🎾 Platelet-Rich Plasma for Epicondylitis Simulator

The Degenerated Extensor / Flexor Tendon Origin

Epicondylitis starts as failed collagen healing, not inflammation.

• Tendinosis: Condition (not tendinitis)
• I → III: Collagen type shift (weaker fibers)
• Low: Vascularity (poor healing supply)
• >6 wks: Symptom duration (chronic threshold)

Origin under repetitive strain

Wrist extensor tendons anchor at the lateral epicondyle.

Microtears outpace repair

Repetitive load creates microtears faster than cells fix them.

Disorganized scar-like tissue

Fibroblasts lay down thin, randomly oriented collagen fibers.

Angiofibroblastic tissue replaces strong parallel collagen with weak, chaotic strands.

Injecting Concentrated Platelets at the Tendon Origin

Autologous blood is spun down and re-injected at the lesion.

• 3–5×: Platelet concentration (above whole blood)
• Tendon origin: Injection target (epicondyle site)
• Peppering: Technique (multiple needle passes)
• ~15 min: Procedure time (outpatient setting)

Centrifuged whole blood

Centrifugation separates platelet-rich plasma from red cells.

Precision placement

Ultrasound guides the needle to the degenerated zone.

Local platelet deposit

Platelets cluster densely right at the injury site.

Higher platelet concentration seeds a stronger regenerative signal from the start.

Platelet Degranulation Releases Regenerative Growth Factors

Activated platelets flood the tendon origin with signaling proteins.

• Released: PDGF (fibroblast mitogen)
• Released: TGF-β (collagen synthesis driver)
• Released: VEGF (new vessel signal)
• ~1 hr: Peak release window (post-activation)

Alpha granule degranulation

Platelet alpha granules dump growth factors on contact.

PDGF drives proliferation

PDGF pushes resident fibroblasts to multiply rapidly.

VEGF restores blood supply

VEGF triggers new capillaries into the starved tendon.

Three growth factors act together: proliferate, synthesize, and revascularize the tendon origin.

Fibroblasts Migrate Toward the Growth Factor Gradient

Chemotaxis pulls fibroblasts from surrounding tissue into the lesion.

• PDGF gradient: Migration cue (chemotactic signal)
• Peritendinous: Fibroblast source (nearby tissue)
• Days 3–14: Recruitment window (post-injection)
• Up to 3×: Density increase (vs baseline)

Directed cell migration

Fibroblasts crawl up the PDGF concentration gradient.

Population expansion

Recruited cells proliferate once anchored at the site.

Dose-dependent response

Higher platelet concentration recruits fibroblasts faster and denser.

Fibroblast density scales with both growth factor dose and elapsed time.

New Collagen Aligns Into Organized Parallel Bundles

Fibroblasts synthesize and remodel collagen over several weeks.

• III → I: Collagen shift (stronger fiber type)
• Mechanical load: Alignment driver (tensile remodeling)
• ~8–12 wks: Organization plateau (typical timeline)
• Substantial: Tensile strength gain (vs pre-treatment)

Collagen type transition

Type III collagen is gradually replaced by stronger type I.

Load-guided alignment

Tendon loading orients new fibers along the strain axis.

Weeks-long remodeling

Organization keeps improving for roughly twelve weeks.

Faster, denser regeneration follows higher platelet concentration and more elapsed weeks.