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• W2068139504 abstract "Low-energy helium–neon lasers (632.8 nm) have been employed in a variety of clinical treatments including vitiligo management. Light-mediated reaction to low-energy laser irradiation is referred to as biostimulation rather than a thermal effect. This study sought to determine the theoretical basis and clinical evidence for the effectiveness of helium–neon lasers in treating vitiligo. Cultured keratinocytes and fibroblasts were irradiated with 0.5–1.5 J per cm2 helium-neon laser radiation. The effects of the helium–neon laser on melanocyte growth and proliferation were investigated. The results of this in vitro study revealed a significant increase in basic fibroblast growth factor release from both keratinocytes and fibroblasts and a significant increase in nerve growth factor release from keratinocytes. Medium from helium–neon laser irradiated keratinocytes stimulated [3H]thymidine uptake and proliferation of cultured melanocytes. Furthermore, melanocyte migration was enhanced either directly by helium–neon laser irradiation or indirectly by the medium derived from helium–neon laser treated keratinocytes. Thirty patients with segmental-type vitiligo on the head and/or neck were enrolled in this study. Helium-neon laser light was administered locally at 3.0 J per cm2 with point stimulation once or twice weekly. The percentage of repigmented area was used for clinical evaluation of effectiveness. After an average of 16 treatment sessions, initial repigmentation was noticed. Marked repigmentation (>50%) was observed in 60% of patients with successive treatments. Basic fibroblast growth factor is a putative melanocyte growth factor, whereas nerve growth factor is a paracrine factor for melanocyte survival in the skin. Both nerve growth factor and basic fibroblast growth factor stimulate melanocyte migration. It is reasonable to propose that helium-neon laser irradiation clearly stimulates melanocyte migration and proliferation and mitogen release for melanocyte growth and may also rescue damaged melanocytes, therefore providing a microenvironment for inducing repigmentation in vitiligo. Low-energy helium–neon lasers (632.8 nm) have been employed in a variety of clinical treatments including vitiligo management. Light-mediated reaction to low-energy laser irradiation is referred to as biostimulation rather than a thermal effect. This study sought to determine the theoretical basis and clinical evidence for the effectiveness of helium–neon lasers in treating vitiligo. Cultured keratinocytes and fibroblasts were irradiated with 0.5–1.5 J per cm2 helium-neon laser radiation. The effects of the helium–neon laser on melanocyte growth and proliferation were investigated. The results of this in vitro study revealed a significant increase in basic fibroblast growth factor release from both keratinocytes and fibroblasts and a significant increase in nerve growth factor release from keratinocytes. Medium from helium–neon laser irradiated keratinocytes stimulated [3H]thymidine uptake and proliferation of cultured melanocytes. Furthermore, melanocyte migration was enhanced either directly by helium–neon laser irradiation or indirectly by the medium derived from helium–neon laser treated keratinocytes. Thirty patients with segmental-type vitiligo on the head and/or neck were enrolled in this study. Helium-neon laser light was administered locally at 3.0 J per cm2 with point stimulation once or twice weekly. The percentage of repigmented area was used for clinical evaluation of effectiveness. After an average of 16 treatment sessions, initial repigmentation was noticed. Marked repigmentation (>50%) was observed in 60% of patients with successive treatments. Basic fibroblast growth factor is a putative melanocyte growth factor, whereas nerve growth factor is a paracrine factor for melanocyte survival in the