Calcium homeostasis × bone remodeling

A focused atlas of calcium dynamics models

Every entry either simulates calcium–phosphate physiology directly or is a documented PTH-driven bone-resorption mechanism used by that integrated model lineage.

View repository ↗
9scope-audited model entries
5Julia source modules
7atlas entries with Julia coverage
2supporting PTH/bone mechanisms, explicitly labeled
Scope audit

Relevant means mechanistically connected

The prior broad bone-model list was narrowed. Genetics, estrogen-only BMD, fatigue, mechanics, and spatial models are not shown because they do not simulate mineral dynamics.

What the atlas now includes

Direct models have calcium or phosphate states, fluxes, endocrine feedback, or calcium-focused clinical outputs. They cover gut absorption, renal handling, parathyroid control, calcitriol, FGF23, bone mineral exchange, CKD-MBD, and hypoparathyroidism.

Supporting mechanisms are retained only where PTH-controlled bone resorption/formation provides a direct biological bridge to calcium mobilization and is part of the Peterson–Riggs lineage. The cards state plainly when serum calcium is not explicit.

Start with physiology

Where the retained models sit

Choose a compartment to filter the atlas. Solid arrows indicate mineral/endocrine flows; dashed arrows are feedback.

mineral or endocrine flowfeedback/signaling
Explore the literature

Choose a calcium-relevant model

9 models shown

Selected model

Physiological interpretation

“Supporting” does not mean a calcium state is hidden: it means the card identifies its precise PTH-to-bone role and its limitation.

Comparison matrix

What is explicit in each model?

Rows use the same clinical-physiology dimensions. Click a row to inspect the model.

ModelRoleCa / PO4EndocrineKidneyBone cellsOutputsJulia