Patients with pemphigus foliaceus have circulating IgG against desmoglein 1 yet develop blisters only in the superficial epidermis and never involve oral mucosa, whereas pemphigus vulgaris patients with antidesmoglein 3 antibodies develop oral erosions first. What best explains this distribution?

• A Oral mucosa lacks desmosomes and relies on gap junctions for cohesion
• B Desmoglein 1 is expressed only in the granular layer of skin and is absent from mucosa, where desmoglein 3 compensates ✓
• C Antibodies against desmoglein 1 cannot cross the basement membrane into mucosa
• D Mucosal keratinocytes express a protease that degrades desmoglein 1

Explanation

The desmoglein compensation theory explains the distribution: skin expresses both desmoglein 1 and 3, while oral mucosa expresses almost exclusively desmoglein 3. Antidesmoglein 1 alone disrupts only the upper epidermal adhesion in skin, causing subcorneal blisters, and leaves mucosa intact because desmoglein 3 maintains cohesion there. Antidesmoglein 3 alone removes all cohesive function in mucosa, producing early oral erosions in pemphigus vulgaris.

Reference: Fitzpatrick's Dermatology, 9th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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