Abstract
Hypertrophic scars (HTSs) are common and cause functional and psychological morbidity. UVA1 (340–400 nm) phototherapy has been previously shown to be effective in the treatment of localized scleroderma, systemic sclerosis, and POEMS syndrome with minimal side effects, all of which are presented as collagen fibrils hyperplasia that is common with scarring in skin histology. In the present study, we aimed to investigate the impact of UVA1 on the protein expression of TGF-β signal pathway and myofibroblasts in a rabbit model of cutaneous scarring. Full-thickness skin wounds (2 cm × 5 cm in diameter) were made in New Zealand white rabbits to establish the hypertrophic scarring model. New Zealand white rabbits were divided into two treatment groups (n=30 wounds per group with an equal number of controls): medium-dose of UVA1 phototherapy group: 60 J/cm2; high-dose of UVA1 phototherapy group: 110 J/cm2. Left ears were used for treatment and the right ones were used for control. Treatment was administered five times weekly for 6 weeks. Treated and untreated control wounds were harvested at various time points and examined by histologic examination, immunohistochemical assessment, and ultrastructural evaluation. The results showed that UVA1 phototherapy caused a significant reduction in dermal thickness by histological features, whereas the scar index was descended significantly in both medium- and high-dose UVA1 groups compared with the control group. Examination of immunohistochemistry also revealed a marked suppression of tissue growth factor-β (TGF-β) (both medium- and high-dose), α smooth muscle actin (α-SMA) (only high-dose), and tissue inhibitor of metalloproteinase 1 (TIMP-1) (only high-dose), and apparent increase in matrix metalloproteinases (MMP-1) (both medium- and high-dose) compared with the control. The ultrastructural evaluation showed the collagen fibers’ diameter had shrunk, and that fibroblastic cytoplasm was not affluent and in a quiescent stage. These findings of the present study suggested that administration of UVA1 irradiation is effective to improve the experimental HTS model and raises a possibility of the therapeutic approach of UVA1 in the scar. Although not directly examined in the present study, MMP inhibition is hypothesized to be responsible for this effect. However, early UVA1 treatment could not prevent the formation of scar model.
Highlights
Keloids and hypertrophic scars (HTSs) are benign hyperproliferative growths of dermal collagen. [1]
We studied the success of our treatment on the animal model of HTS in this challenging clinical scenario
The HTSs were obviously induced in the rabbit ears of group U4, which received irradiation UVA1 while they were locally operated on
Summary
Keloids and hypertrophic scars (HTSs) are benign hyperproliferative growths of dermal collagen. [1]. Keloids and HTS often cause unacceptable disfigurement to the affected individuals. They may be painful or pruritic, and restrict range of motion [3,4]. Management of such conditions remains challenging due to their high rate of recurrence and lack of curative treatment [5]. Several treatments, such as intralesional injection of various agents (e.g. corticosteroids and/or 5-fluorouracil, interferon, bleomycin), surgical removal, occlusive dressing, cryotherapy, radiotherapy, laser therapy, and silicone gel sheeting had been used either alone or in various combinations, some with potential side effects and varying degrees of success [6,7]. The introduction of UV therapy has substantially changed the therapeutic possibilities of HTSs, in providing new insights into the pathogenesis of the disease
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