Narrow‐band ultraviolet‐B stimulates proliferation and migration of cultured melanocytes

Wu, Ching‐Shuang; Yu, Chia‐Li; Wu, Chieh-Shan; Lan, Cheng‐Che E.; Yu, Hsin‐Su

doi:10.1111/j.0906-6705.2004.00221.x

Cited by 107 publications

(92 citation statements)

References 44 publications

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“…(3) Matrix metalloproteinase-2 (MMP-2) is known to enhance migration of melanocytes from adjacent normal skin. Previous study showed that NB-UVB irradiation could significantly increase the activity of MMP-2 in melanocytes [16]. Dermabrasion using fractional Er:YAG laser followed by NB-UVB irradiation would enhance the stimulation of MMP-2 activity in vitiligo lesion.…”

Section: Discussionmentioning

confidence: 89%

Fractional Er:YAG laser assisting topical betamethasone solution in combination with NB-UVB for resistant non-segmental vitiligo

et al. 2017

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Resistant non-segmental vitiligo is difficult to be treated. Ablative erbium-YAG (Er:YAG) laser has been used in the treatment of vitiligo, but the ablation of entire epidermis frustrated the compliance of patients. The purpose of this study is to investigate the effects of fractional Er:YAG laser followed by topical betamethasone and narrow band ultraviolet B (NB-UVB) therapy in the treatment of resistant nonsegmental vitiligo. The vitiligo lesions of each enrolled patient were divided into four treatment parts, which were all irradiated with NB-UVB. Three parts were, respectively, treated with low, medium, or high energy of Er:YAG laser, followed by topical betamethasone solution application. A control part was spared with laser treatment and topical betamethasone. The treatment period lasted 6 months. The efficacy was assessed by two blinded dermatologists. Treatment protocol with high energy of 1800 mJ/P of fractional Er:YAG laser followed by topical betamethasone solution and in combination with NB-UVB made 60% patients achieve marked to excellent improvement in white patches. The protocol with medium energy of 1200 mJ/P of laser assisted approximate 36% patients achieve such improvement. The two protocols, respectively, showed better efficacies than NB-UVB only protocol. However, fractional Er:YAG laser at low energy of 600 mJ/P did not provide such contributions to the treatment of vitiligo. The fractional Er:YAG laser in combination with topical betamethasone solution and NB-UVB was suitable for resistant non-segmental vitiligo. The energy of laser was preferred to be set at relatively high level.

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Section: Discussionmentioning

confidence: 89%

Fractional Er:YAG laser assisting topical betamethasone solution in combination with NB-UVB for resistant non-segmental vitiligo

et al. 2017

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“…Ultraviolet B rays cause DNA damage and formation of pyrimidine dimmers [15]. In addition to T cell apoptosis, UVB radiation triggers changes in cytokine production, local immunosuppression and stimulation of melanocyte-stimulating hormone (MSH), and increases migration, proliferation of melanocytes and melanogenesis [16,17]. A twostep effect of NB-UVB has been proposed -both of them may occur simultaneously though.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Targeted phototherapy

Sanga¹

2015

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“…In another study Wu et al investigated affects of NBUVB on melanocytes proliferation in vitro and they observed a significant increase in bFGF and in endothelin-1 (ET-1) release as bFGF is a natural mitogen for melanocytes and ET-1 can stimulate DNA synthesis in melanocytes. They also suggested that matrix metalloproteinase-2 (MMP-2) activity play important roles in narrow-band UVB-induced migration of melanocytes [36]. In a recent study, Starner et al showed that UVR radiation stimulates prostoglandin E2 (PGE2) secretion in melanocytes that leads cAMP production, tyrosinase activity and proliferation in melanocytes [37].…”

Section: Ultraviolet Radiationmentioning

confidence: 99%

Photo (Chemo) Therapy and Vitiligo

2015

J Turk Acad Dermatol

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Background: Vitiligo is an acquired idiopathic pigmentary skin disorder characterized by sharply demarcated milky white macules with variable size and shape. It has an estimated worldwide incidence of 0.5-4% and occurs in half of the patients before the age of 20 years. Since exact pathogenic mechanism is unknown, several proposed hypotheses are alternation of cellular and humoral immunity, melanocyte damage stimulated by chemicals released from nerve endings, structural aberration of melanocytes, melanocytorrhagia, epidermal cytokines, metabolic dysregulations and convergence theory depended on combination of these etiologic factors. Treatment of vitiligo depends on viable melanocyte reservoirs which induce repigmentation during various therapies. Although melanocyte reservoir mainly shown as hair follicle unit, repigmentation arise from three main sources. These are hair follicle unit, melanocytes located at the edge of vitiligo lesion and unaffected melanocytes within areas of depigmented epidermis. Treatment modalities for vitiligo therapy divided in three main groups as medical therapy, phototherapy and surgical therapy. Vitiligo lesions should be initially treated with topical medical therapy or localized phototherapy. If depigmentation is larger than 10-20% of body surface area, systemic medical therapy or phototherapy should be sought. When depigmentations do not regress in spite of appropriate interventions, surgical therapies should be considered as the lesions become refrectory and stable. In this review, we discuss the literature and evidence base for phototherapy in vitiligo and summarized previous studies.

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Narrow‐band ultraviolet‐B stimulates proliferation and migration of cultured melanocytes

Cited by 107 publications

References 44 publications

Fractional Er:YAG laser assisting topical betamethasone solution in combination with NB-UVB for resistant non-segmental vitiligo

Fractional Er:YAG laser assisting topical betamethasone solution in combination with NB-UVB for resistant non-segmental vitiligo

Targeted phototherapy

Photo (Chemo) Therapy and Vitiligo

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