Erythematosquamous Lesions: Psoriasis
Psoriasis is a chronic, relapsing dermatosis driven by genetic predisposition and autoimmune reactions. The process is characterized by epidermal hyperproliferation combined with dermal inflammation.
Clinically, lesions evolve from small macules to scaly papules that coalesce into extensive plaques.
From a pathologic anatomy perspective, psoriasis is characterized by:
- Parakeratosis (pronounced) and acanthosis (epidermal rete ridges elongate and widen at their tips).
- Thinning of the epidermis directly over the dermal papillae.
- Complete absence of the stratum granulosum.
- Munro microabscesses — neutrophil collections within the parakeratotic zones. In pustular variants, these coalesce into larger Kogoj pustules.
- In the papillary dermis, capillaries are markedly tortuous and dilated, surrounded by infiltrates of lymphocytes and histiocytes.
Papular Dermatoses: Lichen Planus
Lichen planus (Lichen ruber planus) is a chronic inflammatory disease of the skin and mucous membranes most commonly affecting women. The proposed mechanism involves a delayed-type hypersensitivity (DTH) reaction, with tumors, chronic hepatitis, or primary biliary cholangitis serving as potential triggers.
The primary lesion is a flat-topped, polygonal papule (pink to violaceous) with a central depression. A fine lattice network called Wickham striae appears on the surface of the papules.
The histologic picture differs fundamentally from psoriasis:
- In the epidermis: parakeratosis is absent, but prominent hyperkeratosis and hypergranulosis are present (the thickened granular layer forms the striae pattern). Basal cells undergo vacuolar degeneration.
- In the dermis: a band-like (lichenoid) lymphocytic infiltrate forms immediately adjacent to the basement membrane. The dermoepidermal junction becomes obscured, and lymphocytic exocytosis is observed.
Allergic Conditions: Urticaria and Atopic Dermatitis
Both conditions share an allergic etiology but have distinct developmental mechanisms and histology.
Urticaria presents as wheals. Allergens trigger histamine release, leading to vasodilation and marked dermal edema. Acute forms follow a type I immediate hypersensitivity reaction. In chronic cases, the inflammatory infiltrate becomes denser, featuring eosinophils, neutrophils, and mast cells. The process may occasionally progress to leukocytoclastic vasculitis.
Atopic dermatitis is a genetically determined disorder characterized by congenital sensitization and elevated IgE levels, typically presenting within the first year of life.
- In the infantile phase (or during flares), spongiosis predominates with microvesicle formation in the epidermis.
- In adults, the skin becomes thickened (lichenification), with histologic findings of acanthosis, hyperkeratosis, and focal parakeratosis. Perivascular infiltrates in the dermis are notable for a high abundance of mast cells.
Vesiculobullous Diseases: Pemphigus Vulgaris
Pemphigus vulgaris is a severe autoimmune dermatosis with a peak incidence between 40 and 60 years of age.
Autoantibodies form against keratinocyte glycoproteins, leading to the destruction of desmosomes in the suprabasal layers of the epidermis. Cells lose attachment to one another (acantholysis), resulting in microclefts followed by flaccid bullae. Notably, the basal cell layer remains firmly anchored to the basement membrane.
In 60% of patients, the disease begins in the oral mucosa, mimicking refractory stomatitis with painful erosions. Cutaneous blisters develop even with minimal mechanical friction—a specific sign known as Nikolsky's sign. Cytology smears from the erosion base reveal characteristic acantholytic cells.