Pathomorphology of scabies
Let's begin by completing the section on parasitic dermatoses. Scabies is caused by a mite that completes its full life cycle on the host's skin. After fertilization, mature females actively burrow into new areas of the skin. Clinically, this manifests as nocturnal pruritus, which is directly related to the peak activity of the parasite during nighttime hours. Specific scabies burrows, small papular rashes, and multiple scratch marks (excoriations) can be found on the patient's skin.
Under the microscope (with standard hematoxylin and eosin staining), the picture is quite specific:
- Epidermis: pronounced thickening of the spinous layer (acanthosis) combined with moderate hyperkeratosis.
- Stratum corneum: it is precisely here that those multiple burrows are visualized, inside of which the mites themselves or their fragments are localized.
- Spinous layer: intracellular edema and spongiosis of varying severity are noted.
- Dermis: in its upper parts, a moderate inflammatory infiltrate forms, consisting predominantly of lymphocytes.
Epidermal tumors: general information and classification
Epidermal neoplasms exhibit tremendous diversity in both histological structure and clinical presentation. Their primary source (histogenesis) is keratinocytes located directly within the epidermis or in skin appendages. The main trigger and etiological factor in the development of these tumors is recognized as ultraviolet (UV) radiation.
Based on their clinical course, neoplasms are divided into two main groups:
- Benign (acanthomas). Most often, they represent merely a cosmetic defect. Following proper surgical removal, the patient requires no specific follow-up treatment.
- Malignant. Characterized by aggressive behavior. Some forms (especially squamous cell carcinoma, which metastasizes in 8% of cases) are prone to early dissemination throughout the body. At the same time, the prognosis for epidermal tumors is generally favorable—overall mortality does not exceed 0.1%.
Actinic keratosis: a precursor to cancer
Actinic (also known as solar or senile) keratosis is classified as a precancerous skin lesion. According to the 2006 WHO classification, this condition is based on epidermal dysplasia, although the term "epidermal dysplasia" is rarely used in routine practice.
The disease arises from prolonged exposure to UV rays. Men over 60 with fair skin, as well as patients who have undergone PUVA therapy, are at increased risk. The pathology localizes on sun-exposed areas: the face, neck, auricles, lower third of the forearms, and dorsal hands.
Clinically, these are dry, sharply demarcated erythematous spots or plaques (less than 1 cm in diameter) covered with yellowish-brown scales. If a scale is scraped off, punctate bleeding occurs. The background skin is often thinned (atrophied), pigmented, and dotted with telangiectasias. The disease has a protracted course, but with good sun protection, the lesions can spontaneously disappear.
Histological picture: The epidermis shows parakeratosis, hypogranulosis, and cellular atypia of keratinocytes (dyskeratosis, hyperchromasia and nuclear enlargement, polarity disruption, increased mitosis count). The underlying dermis shows solar elastosis, vascular dilation, and infiltration by lymphocytes and plasma cells. If keratosis develops against a background of immunodeficiency, verrucous changes and multinucleated keratinocytes may appear. The risk of malignant transformation (predominantly into squamous cell carcinoma, less frequently into basal cell carcinoma or melanoma) varies from 8 to 20%.
Keratoacanthoma: a dynamic benign tumor
Keratoacanthoma is a rapidly growing benign neoplasm. It is believed that human papillomaviruses (HPV) and chemical carcinogens are implicated in its development. It most commonly affects the faces of elderly men (over 60 years of age).
Macroscopically, the tumor resembles a crater 2–3 cm or more in diameter. The center of the crater is tightly packed with keratin masses, surrounded by a raised border (red, cyanotic, or skin-colored).
The life cycle of keratoacanthoma is divided into three phases: rapid growth (1–2 months), stabilization (6–9 months), and spontaneous regression (resolution with the formation of an atrophic scar).
Microscopic stages:
- Stage one: appearance of an epidermal depression filled with keratin masses. A two-layered epidermal "collar" forms at the edges. The basement membrane is intact. There are many mitoses in the basal layer, but atypical forms are absent.
- Stage two: sharp epidermal hyperplasia, with strands extending into the dermis. Foci of dyskeratosis, mild cellular atypia, and hyperchromasia appear. A robust inflammatory infiltrate accumulates in the dermis.
- Stage three: cellular polymorphism increases, the basement membrane breaks down, and cell clusters detach from the nodule, extending deep into the dermis.
