What is it?

The Burn Wound Simulator implements a spatial agent-based model (ABM) of post-burn wound healing on a 100×100 grid representing a cross-section of skin tissue. Each grid cell hosts at most one mobile cell agent (neutrophil, macrophage, fibroblast, etc.) and two underlying cytokine fields — IL-8 and TGF-β — that diffuse and decay across the tissue over time.

At every simulation step, agents sense their local cytokine environment, move toward relevant signals, produce or consume mediators, and can proliferate, transition phenotype, or die. The collective behaviour of hundreds of interacting agents produces the characteristic temporal dynamics of wound healing: an early inflammatory phase, a resolution phase, and a remodelling phase whose outcome is captured as a scar classification.

The model is based on the mathematical framework from Bumbuc et al. (2026), which combines ordinary differential equations for cytokine dynamics with agent-based rules for cellular behaviour — making it one of the first hybrid ABM-ODE models of burn scar formation.

What can you simulate?

The tool ships with three biologically distinct presets that produce different healing outcomes:

• Normotrophic — balanced inflammation and repair, yielding a flat, functional scar (Collagen I/III ratio 4–8).
• Hypertrophic — excessive myofibroblast activity and collagen deposition leads to a raised, firm scar (ratio > 8).
• Keloid — dysregulated collagen III production outpaces conversion to collagen I, producing an overgrowing scar (ratio < 3).

Beyond presets, you can adjust the wound radius (how large the initial burn is) and the simulation speed. Live charts track cell population dynamics and cytokine concentrations over time, and a scar classification badge updates automatically once sufficient healing has occurred (after ~200 simulation steps).

The six cell types modelled

The simulation tracks six distinct cell populations, each with biologically realistic movement rules, lifespans, and cytokine interactions:

Two cytokines driving everything

Cell behaviour is orchestrated by two cytokine fields that diffuse across the tissue and decay over time:

• IL-8 (Interleukin-8) — the pro-inflammatory signal. Released by dead endothelial cells at injury onset, then amplified by neutrophils and M1 macrophages. IL-8 recruits and activates immune cells, driving the inflammatory phase.
• TGF-β (Transforming Growth Factor-β) — the resolution/repair signal. Produced by M2 macrophages and mast cells as inflammation resolves. TGF-β stimulates fibroblast migration, collagen synthesis, and the fibroblast → myofibroblast transition that closes the wound.

The balance between these two signals — and particularly how long IL-8 dominates before TGF-β takes over — determines the scar outcome. Prolonged IL-8 dominance tends toward hypertrophic scarring; excessive TGF-β signalling promotes keloid formation.

How to use it

1. Select a preset from the dropdown (Normotrophic is a good starting point).
2. Adjust the wound radius slider if desired (default: 20 grid units).
3. Click Run to start the simulation.
4. Watch the wound fill in on the grid canvas as repair cells arrive.
5. After ~200 steps, a Scar Classification badge will appear based on the Collagen I/III ratio produced during healing.
6. Use Reset to start over, or switch presets to compare outcomes.