🩸 Ulcers, Blisters & Bullae: How Dentists Decode Oral Mucosal Damage

ToothOps
Jan 8
3 min read

Understanding the clues hidden in the oral cavity — inspired by Case 2905

When a patient walks in with painful oral ulcers, erosions, and mysterious blisters, it can feel like someone dumped your entire oral path textbook on the floor and said, “Good luck.”

But take a breath — because behind every ulcer is a pattern.Behind every blister is a mechanism.And behind every scary-looking lesion is a story the oral mucosa is trying to tell you.

Today’s ToothOps breakdown uses Ms. Wiltshire’s symptoms as a real-world anchor to decode what ulcers, blisters, and mucosal erosions actually mean — and how clinicians work through the differential like pros.

1️⃣ What Are We Even Looking At? (Blisters, Erosions, Ulcers)

Before we diagnose anything, we identify the type of mucosal damage:

💧 Blister (Vesicle/Bulla)

A raised, fluid-filled lesion.

Vesicle = <5 mm
Bulla = >5 mmWhen they rupture → erosion or ulcer

⚠️ Erosion

Shallow loss of epithelium but basement membrane stays intact→ Heals without scarring→ Harder to notice; shiny, red, painful

🩸 Ulcer

Deep lesion extending through the basement membrane→ Yellow base, red halo→ Much more painful→ Heals slower

🧠 ToothOps Analogy:Think of the oral mucosa like carpet:

Erosion = scratching off the top fibers
Ulcer = ripping a chunk out

2️⃣ Why Ms. Wiltshire’s Case Raised Red Flags

Ms. Wiltshire presents with:

Multiple mucosal sites involved
Flaccid blisters
Easily ruptured bullae → erosions + ulcers
Severe pain preventing eating → 20 lb weight loss
No improvement with nystatin or Mycelex

These features do NOT match:

Trauma
Simple aphthous ulcers
Localized infection

But they do strongly match:

🔥 Autoimmune blistering disease — especially Pemphigus Vulgaris

Because PV = intraepithelial blistering → flaccid bullae…and that’s exactly what she has.

3️⃣ Differential Diagnosis Breakdown (The ToothOps Way)

Here's the cheat sheet every dental student needs:

A) Traumatic Ulcer

✔ Common (cheeks, tongue, lips)

✔ Yellow-gray center

❌ Usually solitary

❌ No blisters

📌 Not consistent with Ms. W.

B) Aphthous Ulcer (RAS)

✔ Painful, recurrent

✔ Stress-triggered

❌ No blisters

❌ Not widespread

❌ No weight loss

C) Herpes Simplex Virus (HSV-1)

✔ Vesicles → rupture → shallow painful ulcers

✔ Often on lips & gingiva

❌ Typically clustered

❌ Not months-long

❌ Not flaccid bullae

D) Erythema Multiforme / SJS

✔ Target lesions on skin

✔ Oral erosions & bullae

❌ Usually acute, not chronic

❌ Often linked to drug exposure/infection

⭐ E) Pemphigus Vulgaris (Most Likely)

✔ IgG attacks desmosomes

✔ Acantholysis → suprabasal split

✔ Flaccid bullae that rupture easily

✔ “Tombstone basal layer”

✔ Positive Nikolsky sign

✔ Oral cavity often first site

This matches Ms. W. nearly perfectly.

F) Bullous Pemphigoid

✔ Hemidesmosome autoantibodies

✔ Subepithelial, tense bullae

✔ Older adults

❌ Oral mucosa often spared

❌ Bullae not flaccid

G) Lupus Erythematosus

✔ Painful erythematous & ulcerative patches

✔ Keratotic white radiating borders

❌ No flaccid blisters

❌ Doesn’t match presentation

4️⃣Why Pemphigus Vulgaris Is So Dangerous

PV isn’t just painful — it’s life-threatening if untreated.

Patients struggle to eat → rapid weight loss
High infection risk due to broken epithelium
Chronic pain → reduced oral intake & dehydration

And most importantly:

PV requires systemic immunosuppressants

→ corticosteroids→ rituximab→ careful medical-dental coordination

This is why recognizing PV early is crucial.

5️⃣ Understanding the Oral Mucosa (Why It Breaks Down)

(Cited from Regezi Oral Pathology & Taylor’s Dermatology)

Your oral mucosa is built for war:

Stratified squamous epithelium
Minor salivary glands
Continuous turnover
Biofilm exposure
Constant mechanical stress

But autoimmune IgG antibodies →obliterate the bonds (desmosomes) between keratinocytes,turning the mucosa from a shield → to wet tissue paper.

This is the mechanism behind Ms. W’s erosions and chronic pain.

6️⃣ Takeaway — How Students Should Approach Cases Like This

💡 1. Identify the lesion type first

Ulcer vs erosion vs vesicle vs bulla = the diagnostic backbone.

💡 2. Check the distribution

One area → traumaMultiple mucosa → systemic disease

💡 3. Evaluate blister quality

Flaccid? = PVTense? = BPClusters? = HSV

💡 4. Ask the “eating question”

If the patient can’t eat → think deeper pathology

💡 5. Medications matter

Polyene antifungal failure = consider azolesAntifungal failure overall = consider autoimmune disease

🌟 Final Message

Oral mucosal disease is like detective work —every lesion is a clue, every blister is a signal, and every ulcer tells a story.

When you learn how to read those clues, you stop memorizing…and start diagnosing.

You’ve got this. Keep studying smart, not scared. 🦷✨