It is important to remember that regression is possible only in the first and second stages. In this case, the inflammation subsides, giving way to fibroblasts and foreign body giant cells. If regression does not occur, keratoacanthoma may undergo malignant transformation into squamous cell carcinoma.
Basal cell carcinoma (Basalioma)
Basalioma is a malignant epidermal tumor consisting of clusters of so-called basaloid cells. The tumor grows extremely slowly and exhibits a multicentric growth pattern, which can result in multiple lesions.
Clinical presentation: Usually a solitary hemispherical nodule of grayish-red or pink color with a characteristic pearly luster. The surface is smooth, with spider veins (telangiectasias). The center often features a depression covered by a crust (its removal exposes an erosion). If the tumor ulcerates, its edges become crateriform, consisting of whitish "pearly" nodules. It grows on sun-exposed skin areas, both on healthy skin and on a background of lupus erythematosus, psoriasis, or actinic keratosis.
Histology (hematoxylin and eosin staining): The tumor forms solid strands, tubular, and alveolar structures. They consist of epithelial cells with sparse cytoplasm and dark oval nuclei (basaloid cells). A fibromucinous stroma surrounds the tumor cell clusters. At the periphery of the clusters, cells arrange themselves in a palisading pattern (like a fence). A characteristic histological artifact is the presence of artificial clefts between the tumor and the stroma. These occur during specimen preparation due to weak hemidesmosomes, leading to tissue tearing.
Briefly: answers to topical questions
What histological features are characteristic of pemphigus vulgaris?
Pemphigus vulgaris (Pemphigus vulgaris) is characterized by the formation of an intraepidermal blister and suprabasal clefts.
Main histological features:
- Intraepidermal blister — contains lymphocytes and acantholytic cells (round in shape with large vesicular nuclei and pale cytoplasm).
- Suprabasal clefts — form in the epidermis and the epithelium of hair follicles.
- Blister base — becomes multilayered as epithelialization progresses.
- Changes in the dermis — inflammatory infiltrates of eosinophils and lymphocytes are present.
Direct immunofluorescence microscopy reveals deposition of IgG and the C3 complement component in the intercellular spaces.
What are the clinical and morphological forms of basal cell carcinoma?
There are numerous clinical and morphological forms and types of cutaneous basal cell carcinoma.
Main clinical types of basaliomas:
- Nodular — firm nodules merging into a tumor with a tuberous surface.
- Ulcerative (ulcus rodens) — extensive lesions with central necrosis.
- Pigmented — a gray-black spot or nodule.
- Sclerodermiform variant — a scar-like whitish patch with blurred margins.
- Pinkus fibroepithelioma — a pink nodule of firm-elastic consistency.
- Metatypical — combines features of both basal cell and squamous cell carcinoma.
The classification also mentions the destructive-perforating, eczematous, and scar-atrophic types, while histological variants include nodular, superficial, micronodular, infiltrative, and others.
What are the microscopic features of well-differentiated cutaneous squamous cell carcinoma?
The microscopic picture of well-differentiated squamous cell carcinoma is characterized by squamous differentiation with prominent extracellular keratinization.
Key histological features:
- "Cancer pearls" — concentrically laminated, intensely eosinophilic masses of extracellular keratin in the center of tumor nests.
- Stratification — tumor cells retain layering and complex architectural structure, resembling normal stratified squamous epithelium.
- Intercellular bridges — preserved desmosomal contacts between cells, visualized as fine bridges.
In this form, cells form keratohyalin granules, and mitoses are relatively rare.
Class and exam questions
Why do clefts appear in basal cell carcinoma histological slides?
These are artifactual clefts arising during histological processing. They form due to weakness and insufficiency of hemidesmosomes, leading to detachment of the tumor tissue from the surrounding stroma.
At what stage can keratoacanthoma resolve spontaneously?
Spontaneous regression with the formation of an atrophic scar is possible only in the first and second morphological stages of tumor development.
What is found inside the specific burrows in scabies?
Inside the scabies burrows located in the stratum corneum of the epidermis are the parasites (mites) themselves or their fragments.
What else to study on this topic
- Bowen's disease and intraepidermal carcinomas
- Bowenoid papulosis
- Cutaneous squamous cell carcinoma and its propensity for early metastasis
- Mechanisms of PUVA therapy effects on epidermal dysplasia
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