Biomaterials: Drug Release from a Hydrogel Scaffold

Hydrogel Scaffold

Porosity 55%

Drug mobility 1.0×

Scaffold degradation 0.006/h

Released

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Elapsed time

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Scaffold integrity

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How it works

A biodegradable polymer/hydrogel scaffold — the strut lattice you see — holds an encapsulated drug payload (amber points) near its core. Each drug molecule performs a random walk (Brownian diffusion) through the pores of the matrix; once it crosses the scaffold's outer boundary it counts as "released" (teal). The lattice itself slowly erodes over time, exactly as a real bioresorbable implant does, which opens more channels and accelerates diffusion as the run progresses.

Fick's 2nd law:  ∂C/∂t = D·∂²C/∂x²
Higuchi model:   Q(t) = k·√t
effective D  ∝  mobility · (0.4 + porosity) · (1 + erosion)

Porosity — the void fraction of the scaffold at t=0. A denser (low-porosity) matrix obstructs the drug more, slowing the early release rate.
Drug mobility — the intrinsic diffusivity of the payload molecule itself (small molecules diffuse faster than proteins).
Scaffold degradation — the polymer's hydrolytic erosion rate; as struts thin and vanish, effective porosity rises and release accelerates — the coupling real bioresorbable implants rely on for a sustained-then-rising release profile.
Released fraction — cumulative drug that has diffused past the scaffold boundary; for a simple porous matrix this tracks the classic Higuchi square-root-of-time law until the payload is exhausted.

Real-world relevance: this is the working principle behind drug-eluting orthopedic implants, resorbable sutures and tissue-engineering scaffolds — the same porosity/degradation trade-off engineers tune when designing PLGA, PCL or hydrogel carriers for controlled release.

Scaffold strut Encapsulated drug Released drug

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