💊 Chemotherapy-Induced Alopecia & Scalp Cooling Simulator
This simulator illustrates hair loss during chemotherapy due to damage to follicles in the active growth phase and the mechanism of scalp cooling, which narrows blood vessels in the scalp.
Anagen-Phase Hair Follicles
Follicle matrix cells divide fast, rivaling cancer cell turnover rates.
- ~90%: Follicles in anagen phase (scalp at any time)
- ~24-72h: Matrix cell cycle time (among fastest in body)
- 2-7 yrs: Anagen phase duration (active growth)
- ~0.35mm: Daily scalp hair growth (per follicle)
Why follicles divide so fast
Matrix cells rival tumor cells in division speed.
Fast division makes follicles collateral chemo targets.
Anatomy of the follicle
Bulb, matrix, dermal papilla, and shaft, briefly.
The hair growth cycle
Anagen growth, catagen transition, telogen rest phases.
Chemotherapy Circulation to the Scalp
Cytotoxic drugs travel systemically, unable to distinguish target cells.
- >80%: Alopecia risk, anthracyclines (without protection)
- >80%: Alopecia risk, taxanes (without protection)
- Bloodstream: Drug reaches scalp via (systemic circulation)
- Days: Onset after infusion (to first cycle)
Systemic, non-selective delivery
Blood carries drug everywhere, healthy tissue included.
Fast-dividing cells anywhere are vulnerable collateral targets.
Regimen-dependent severity
Different chemo classes carry different alopecia risk.
Why hair follicles are hit hard
High blood flow scalp region gets strong exposure.
Matrix Damage & Hair Shedding
Damaged matrix cells weaken the shaft, causing breakage and shedding.
- 2-3 wks: Shedding onset (after first cycle)
- Diffuse: Pattern (across whole scalp)
- Breakage: Shaft failure mode (not root loss)
- ~1-2 mo: Peak shedding window (during treatment)
Timeline of visible loss
Weakened shafts snap near the scalp surface.
Loss is typically abrupt, diffuse, and treatment-cycle linked.
Anagen effluvium mechanism
Growth-phase follicles are abruptly disrupted mid-cycle.
Regrowth after treatment
Follicles usually recover once chemo exposure ends.
Scalp Cooling & Vasoconstriction
Cooling caps chill the scalp, narrowing vessels feeding follicles.
- ~18-22°C: Scalp temp during cooling (target skin temperature)
- ~20-40%: Blood flow reduction (estimated local decrease)
- Pre/post infusion: Cooling duration (plus infusion time)
- ~1.5-3h: Cap contact time (per session typical)
Vasoconstriction mechanism
Cold narrows vessels, cutting local blood delivery.
Less blood flow means less chemo reaching follicles.
Reduced cellular uptake
Cooler tissue also slows drug metabolic uptake.
Device & protocol basics
Cap fitted snugly, cooled before, during, after dosing.
Hair Preservation Outcomes
Cooling gives partial-to-substantial hair preservation, not a guarantee.
- ~50-65%: Success rate (varies) (meaningful preservation)
- Regimen type: Effectiveness driver (drug class dependent)
- Risk reduction: Approach (not full prevention)
- Growing: Adoption (oncology centers worldwide)
Variable effectiveness
Outcomes differ by drug, dose, and individual patient.
Cooling shifts odds toward preservation, not certainty.
Patient experience factors
Cold tolerance and cap fit affect real-world use.
Weighing the tradeoff
Extra session time for a chance at preserved hair.
This simulator illustrates hair loss during chemotherapy due to damage to follicles in the active growth phase and the mechanism of scalp cooling, which narrows blood vessels in the scalp.
2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install