💧 Radiation-Induced Xerostomia Simulator

Pre-Treatment Salivary Gland Function

Healthy parotid and submandibular glands secrete steady protective saliva.

• 0.3–0.4: Unstimulated flow (mL/min normal)
• ~1.5 L: Daily saliva output (per day)
• Slow: Acinar cell turnover (low mitotic rate)
• 0 Gy: Radiation dose so far (no exposure)

Acinar cell architecture

Grape-like acinar clusters drain into branching collecting ducts.

Serous vs mucous glands

Parotid glands are serous, watery and highly radiosensitive.

Parotid serous acini are the first tissue radiotherapy damages.

Saliva's protective role

Saliva buffers acid, clears food, and prevents dental decay.

Early Radiation Exposure to Acinar Cells

Acinar cells die early despite being mostly non-dividing tissue.

• ~10 Gy: Dose at onset (first flow drop)
• ~50%: Flow decline (within week one)
• Apoptosis: Mechanism (non-mitotic death)
• Partial: Reversibility (early on)

Why acinar cells are so sensitive

Membrane and DNA damage trigger apoptosis despite low turnover.

Damage appears within the first radiotherapy fraction, not weeks later.

Beam pathway through tissue

Fractionated beams cumulatively strike acinar membranes daily.

Early flow measurement

Sialometry already detects reduced output during week one.

Significant Flow Reduction in Early Treatment

Flow falls sharply as cumulative dose passes mid-treatment levels.

• ~45 Gy: Typical dose (mid-course)
• ~75%: Flow reduction (from baseline)
• Weeks 2–3: Patient symptom onset (of therapy)
• Common: Taste changes (concurrent effect)

Threshold dose effects

Above 30 Gy, flow reduction becomes clinically severe.

A single course can push flow below 25% of baseline.

Symptom burden

Dry mouth, difficulty swallowing, and altered taste emerge.

Sparing techniques

IMRT contouring tries to limit dose to spared parotid tissue.

Fibrotic Replacement of Gland Tissue

Over months, dead acini are replaced by dense fibrotic scar.

• ~3–6 mo: Onset of fibrosis (post-treatment)
• Progressive: Fibrosis extent (dose dependent)
• Present: Vascular damage (microvessel loss)
• <20%: Flow at 6 months (of baseline)

Fibrotic cascade

TGF-beta signaling drives collagen deposition around dead acini.

Fibrosis, unlike acute injury, does not resolve with time.

Stem cell depletion

Radiation also kills the progenitor cells needed for repair.

Imaging correlates

MRI shows gland shrinkage and fatty fibrotic replacement.

Chronic Xerostomia and Lifelong Dry Mouth

Gland architecture cannot regenerate once fibrosis is established.

• >60%: Chronic prevalence (head and neck RT)
• Minimal: Flow recovery (beyond 2 years)
• High: Dental caries risk (lifelong)
• Palliative: Management (saliva substitutes)

Irreversible endpoint

Acinar and stem cell loss makes damage permanent.

Chronic xerostomia can persist unchanged for the rest of life.

Quality of life impact

Eating, speaking, and sleep are affected daily.

Preventive strategies

Sparing techniques and sialogogues reduce long-term severity.