Radiation dermatitis

Radiation dermatitis develops as a result of exposure to ionizing radiation. The nature of skin changes depends on the intensity of radiation exposure. They can be acute, developing after a short latent period, and chronic, occurring several months or even years after irradiation. Acute radiation skin lesions can be in the form of erythematous, bullous or necrotic reactions, after the disappearance of which atrophic, cicatricial changes, telangiectasias, and long-term non-healing ulcers may remain. Chronic radiation injuries usually occur with exposure to small doses of ionizing radiation. They are characterized by mild inflammation, poikiloderma, a tendency to hyperplastic processes in the epidermis, especially with ulcerative lesions. Against the background of such changes, skin cancer often occurs.

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Pathomorphology of radiation dermatitis

The typical microscopic picture in acute radiation dermatitis is characterized by severe edema of the upper dermis, as a result of which the epidermis flattens, epidermal outgrowths are absent. In the dermis - homogenization of collagen and swelling of the endothelium of capillaries, accompanied by narrowing and closure of their lumens; occasionally, infiltration of neutrophilic granulocytes and lymphocytes around the sweat glands is observed. The sebaceous glands are not changed. Sometimes vacuolization of the cells of the basal layer of the epidermis is observed, the appearance of large atypical multinucleated cells in it, reminiscent of those in Korn's disease.

Around the lesion, thinning of the epidermis, an increase in the amount of pigment in the basal cells and melanocytes, as well as in the melanophages of the dermis are noted. The number of fibroblastic elements increases around the dilated vessels. Hyperkeratosis, atrophy of the epidermis and hair follicles, and vacuolization of the cells of the basal layer subsequently develop.

In chronic radiation dermatitis, the histological picture depends on the degree of damage. Almost always, fibrous changes in the walls of blood vessels are found, especially in the deep parts of the dermis, with a greater or lesser narrowing of their lumen, fibrosis and homogenization, and sometimes hyalinization of the connective tissue. In cases clinically accompanied by telangiectasias, significant changes in the vessels in the upper parts of the dermis are observed. Changes in the epidermis vary, from atrophy to acanthosis and hyperkeratosis. In the germ layer of the epidermis, cell lesions are visible, reminiscent of those in Bowen's disease: dyskeratosis and atypia, uneven outgrowths of the epidermis into the dermis. As a result of vascular obliteration, ulcers can form, along the edges of which pseudo-epitheliomatous hyperplasia of the epidermis is often found. In the dermis, there is an overgrowth of connective tissue with a large number of cellular elements and melanin both inside and outside the melanophages. Many collagen fibers are fragmented, located unoriented, and elastic fibers also show fragmentation phenomena, but to a lesser extent. Skin appendages atrophy until they disappear completely. These changes can lead to the development of squamous cell skin cancer.