Radiation induced skin damage

There is a range of effects that can occur in irradiated skin over time. In general radiation can damage cells by directly disrupting DNA or through free radical production. This damage results in disorganized fibroblast activity, micro-vascular thrombosis and inadequate tissue oxygenation. During the 3rd to 6th week of therapy, populations of basal layer stem cells become depleted in the treated area. The gross skin changes occurring with standard schedules and doses of radiotherapy to the breast are categorized as early or late effects, as determined by the time at which they present.

Early effects are defined as those that occur within 90 days of the 1st radiation therapy. The skin reactions include dryness, epilation, pigmentation changes and erythema. Dryness and epilation are results from destruction of the dermal layer. Hyperpigmentation is a result of epidermal melanocyte stimulation. Some patients may develop hypopigmentation due to complete eradication of all melanocytes. Acute erythema is caused by cytokine- mediated inflammatory reactions.

Late effects are considered the effects that present more than 90 days from the first radiotherapy. These effects are related to dermal injury. Until the moment that late effects appear the skin can appear “normal”. Late effects can appear after months or even up to 15 years later. These late effects are directly related to the dermal fibroblast response to radiotherapy and the reabsorption of collagen fibers. Telangiectasia is another effect of radiation that can manifest months or multiple years after the therapy. If necrosis appears this is associated with doses of radiation higher than those used in breast cancer treatment.

Unfortunately melasma and postinflammatory hyperpigmentation are cosmetic problems with limited options for treatment.

Many dermatological treatments are proposed in letterature, but without any optimal result for the moment (selective photothermolysis of pigmented cells by Q-switched ruby laser, MedLite C6 Q-switched Nd:YAG laser, laser resurfacing).

Promising results have been observed with the use of lipofilling. The injection of body-own fat into the subdermal layers have induced improved pigmentation, increased suppleness and better elasticity of the skin. The working mechanism is unclear for the moment but the positive influence and reparatory function of stem-cells on the damaged tissue seem to be the most logical explanation today.

Camouflage options are discussed in the session make-up and camouflage*.



Depression is associated with some patient-perceived cosmetic changes, but not with radiotherapy-induced late toxicity, in long-term breast cancer survivors.

Brunault P, Suzanne I, Trzepidur-Edom M, Garaud P, Calais G, Toledano A, Camus V.

Psychooncology. 2013 Mar;22(3):590-7. doi: 10.1002/pon.3038. Epub 2012 Feb 7.


Dose and polymorphic genes xrcc1, xrcc3, gst play a role in the risk of articledeveloping erythema in breast cancer patients following single shot partial breast irradiation after conservative surgery.

Falvo E, Strigari L, Citro G, Giordano C, Arcangeli S, Soriani A, D'Alessio D, Muti P, Blandino G, Sperduti I, Pinnarò P.

BMC Cancer. 2011 Jul 12;11:291. doi: 10.1186/1471-2407-11-291.


1550-nm nonablative laser resurfacing for facial surgical scars.

Pham AM, Greene RM, Woolery-Lloyd H, Kaufman J, Grunebaum LD.

Arch Facial Plast Surg. 2011 May-Jun;13(3):203-10. doi: 10.1001/archfacial.2011.28.


Treatment of refractory dermal melasma with the MedLite C6 Q-switched Nd:YAG laser: two case reports.

Polnikorn N.

J Cosmet Laser Ther. 2008 Sep;10(3):167-73. doi: 10.1080/14764170802179687.


Ineffective treatment of refractory melasma and postinflammatory hyperpigmentation by Q-switched ruby laser.

Taylor CR, Anderson RR.

J Dermatol Surg Oncol. 1994 Sep;20(9):592-7.