Pathomorphology of Scabies
We begin with the conclusion of parasitic dermatoses. Scabies is caused by a mite that completes its entire life cycle on the host's skin. After fertilization, mature female mites actively burrow into new areas of the skin. Clinically, this presents as nocturnal pruritus, which directly correlates with the peak activity of the parasite during nighttime hours. Characteristic 'burrows' (cuniculi), small papular eruptions, and multiple scratch marks (excoriations) can be found on the patient's skin.
Under the microscope (using standard hematoxylin and eosin staining), the histological picture is quite specific:
- Epidermis: Marked thickening of the stratum spinosum (acanthosis) combined with moderate hyperkeratosis.
- Stratum corneum: Multiple burrows are visualized here, containing the mites themselves or their fragments.
- Stratum spinosum: Intracellular edema and spongiosis of varying severity.
- Dermis: A moderate inflammatory infiltrate consisting predominantly of lymphocytes forms in the upper dermis.
Epidermal Tumors: General Overview and Classification
Epidermal neoplasms feature tremendous diversity in both histological structure and clinical presentation. Their primary source (histogenesis) is keratinocytes located directly within the epidermis or skin appendages. Ultraviolet (UV) radiation is recognized as the main trigger and etiological factor in the development of these tumors.
Based on their clinical course, neoplasms are divided into two main groups:
- Benign (acanthomas). Most often, they represent merely a cosmetic defect. After proper surgical removal, patients require no specific follow-up treatment.
- Malignant. Characterized by aggressive behavior. Some forms (especially squamous cell carcinoma, which metastasizes in 8% of cases) tend to spread early throughout the body. At the same time, the overall prognosis for epidermal tumors is generally favorable, with total mortality not exceeding 0.1%.
Actinic Keratosis: A Precursor to Carcinoma
Actinic (solar or senile) keratosis is classified as a precancerous epidermal lesion. According to WHO classifications, this condition is rooted in epidermal dysplasia, although the term 'epidermal dysplasia' is rarely used in routine pathology practice.
The disease arises from prolonged UV exposure. High-risk groups include fair-skinned men over 60 years of age and patients who have undergone PUVA therapy. The lesions localize to sun-exposed areas: the face, neck, auricles, lower third of the forearms, and dorsal hands.
Clinically, lesions present as dry, sharply demarcated erythematous macules or plaques (less than 1 cm in diameter) covered with yellowish-brown scales. Removing a scale reveals pinpoint bleeding. The surrounding skin is often thinned (atrophic), pigmented, and peppered with telangiectasias. The disease has a chronic course, but with rigorous sun protection, lesions may spontaneously resolve.
Histological Features: The epidermis shows parakeratosis, hypogranulosis, and keratinocyte cellular atypia (dyskeratosis, hyperchromasia, nuclear enlargement, loss of polarity, and an increased mitotic rate). The underlying dermis demonstrates solar elastosis, vascular dilation, and an infiltrate of lymphocytes and plasma cells. When keratosis develops in the setting of immunodeficiency, verrucous changes and multinucleated keratinocytes may appear. The risk of malignant transformation (predominantly to squamous cell carcinoma, less frequently to basal cell carcinoma or melanoma) ranges from 8 to 20%.
Keratoacanthoma: A Dynamic Benign Tumor
Keratoacanthoma is a rapidly growing benign neoplasm. Human papillomaviruses (HPV) and chemical carcinogens are implicated in its pathogenesis. It most frequently affects the faces of elderly men (over 60 years).
Macroscopically, the tumor resembles a cup-shaped crater 2–3 cm or more in diameter. The center of the crater is tightly plugged with keratin masses, surrounded by a raised border (red, violaceous, or skin-colored).
The life cycle of a keratoacanthoma consists of 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 1: Formation of an epidermal depression filled with keratin masses. A double-layered epithelial 'collar' forms at the edges. The basement membrane remains intact. The basal layer shows numerous mitoses, but atypical forms are absent.
- Stage 2: Marked epidermal hyperplasia, with cords extending into the dermis. Foci of dyskeratosis, mild cellular atypia, and hyperchromasia appear. A dense inflammatory infiltrate accumulates in the dermis.
- Stage 3: Cellular polymorphism increases, the basement membrane breaks down, and cell nests detach from the main node, invading deep into the dermis.
It is important to remember that regression is possible only during stages 1 and 2. In this case, inflammation subsides, giving way to fibroblasts and foreign-body giant cells. If regression fails to occur, keratoacanthoma may undergo malignant transformation into squamous cell carcinoma.
Basal Cell Carcinoma (Basalioma)
Basal cell carcinoma is a malignant epidermal tumor composed of nests of so-called basaloid cells. The tumor grows extremely slowly and exhibits a multicentric growth pattern, meaning lesions can be multiple.
Clinical Presentation: Typically, it presents as a solitary hemispherical nodule, grayish-red or pink in color, with a characteristic pearly sheen. The surface is smooth with telangiectasias (spider veins). The center often exhibits a depression covered by a crust (upon removal, an erosion is exposed). If the tumor ulcerates, its borders become crateriform, consisting of whitish 'pearly' nodules. It develops on sun-exposed skin, arising either on normal skin or against the background of discoid lupus erythematosus, psoriasis, or actinic keratosis.
Histology (H&E Stain): The tumor forms solid cords, tubular, and alveolar structures. These consist of epithelial cells with scant cytoplasm and dark oval nuclei (basaloid cells). A fibromucinous stroma surrounds the tumor nests. At the periphery of the nests, cells align in a palisading pattern. A characteristic histological artifact is the presence of artificial clefts between the tumor nests and the stroma, which arise during tissue processing due to fragile hemidesmosomes leading to tissue tearing.