Articular cartilage is a biphasic material: an ~75% water/interstitial-fluid phase trapped in a solid matrix of collagen fibers and proteoglycan (PG) aggrecans. Under a step compressive stress σ, the fluid is nearly incompressible and initially carries almost the entire load — the classic biphasic consolidation result (Mow et al. 1980):
∂p/∂t = c_v · ∂²p/∂z² (1D pore-pressure diffusion)
c_v = k · H_A (consolidation coefficient)
σ'(z,t) = σ(t) − p(z,t) (effective / solid-matrix stress)
p is interstitial fluid pressure, k is hydraulic permeability, H_A is the aggregate (solid-matrix) modulus, and σ' is the stress actually carried by the collagen–PG solid network. The free articular surface is fluid-draining (p = 0 there); the deep zone against subchondral bone is essentially sealed (no flux). So the surface layer loses its fluid pressure support first and its solid matrix takes on load soonest — matching the clinical observation that early osteoarthritic fibrillation starts at the cartilage surface, not the deep zone.
Losing proteoglycan (as in early OA) does two things at once: it lowers H_A (a softer matrix) and raises k (a leakier one), so pressure dissipates faster and the solid network is exposed to damaging stress sooner and more often — a self-reinforcing degradation loop. This simulator integrates the PDE above on a 1D depth grid each frame and accumulates a simple fatigue-damage law, dDamage/dt ∝ max(0, σ' − σ_threshold)², visualized as instance color/erosion on a cylindrical explant under confined compression, the same geometry used in real biphasic-property testing.
- Applied stress — peak joint contact stress (walking loads the knee at roughly 3–5 MPa).
- Proteoglycan content — 100% is healthy cartilage; dragging it down softens and speeds up the tissue's fluid response, the way early PG loss does in vivo.
- Static hold vs. cyclic gait — a constant load lets fluid drain once; cyclic loading (like walking) repeatedly re-pressurizes and re-drains the tissue, accumulating fatigue damage over many cycles.
This is a simplified, pedagogical 1D model, not a clinical-grade finite-element solve — but the governing equations and the surface-first degeneration pattern are the real biomechanics behind cartilage breakdown in osteoarthritis.