Tendinopathy as Cyclic-Fatigue Unjamming of the Tendon Collagen Network

Tendinopathy is the tendon analogue of osteoarthritis: cyclic-fatigue unjamming of a load-bearing collagen network. Overuse drives the same Paris/Basquin damage law (§12) on the tendon contact number, so fibres are lost progressively — 25.6% at overuse — while sub-threshold use is protected and loss accelerates with overuse. Shape verified [V] on the cited damage-law form.

A tendon is a load-bearing collagen contact network; tendinopathy is its cyclic-fatigue degeneration under overuse. Reusing the OA Paris/Basquin law (exponent m=2, FORM cited) on the tendon contact number: sub-threshold use is protected, fibre loss rises with overuse load and is convex. Same kernel, different tissue. Shape [V]; damage-law form [L]; absolute progression rate [O].

The same unjamming, a different tissue

Tendon is modelled as a load-bearing collagen network — the same kind of contact-number order parameter as cartilage. Tendinopathy is overuse fatigue of that network: repetitive supra-threshold loading accumulates damage and progressively degrades the collagen, exactly as cyclic loading unjams cartilage in OA. So the OA fatigue kernel transfers directly, with no new mechanism, only a different tissue.

Sub-threshold protected, overuse accelerates

loadingσ/σ*final contact no.fibre loss
rest (sub-threshold)0.8×1.0000.000
normal use1.3×0.9640.036
overuse1.8×0.7440.256
severe overuse2.3×0.3240.676

Rest and sub-threshold use are protected (no loss); fibre loss rises with overuse load and is convex — the documented dose effect of training overload. The mechanism is collagen-network unjamming under cyclic fatigue.

What is NOT claimed

The SHAPE is the result and the Paris/Basquin damage-law FORM is cited [L]; the absolute progression rate (the rate constant) is not fixed by the substrate and stays [O]. Tendinopathy was a registered open-material item in the previous version; giving it the OA kernel moves it from [O] to a verified shape, while the absolute rate remains open.

Analgesic lever map (cross-reference)

Tendinopathy pain reuses the same cyclic-fatigue kernel, so the L2 (deload) lever lowers both the crossing rate and the tendon contact loss; the mirror disease-modifying step then ADDS eccentric loading, a separate up-step that is not analgesia. See §25 the three-lever threshold logic for the inherited technique (concept DOI 10.5281/zenodo.20733420), and §26 L2 convergence for the worked lever sweeps. The analgesic axis adds no new physics: pain is a threshold-crossing rate on the same R19 barrier this chapter already uses.