Changes in cellular composition in atopic dermatitis
The histological picture and morphology of skin cells directly depend on the phase of disease development. In the infantile phase, as well as during periods of acute exacerbation, tissue changes visually resemble eczema. The leading process is spongiosis, which leads to the formation of small vesicles. These elements are localized predominantly in the upper parts of the epidermis and in the stratum corneum.
As the patient grows older (in childhood and adulthood), the cellular architecture changes, acquiring features of neurodermatitis. During this period, moderately pronounced acanthosis and hyperkeratosis are observed. When evaluating histological preparations, it is important to perform a differential diagnosis with manifestations of hypergranulosis, dyskeratosis, and pronounced spongiosis, since the formation of foci of parakeratosis is most typical for this stage, indicating impaired cell keratinization processes.
Significant transformations also affect the dermis. Collagen fibers located at the dermal-epidermal junction undergo fibrotic changes. The dermis itself becomes edematous. In its upper part, perivascular lymphohistiocytic infiltrates are formed. Their severity varies, but most often they are mild. A crucial diagnostic sign is the admixture of mast cells in these infiltrates—their presence is considered a highly characteristic histological marker for this dermatosis.
Destruction of intercellular connections: pemphigus vulgaris
Pemphigus vulgaris is a chronic autoimmune disease belonging to the group of non-infectious vesiculobullous and vesiculopustular skin diseases. It is based on the production of autoantibodies. During laboratory diagnostics, potential targets may include type VII collagen, desmoglein 1, or class E immunoglobulins (IgE), but it has been reliably established that in this pathology, antibodies are formed specifically against keratinocyte glycoprotein.
Epidemiologically, this pathology accounts for up to one percent of all skin diseases. Although manifestation is possible at absolutely any age, a pronounced peak incidence is recorded between the ages of forty and sixty, with women being more frequently affected than men.
The pathological anatomy of the vulgaris form begins with the development of intercellular edema. The main morphological defect is the destruction of desmosomes, which ensure contacts between cells. This process is localized strictly in the suprabasal layers of the epidermis. As a result of the loss of connection between keratinocytes, microclefts form first, which then transform into microvesicles. Notably, the cells of the basal layer retain their structural integrity and do not lose their connection with the basement membrane.
Cytological picture and clinical manifestations
Changes in cell shape and state have a direct clinical reflection. In the common form of the disease, blisters appear on visually unchanged skin or the oral mucosa. They tend to increase rapidly in size, and their walls acquire a characteristic flaccid consistency. In sixty percent of patients, the pathological process starts precisely from the oral mucosa, where painful erosions form. Such a course can mimic stomatitis for a long time, making timely diagnosis difficult.
A crucial clinical marker of impaired cellular connections is Nikolsky's sign — the appearance of new blisters upon mechanical friction of outwardly healthy skin. To confirm the diagnosis, the cytological method is used: in imprint smears taken from the surface of erosions, specific acantholytic cells are detected, which have changed their normal shape due to the loss of desmosomal contacts. As an outcome of these elements, eroded areas are covered with new epithelium (re-epithelialize) fairly quickly, leaving behind only pigmented spots.
Morphological features of other forms of pemphigus
In addition to the vulgaris (common) form, the classification of pemphigus includes several other variants, each of which has its own features of cellular and tissue changes:
- Pemphigus seborrheicus: characterized by the appearance of small blisters on the face, scalp, chest, and back. The elements quickly dry up, forming yellowish crusts that cover the erosions. It is important to note that diagnostic acantholytic cells in this form are far from always detected.
- Pemphigus foliaceus: proceeds as an erythematous-squamous large-lamellar dermatosis. In this form, clinical Nikolsky's sign becomes sharply positive, indicating massive impairment of intercellular adhesion in the epidermis.
- Pemphigus vegetans: differs in that abundant vegetations form on the surface of erosions, which can sometimes bleed. Visually, this clinical picture can strongly resemble vegetative pyoderma.
To remember the localization of destruction in pemphigus: the SUPRAbasal layer loses connections (desmosomes are destroyed), while the basal layer SECURELY holds onto the membrane.
Class and exam questions
Which cells are a marker of atopic dermatitis in the dermis?
For atopic dermatitis, the presence of mast cells is extremely characteristic. They are found as part of perivascular lymphohistiocytic infiltrates in the upper part of the edematous dermis.
What happens to basal layer cells in pemphigus vulgaris?
Basal layer cells do not lose their connection with the basement membrane. Desmosome destruction and microcleft formation occur exclusively in the suprabasal layers of the epidermis.
How are acantholytic cells detected?
They are detected during cytological diagnostics in imprint smears taken directly from the eroded surface of the skin or mucous membranes.
Where does the pathological process begin in pemphigus at the cellular level?
The process starts with intercellular edema and the destruction of desmosomes between keratinocytes, leading to the formation of microclefts and subsequent microvesicle formation.
What else to study on this topic
- Mechanisms of spongiosis and microvesicle formation in the stratum corneum.
- Differential diagnosis of acanthosis, hyperkeratosis, and parakeratosis.
- The role of autoantibodies to keratinocyte glycoprotein in the pathogenesis of pemphigus.
- Clinical significance and physical basis of Nikolsky's sign.
- Cytological features of imprint smears in the seborrheic form of pemphigus.
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