Out-of-Class and Material Diseases: Honest Open Grades and Seam Routing

Some musculoskeletal-presenting diseases are deliberately NOT emerged here. Material diseases (osteogenesis imperfecta, Ehlers-Danlos / Marfan) and signatureless ones (Paget, scoliosis) are carried as honest [O] with stated obstacles; degenerative disc disease is left to an existing kernel to avoid a duplicate page. Diseases whose CAUSE is out-of-class are ROUTED to siblings via a named seam — single-source-of-truth.

This register keeps honesty explicit. The substrate already grades absolute bone density and material strength [O]; connective-tissue diseases inherit that obstacle rather than forcing a claim. Out-of-class diseases are listed so they are not silently dropped, each with the sibling owner and the single seam variable cited — SSOT, no duplicate emergence.

Material and signatureless diseases — honest [O], not forced

The kit fixes the SHAPE of bone and cartilage mechanics but not their absolute material constants; that boundary is graded [O] throughout. The following connective-tissue diseases live in that open region and are recorded with their obstacle, not overclaimed:

• Osteogenesis imperfecta (COL1A1/2) — a qualitatively lower matrix yield threshold is plausible [V?], but the quantitative brittleness is a material property the substrate does not fix [O].
• Ehlers-Danlos / Marfan (collagen, fibrillin) — connective-tissue laxity; a material compliance change, [O].
• Tendinopathy — NOW IMPLEMENTED in §17: the OA cyclic-fatigue kernel applied to a tendon collagen contact number gives a verified shape [V]; only the absolute progression rate remains [O]. (Moved out of this open-material list this cycle.)
• Paget's disease — disorganised runaway cross-basin remodelling; no clean single-switch signature [O]. Renal osteodystrophy / osteomalacia — a mineralization-supply defect, outside the switch-threshold scope [O].
• Scoliosis, developmental dysplasia of the hip, clubfoot — three-dimensional structural / developmental deformities with no clean single-switch signature to perturb; the substrate fixes load-bearing mechanics, not three-dimensional skeletal geometry. Carried as honest [O], the same category as Paget's. (Out of current scope; the posture / mechanical-load seam is where any future treatment would attach.)

Covered by an existing kernel — deliberately not duplicated

One residual disease is not open for lack of a mechanism — it is deliberately left un-emerged to avoid a duplicate. Degenerative (intervertebral) disc disease is a cyclic-fatigue unjamming of a load-bearing collagen matrix, mechanically identical to osteoarthritis (§12) and tendinopathy (§17). The same CITED Paris/Basquin damage law (m=2) applied to an intervertebral-disc contact number would reproduce the same signature — sub-threshold protected, loss convex in cyclic load — a verified SHAPE [V] with only the absolute rate left [O]. It is a one-function reuse of the existing kernel. We deliberately do NOT give it a third identical-kernel page: that would duplicate a source of truth (SSOT) without adding physics. The distinction is honest book-keeping — a parsimony choice, not a capability gap — and it couples through the same posture / mechanical-load seam.

Out-of-class diseases — routed via seams (SSOT)

These are real musculoskeletal presentations whose CAUSE belongs to another physical class. They are emerged in the sibling package and only the seam variable is cited here; re-deriving them would duplicate a source of truth.

The bone-metastasis row is the instructive one: the bone microenvironment (osteoclast/osteoblast coupling) IS in-class and couples to the T3/T6 remodelling axis, but the primary tumour is owned by its own sibling. The seam carries only what crosses the boundary.