Biodegradable Stent Polymer Degradation

Timeline

Implant age 0.0 mo

Polymer Composition

Glycolide content (PLGA) 15%

Autocatalysis strength A 1.2

Scaffold State

Molecular weight

100%

Radial strength

100%

Scaffold mass

100%

Phase

Intact

How it works

Bioresorbable coronary scaffolds (e.g. PLLA/PLGA-based devices) degrade by bulk hydrolysis: water penetrates the whole strut cross-section and randomly cleaves ester bonds. The chain-scission rate follows the Pitt–Schindler relation for the number-average molecular weight M_n:

d(1/Mn)/dt = k_eff(t)
k_eff(t) = k0 · (1 + A · x(t)),   x(t) = Mn0/Mn(t) − 1

x(t) is the fraction of ester bonds already cleaved. Because the acidic scission products (lactic/glycolic acid oligomers) catalyze further hydrolysis before they can diffuse out, k_eff grows with x — this is the well-documented autocatalytic bulk-erosion mechanism, and A sets how strongly it self-accelerates.

Radial strength collapses once M_n falls below the critical entanglement weight M_c — chains too short to entangle can't transmit load, so mechanical support is lost well before the material physically disappears (real devices lose most radial strength by ~6 months).
Scaffold mass stays high much longer: oligomer fragments must shrink below a diffusible size before they leave the strut, so bulk mass loss lags both M_n and strength by roughly a year (full resorption ~2–3 years).
Glycolide content raises k0 — glycolide's extra hydrophilicity speeds water uptake and ester hydrolysis versus lactide-rich (PLLA-like) copolymers.

Strut color tracks molecular-weight retention (cyan → amber → red) and strut thickness tracks local mass loss, applied with per-strut random erosion thresholds — real bulk erosion is heterogeneous, not uniform, because local water/acid concentration varies across the scaffold.

Intact polymer Weakened (below Mc) Eroding / fragmenting

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