Many fibroblasts eventually undergo apoptosis (programmed cell death) once their job is complete.

Summary: 

In bone healing, fibroblasts

·      create the early collagen scaffold,

·      help form the soft callus that stabilizes the fracture,

·      signal and support osteoblasts/chondrocytes,

·      and aid in remodeling the extracellular matrix.

They are the scaffold builders and coordinators, while osteoblasts are the bricklayers that deposit new bone.

The skin

Fibroblasts are absolutely essential in skin wound healing, because they’re the main cells responsible for rebuilding the tissue framework after injury. Here’s how they work step by step:

1. Inflammatory Phase (first 48–96 hrs)

• Fibroblasts are recruited into the skin cells bed by signals from platelets and immune cells.

• They remain relatively inactive at first while immune cells clear debris and pathogens.

2. Proliferative Phase (days → weeks)

• Collagen & ECM production: Fibroblasts begin producing collagen type III, fibronectin, and proteoglycans, forming the extracellular matrix (ECM) scaffold.

• Granulation tissue: This scaffold + new capillaries form granulation tissue, filling in the wound gap.

• Growth factors: Fibroblasts release VEGF, PDGF, and FGF to stimulate angiogenesis (new blood vessel growth) and support keratinocyte migration (for re-epithelialization).

• Myofibroblast transformation: Many fibroblasts differentiate into myofibroblasts, which have contractile properties that physically pull the wound edges together.

3. Remodeling / Maturation Phase (weeks → months)

• Collagen remodeling: Fibroblasts switch from producing collagen type III (temporary, weaker) to collagen type I (stronger, more durable).

• Matrix organization: They align collagen fibers along stress lines, strengthening the new skin.

• Scar formation: The result is a scar—less elastic and without hair or glands, but structurally sound.

• Apoptosis: Once healing stabilizes, many fibroblasts die off, leaving fewer cells in the scar tissue.

✅ Summary: In skin healing, fibroblasts

• migrate into the wound,

• build the collagen/ECM scaffold,

• contract the wound edges,

• support blood vessel and skin cell growth, and

• remodel tissue into a strong (though scarred) structure.