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.