A 52-year-old woman presents with a 6-month history of pruritic, violaceous papules on her wrists and forearms. Intraoral examination reveals a bilateral white lacy reticular pattern on the buccal mucosa. The structure marked **A** in the diagram shows fine white striae overlying the mucosal lesions. Which of the following best explains the pathogenesis of the lesions marked **A**?
A. CD8+ cytotoxic T-cell-mediated apoptosis of basal keratinocytes triggered by altered antigen recognition
B. Mast cell degranulation with release of histamine and tryptase
C. IgG immune complex deposition along the basement membrane zone
D. Neutrophilic infiltration with formation of microabscesses at the dermoepidermal junction
Explanation
Why CD8+ cytotoxic T-cell-mediated apoptosis is right
Wickham's striae (marked A) are a pathognomonic finding in lichen planus resulting from focal hypergranulosis. The underlying pathogenesis of lichen planus is a chronic T-cell mediated inflammatory disease in which CD8+ cytotoxic T cells recognize altered basal keratinocyte antigens (possibly viral or drug-induced) and trigger apoptosis via Fas/FasL and perforin/granzyme pathways. This CD8+ T-cell response is the fundamental mechanism driving the disease, and the fine white lacy striae represent the microscopic manifestation of this cytotoxic injury and subsequent hyperkeratosis (Bolognia Dermatology 5e, Ch 11; Fitzpatrick 9e).
Why each distractor is wrong
Neutrophilic infiltration with microabscesses: While neutrophils may be present in erosive oral lichen planus, the primary infiltrate in lichen planus is lymphocytic (band-like at the dermoepidermal junction), not neutrophilic. Microabscesses are characteristic of pustular dermatoses, not lichen planus.
IgG immune complex deposition: Immune complex disease (Type III hypersensitivity) is seen in conditions like lupus erythematosus and serum sickness, not lichen planus. Direct immunofluorescence in LP shows fibrinogen at the basement membrane zone, not IgG complexes.
Mast cell degranulation: Mast cell-driven histamine release is the mechanism in urticaria and pruritus, not the chronic T-cell mediated inflammation of lichen planus. Mast cells are not the primary pathogenic cell type in LP.
High-YieldNEET PG
Wickham's striae = focal hypergranulosis from CD8+ T-cell cytotoxic injury; screen all LP patients for hepatitis C virus (strong association, especially in Mediterranean/Asian populations).
Bolognia Dermatology 5e Ch 11; Fitzpatrick 9e
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