Background/Purpose: Ultraviolet A1 (UVA1) phototherapy implications for systemic sclerosis still remain the area of research. The aim of the study was to evaluate narrow band 365 nm ± 5 nm light effectiveness and safety for the treatment of dermal fibrosis in bleomycin-induced mouse model of scleroderma using light emitting diodes device.

Methods: DBA/2 strain mice were randomly divided to 6 groups: I – healthy animals; II – control group with bleomycin-induced scleroderma, III and IV – mice with established scleroderma, treated with high- and medium-dose of UVA1 light; V and VI – healthy mice treated with high- and medium-dose of UVA1 light. Light source emitting a narrow band UVA1 light of 365±5 nm and 21 mW/cm² power density was used in the study. Phototherapy was performed 3 times weekly for 5 weeks. The average cumulative doses were 600 J/cm² for medium- and 1200 J/cm² for high-dose treatment. Histological analysis with hematoxylin – eosin staining for dermal thickness measurement was performed. The immunohistochemical staining for p53 and Ki-67 proteins was performed using specific antibodies. Statistical significance was expressed by a P-value < 0.05.

Results: Phototherapy course was well tolerated by the animals. The dermal thickness of mice treated with high- and medium dose of UVA1 was significantly reduced to 272.9 ± 113.2 and 394 ± 125.9 µm, respectively, in comparison to control group II (599 ± 55.7 µm) (p<0.05). Parallel data were analyzed of UVA1- treated healthy mice skin: there was no dermal thickness change in both medium- and high-dose groups. The progression of dermal thickness is summarized in Figure 1. In the healthy mice group (I) the percentage of Ki-67-positive cells was 50.4 ± 2.6% and the number of these positive cells were reduced to 36.1 ± 3% in control group (II) after bleomycin injections (p < 0.05). The percentage of Ki-67 positive cells after medium- and high-dose UVA1 treatment of scleroderma skin (group IV and III) was 37.2 ± 2.8% and 35.4 ± 3.2%, respectively, and did not differ from the control group (II). The expression of p53 was significantly higher in the skin of control group (II) compared to healthy mice skin (I). After UVA1 treatment of mice with scleroderma, the expression of p53 did not differ in comparison to the control group without phototherapy (II). There was no statistically significant change of both p53 and Ki-67 expression between healthy (I) and UVA1-treated healthy mice skin (groups V and VI).

Conclusion: Medium- and high-dose 365 nm UVA1 effect on reducing dermal thickness is dose-dependent. This irradiation does not affect dermal thickness in healthy skin. Cell apoptosis (p53) and proliferation (Ki-67) changes in the dermal and subcutaneous layers suggest a favorable narrow light effect in the experimental sclerosis and healthy mice groups. Narrow band UVA1 phototherapy using light emitting diodes device might be the new era of dermal fibrosis phototherapy.