Inflammatory Dermatoses

Erythematosquamous lesions: psoriasis

Psoriasis is a chronic relapsing dermatosis based on genetic predisposition and autoimmune reactions. The process is characterized by epidermal hyperproliferation combined with dermal inflammation.

Clinically, the elements evolve from small spots to scaly papules that coalesce into extensive plaques.

From a pathomorphological perspective, psoriasis is characterized by:

• Parakeratosis (pronounced) and acanthosis (epidermal ridges elongate and widen at the ends).
• Thinning of the epidermis directly over the dermal papillae.
• Complete disappearance of the granular layer.
• Munro's microabscesses are accumulations of neutrophils within the area of parakeratosis. Upon progression to the pustular form, they merge into large Kogoj's pustules.
• In the papillary dermis, capillaries are markedly tortuous and dilated, with lymphocytes and histiocytes accumulating around the vessels.

Papular dermatoses: lichen planus

Lichen planus (Lichen ruber planus) is a chronic disease of the skin and mucous membranes, more commonly affecting women. A possible mechanism involves delayed-type hypersensitivity (DTH), with tumors, chronic hepatitis, or biliary cirrhosis acting as potential triggers.

The primary element is a flat polygonal papule (ranging from pink to violet) with a central depression. Wickham's striae form on the surface of the papules.

The histological picture is fundamentally different from psoriasis:

1. In the epidermis: parakeratosis is absent, but marked hyperkeratosis and hypergranulosis are present (it is the thickened granular layer that produces the striae pattern). Basal cells undergo vacuolar degeneration.
2. In the dermis: a diffuse band-like lymphocytic infiltrate forms, closely adjoining the basement membrane. The dermo-epidermal junction becomes blurred, and lymphocytic exocytosis is observed.

Allergic diseases: urticaria and atopic dermatitis

Both diseases are of allergic origin, but have different pathogenetic mechanisms and histology.

Urticaria manifests as wheals. Allergens trigger histamine release, vessels dilate, and acute dermal edema occurs. The acute form proceeds as an immediate-type hypersensitivity (ITH) reaction. In the chronic course, the inflammatory infiltrate becomes denser, containing eosinophils, neutrophils, and mast cells. Occasionally, the process progresses to leukocytoclastic vasculitis.

Atopic dermatitis is a genetically determined disease with congenital sensitization and elevated IgE levels, usually beginning in the first year of life.

• In the infantile phase (or during exacerbation), spongiosis predominates with microvesicle formation in the epidermis.
• In adults, the skin thickens (lichenification), and histology reveals acanthosis, hyperkeratosis, and focal parakeratosis. Perivascular infiltrates rich in mast cells are highly characteristic of the dermis.

Vesiculobullous diseases: pemphigus vulgaris

Pemphigus vulgaris is a severe autoimmune dermatosis. The peak incidence occurs at ages 40–60.

Antibodies against keratinocyte glycoproteins are produced in the body, leading to the destruction of desmosomes in the suprabasal layers of the epidermis. Cells lose connection with each other (acantholysis), resulting in microclefts and subsequently flaccid blisters. Notably, basal layer cells remain firmly attached to the basement membrane.

In 60% of patients, the disease begins in the oral mucosa, mimicking prolonged stomatitis with painful erosions. Cutaneous blisters arise even from minor friction—this is the specific Nikolsky's sign. Smears from the eroded surface reveal characteristic acantholytic cells.

Class and exam questions

What else to study on this topic

• Clinical forms of psoriasis (pustular, arthropathic, erythroderma)
• Variants of lichen planus (hypertrophic, bullous, atrophic)
• Morphology of leukocytoclastic vasculitis in chronic urticaria
• Differences between pemphigus vulgaris and foliaceus and vegetans forms
• Pathogenesis of Munro's microabscesses and Kogoj's pustules

Other topics in "Chapter 23. Skin Diseases"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.