Osteoarthritis as Cyclic-Fatigue Unjamming of the Cartilage Contact Network

Osteoarthritis is cartilage unjamming. Cartilage load capacity is the T2 contact number; cyclic SUPRA-threshold load fatigues that contact network, so the matrix progressively loses load-bearing contacts — the joint-space-narrowing analogue. Sub-threshold exercise is protected (100% matrix retained), but at overload with high BMI the matrix loss climbs to 25.6% and accelerates convexly with load. Shape verified [V] on a CITED fatigue-damage law.

A cited Paris/Basquin cyclic fatigue-damage law (exponent m=2, FORM cited [L]) is applied to the cartilage contact number under load σ/σ*. Below threshold (0.8×) the matrix is protected (loss 0.000); at normal load loss is modest (0.036), rising convexly to 0.256 at overload+BMI and 0.676 at severe overload. Loss accelerates with load magnitude and BMI, the OA epidemiology. Shape [V]; damage-law form [L]; absolute progression rate [O].

A joint as a load-bearing contact network

Cartilage is modelled as load-bearing jammed matter, and its integrity is the same order parameter as muscle force in T2: the number of load-bearing contacts. Osteoarthritis is the fatigue of that network. Unlike bone (which can remodel back across the T3 yield threshold), cyclic supra-threshold loading accumulates irreversible damage in the contact number — progressive loss of load-bearing matrix, the mechanical analogue of joint-space narrowing.

A cited damage law, not a fitted one

This is the one disease in the battery that needs a small ADDED mechanism, so it is held to the cited-anchor discipline: damage accumulates by a Paris/Basquin-type cyclic-fatigue law with a CITED exponent (m=2), not a curve tuned to land. Applied to the contact number under normalised contact stress σ/σ*:

Three signatures emerge and match OA epidemiology: (1) a threshold — sub-threshold moderate exercise is PROTECTED (no loss), consistent with exercise not causing OA; (2) monotonic acceleration — loss rises with load magnitude; (3) convexity in load and BMI — the documented dose effect of joint overload and obesity. The mechanism is cartilage UNJAMMING under cyclic fatigue.

What is NOT claimed

The SHAPE (threshold, monotonic, convex, BMI-sensitive) is the result and the damage-law FORM is cited [L]. The absolute progression rate — the rate constant A that sets years-to-narrowing — is NOT fixed by the substrate and stays [O]; only relative, normalised loss is claimed.

Analgesic lever map (cross-reference)

Osteoarthritis is the primary L2-coupled case: the joint load that hurts is the load that erodes the cartilage, so the unloading (L2) analgesic move is the same operation that arrests the lesion, while a peripheral block (L1) relieves pain with the cartilage left unchanged. See §25 the three-lever threshold logic for the inherited technique (concept DOI 10.5281/zenodo.20733420), and §26 L2 convergence, §27 L1 coupled/decoupled discriminant 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.