In ocular cicatricial pemphigoid (OCP), forniceal scarring leads to symblepharon formation. The pathological mechanism differs from Stevens-Johnson syndrome because in OCP:
- A The primary target is type VII collagen at the dermoepidermal junction, causing subepithelial blistering
- B Linear IgG, IgA, and complement deposition occurs at the epithelial basement membrane zone (BMZ), with autoantibodies against BMZ antigens (β4 integrin, BP180, laminin-332) driving progressive subepithelial fibrosis ✓
- C T-cell mediated cytotoxicity targets conjunctival goblet cells specifically, causing mucin deficiency without subepithelial scarring
- D Circulating pemphigus vulgaris IgG antibodies against desmoglein-3 cause conjunctival acantholysis
Explanation
OCP is a type II autoimmune hypersensitivity disorder where autoantibodies (IgG and IgA, rarely IgM) target components of the conjunctival epithelial basement membrane zone — identified targets include β4 integrin (BPAG2/BP180), laminin-332 (epiligrin), and BP230. Direct immunofluorescence shows linear IgG and complement deposition at the BMZ. This triggers complement-mediated and eosinophil-mediated damage to subepithelial structures, causing progressive fibrosis and cicatrization. SJS/TEN is a T-cell-mediated cytotoxic reaction (type IVc hypersensitivity) to drugs, causing acute keratinocyte apoptosis — rapid but potentially self-limiting. OCP is progressive, chronic, and requires systemic immunosuppression (dapsone, cyclophosphamide, rituximab for refractory cases).
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.