Radiation dermatitis

Acute radiation dermatitis is an inflammatory skin reaction caused by exposure to ionizing radiation, most commonly occurring as an acute adverse effect of radiotherapy in cancer patients.

The pathophysiology of radiation dermatitis involves radiation-induced cellular injury, impaired epidermal regeneration, and inflammatory signaling. Early skin reactions result from cell cycle arrest in basal keratinocytes, which limits the replacement of cells shed from the stratum corneum. This adaptive response reduces stem cell vulnerability to radiation but contributes to epidermal thinning and desquamation. Inflammatory cytokines cause tenderness, swelling, and erythema, though erythema may be less apparent or appear differently in darker skin tones. With increasing dose or prolonged exposure, complete loss of the stratum corneum can lead to moist desquamation. Regeneration begins from follicular stem cells in the bulge region, forming islands of new epidermis that expand and merge. Chronic radiation dermatitis may occur when pro-inflammatory and profibrotic cytokine activity remains unbalanced, resulting in fibrosis, pigmentary changes, and vascular damage.

Radiation dermatitis is one of the most common side effects of radiotherapy, affecting up to 95% of patients receiving treatment involving the skin surface. It is especially prevalent in individuals undergoing radiotherapy for breast, head and neck, anal, or vulvar cancers, where treatment fields are superficial or involve skin folds.

Multiple intrinsic and extrinsic factors influence the risk and severity of radiation dermatitis. Intrinsic factors include individual susceptibility, such as pre-existing autoimmune skin conditions (such as lupus erythematosus and psoriasis), and rare genetic disorders such as ataxia-telangiectasia, which involve mutations in the ATM gene and impair DNA repair. Extrinsic and treatment-related risk factors include high total or boost radiation dose, large treatment volume, prolonged fractionation schedules, use of bolus, and anatomical sites where the skin lies close to the target volume (such as breast, head and neck, anal, or vulvar regions). Additional contributors include obesity (due to skin folds increasing local dose), concurrent chemotherapy or targeted therapy, and radiation techniques that increase surface dose exposure.

Radiation dermatitis typically begins within the first few weeks of radiotherapy and progresses through well-defined clinical stages. Grade 1 presents with faint or mild generalized erythema, dry desquamation, pruritus, epilation, scaling, and dyspigmentation due to damage to sebaceous glands and hair follicles. Grade 2 is marked by persistent erythema, tenderness, and patchy moist desquamation, particularly in skin folds, developing after approximately 4-5 weeks of treatment or with cumulative doses ≥40 Gy. Moist desquamation involves epidermal necrosis, fibrinous exudate, pain, and increased susceptibility to infection; histologically, fibrin thrombi and edema are observed. Grade 3 involves confluent moist desquamation in areas beyond skin folds and may be accompanied by bleeding with minor trauma. Grade 4 is characterized by full-thickness dermal ulceration, necrosis, spontaneous bleeding, and potentially systemic inflammatory response syndrome. Healing typically begins 1-2 weeks after the last radiation session, with complete epidermal regeneration occurring within 1-3 months, provided no superinfection or chronic complications develop. Chronic radiation dermatitis is a delayed complication of radiotherapy characterized by persistent skin changes such as fibrosis, atrophy, telangiectasia, and, in severe cases, ulceration or necrosis.