# Vesiculobullous Disorders of the Oral Cavity

> Vesiculobullous disorders for BDS Oral Medicine: pemphigus vulgaris, mucous membrane pemphigoid, Nikolsky sign, Tzanck smear, biopsy and steroid management.

- Canonical URL: https://prepelephant.com/topics/bds/oral-medicine-and-radiology/vesiculobullous-management-bds
- Exam / course: BDS · Subject: Oral Medicine and Radiology
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Vesiculobullous Disorders of the Oral Cavity", PrepElephant, https://prepelephant.com/topics/bds/oral-medicine-and-radiology/vesiculobullous-management-bds

## Direct answer

Blisters in the mouth rupture within a day, so what the clinician sees are shallow erosions with ragged epithelial tags — which is why the level of the split, not the blister, is the organising principle. Intraepithelial (suprabasal) split with acantholysis defines pemphigus vulgaris: fragile flaccid blisters, oral lesions preceding skin disease in most patients, positive Nikolsky sign, acantholytic Tzanck cells on smear, and intercellular "fishnet" immunoglobulin G on direct immunofluorescence. Subepithelial split defines the pemphigoid group: tense intact bullae on skin, desquamative gingivitis and mucosal erosions in the mouth, linear immunoglobulin G and C3 along the basement membrane zone, scarring of conjunctiva in mucous membrane pemphigoid — and a far better prognosis. Erythema multiforme sits apart: an acute, self-limiting hypersensitivity reaction with target skin lesions and haemorrhagic crusted lips. Management is built on biopsy plus perilesional immunofluorescence: topical steroids suffice for pemphigoid, while pemphigus vulgaris demands early systemic corticosteroids with steroid-sparing agents.

## What you must remember

- **Classification by depth:** intraepithelial split — pemphigus vulgaris (suprabasal acantholysis), pemphigus foliaceus (superficial, rarely oral); subepithelial split — mucous membrane (cicatricial) pemphigoid, bullous pemphigoid, linear immunoglobulin A disease.
- **Pemphigus vulgaris:** oral erosions are the presenting feature in the majority; flaccid blisters, positive Nikolsky sign, suprabasal split with acantholytic cells, intercellular fishnet immunoglobulin G and C3 on direct immunofluorescence; untreated it was historically fatal — systemic prednisolone (about 1 mg per kg) with azathioprine, mycophenolate or rituximab is life-saving.
- **Mucous membrane pemphigoid:** older patients, desquamative gingivitis as the oral hallmark, tense skin bullae, linear immunoglobulin G/C3 at the basement membrane zone; conjunctival scarring threatens vision and mandates ophthalmology referral.
- **Linear immunoglobulin A disease:** subepithelial blister with linear immunoglobulin A deposition; dapsone responsive.
- **Erythema multiforme:** acute onset, target lesions on hands and feet, blood-crusted lips, mouth erosions; triggers — recurrent herpes simplex (the classic) and drugs (sulphonamides, non-steroidal anti-inflammatories, anticonvulsants); self-limiting, with severe forms grading into Stevens-Johnson syndrome.
- **Nikolsky sign:** firm sliding pressure shears superficial epithelium — positive in pemphigus (and often in pemphigoid variants as a "mucosal" Nikolsky); the Tzanck smear shows acantholytic cells but cannot distinguish pemphigus from pemphigoid.
- **Diagnostic pairing:** one biopsy in formalin for haematoxylin-eosin, one perilesional biopsy in Michel's medium or frozen for direct immunofluorescence — sending a single sample for both is the classic system error.

## Working through a desquamative gingivitis case

A 55-year-old woman presents with six months of sore, red, glazed gingiva that desquamates when she brushes; intact blisters are absent, but two shallow erosions sit on the palate and her left conjunctiva has been treated for scarring. The clinical label desquamative gingivitis is a sign, not a diagnosis — its three great causes are mucous membrane pemphigoid, pemphigus vulgaris and erosive lichen planus. Two biopsies follow: perilesional tissue for direct immunofluorescence, adjacent tissue for routine histology. Histology shows a clean subepithelial split; immunofluorescence shows linear immunoglobulin G and complement along the basement membrane zone — mucous membrane pemphigoid.

Management runs on three tracks. Locally: clobetasol 0.05 per cent gel in a custom tray for the gingiva, chlorhexidine rinses, treatment of any candidiasis. Systemically, for progressive disease: dapsone or low-dose prednisolone with a steroid-sparing agent under dermatology. And the sight-threatening track: ophthalmology review, because symblepharon formation converts a mucosal disease into blindness. Had the histology shown suprabasal acantholysis with fishnet immunofluorescence, every track changes — immediate systemic corticosteroids, rituximab or azathioprine maintenance — because pemphigus vulgaris is a medical emergency by comparison.

## How the exam frames it

Two organising questions decide most vesiculobullous marks: "at what level does the split occur and in which disease?" — suprabasal intraepithelial for pemphigus, subepithelial for pemphigoid — and "what does direct immunofluorescence show?" — intercellular fishnet immunoglobulin G in pemphigus, linear basement-membrane immunoglobulin G/C3 in pemphigoid, linear immunoglobulin A in linear immunoglobulin A disease, shaggy fibrinogen in lichen planus. The viva classics follow: Nikolsky sign mechanism, Tzanck smear contents (acantholytic cells, unable to separate the two diseases), tense versus flaccid blisters (depth of split and roof thickness). The management trap is prescribing topical steroids alone for pemphigus vulgaris — oral lesions are the presenting sign, and early systemic therapy prevents the fatal generalised phase; the examinable sentence is "pemphigus is treated systemically from the outset; pemphigoid is treated topically unless progressive".

## Frequently asked questions

### How are vesiculobullous disorders classified by level of blister formation?
Intraepithelial (suprabasal) splits with acantholysis define pemphigus vulgaris; subepithelial splits define mucous membrane pemphigoid, bullous pemphigoid and linear immunoglobulin A disease — histology of the blister base is the discriminator.

### What does direct immunofluorescence show in pemphigus and pemphigoid?
Pemphigus vulgaris shows intercellular fishnet-pattern immunoglobulin G and C3 throughout the epithelium; mucous membrane pemphigoid shows linear immunoglobulin G and C3 along the basement membrane zone.

### Why do oral blisters of pemphigus rupture so easily?
The split lies high and the blister roof is a thin suprabasal layer of fragile keratinocytes, so the slightest trauma converts the bulla into a broad shallow erosion with ragged tags.

### What is the main danger of mucous membrane pemphigoid?
Progressive scarring of mucous membranes — especially the conjunctiva (symblepharon, vision loss) — so ophthalmological surveillance is mandatory alongside topical or systemic immunosuppression.

### Which factors typically trigger erythema multiforme?
Recurrent herpes simplex infection is the classic trigger, followed by drugs such as sulphonamides, non-steroidal anti-inflammatories and anticonvulsants; episodes are self-limiting but recurrent disease is treated with herpes suppression.