skin. Both nerve growth factor and basic fibroblast growth factor stimulate melanocyte migration. It is reasonable to propose that helium-neon laser irradiation clearly stimulates melanocyte migration and proliferation and mitogen release for melanocyte growth and may also rescue damaged melanocytes, therefore providing a microenvironment for inducing repigmentation in vitiligo. endothelin-1 hepatocyte growth factor stem cell factor Low-energy laser is capable of producing an energy density so low that any biologic alterations are the results of a direct irradiation effect, not thermal events. In this system, the temperature elevations in irradiated tissues are limited to less than 0.1°C–0.5°C (Basford, 1989Basford J.R. Low-energy laser therapy: controversies and new research findings.Laser Surg Med. 1989; 9: 1-5Crossref PubMed Scopus (189) Google Scholar;Yu et al., 1994Yu W. Naim J.O. Lanzafame R.J. The effect of laser irradiation on the release of bFGF from 3T3 fibroblast.Photochem Photobiol. 1994; 59: 167-170Crossref PubMed Scopus (190) Google Scholar;Babapour et al., 1995Babapour R. Glassberg E. Lask G.P. Low-energy systems.Clin Dermatol. 1995; 13: 87-90Abstract Full Text PDF PubMed Scopus (20) Google Scholar). Unlike traditional high-powered surgical lasers (their energy output can be up to 100 W), such as carbon dioxide, ruby, and neodymium–yttrium–aluminum–garnet (Nd-YAG) lasers, low-energy lasers are compact, low cost devices with an output power measured in milliwatts (Walsh, 1997Walsh L.J. The current status of low level laser therapy in dentistry. Part 1. Soft tissue applications.Aust Dent J. 1997; 42: 247-255Crossref PubMed Scopus (207) Google Scholar). Recent studies demonstrated that low-energy lasers are potential therapeutic instruments for rheumatoid arthritis management (Goldman et al., 1980Goldman J.A. Casay H. Bass N. et al.Laser therapy of rheumatoid arthritis.Lasers Surg Med. 1980; 1: 93-101Crossref PubMed Scopus (139) Google Scholar), modulation of wound healing (Lyon et al., 1987Lyon R.F. Abergel R.P. White R.A. Dwyer R.M. Castel J.C. Uitto J. Biostimulation of wound healing in vivo by a helium–neon laser.Ann Plast Surg. 1987; 18: 47-50Crossref PubMed Scopus (203) Google Scholar), postherpetic neuralgia (Kemmotsu et al., 1991Kemmotsu O. Sato K. Furumido H. et al.Efficacy of low reactive-level laser therapy for pain attenuation of post-herpetic neuralgia.Laser Ther. 1991; 3: 71-75Crossref Scopus (58) Google Scholar;Yaksich et al., 1993Yaksich I. Tan L.C. Previn V. Low energy laser for treatment of post-herpetic neuralgia.Ann Acad Med Singapore. 1993; 22: 441-442PubMed Google Scholar), and recovery of nerve injury (Khullar et al., 1996Khullar S.M. Bordin P. Barkvoll P. Haanaes H.R. Preliminary study of low-level laser for treatment of longstanding sensory alternation in the inferior alveolar nerve.J Oral Maxillofac Surg. 1996; 54: 2-7Abstract Full Text PDF PubMed Scopus (86) Google Scholar). The continuous wave helium–neon (He–Ne) laser (632.8 nm) has been employed most commonly for these clinical treatments (Pötinen and Pötinen, 1992aPötinen P.J. Indications for LLLT and results.in: Pötinen P.J. Low Level Laser Therapy as a Medical Treatment Modality. Art Urpo Ltd, Tampere1992: 116-141Google Scholar). Recently in vitro studies have shown that low-energy lasers induce biostimulatory effects on cultured cells. Low-energy lasers induced macrophages to release factors that stimulate fibroblast proliferation (Young et al., 1989Young S. Bolton P. Dyson M. Harvey W. Diamantopoulos C. Macrophage responsiveness to light therapy.Lasers Surg Med. 1989; 9: 497-505Crossref PubMed Scopus (261) Google Scholar). An increase in production of pro-collagen, collagen, basic fibroblast growth factors (bFGF) and proliferation of fibroblasts after exposure to low-energy laser irradiation were noticed (Abergel et al., 1987Abergel R.P. Lyon R.F. Castel J.C. Dwyer R.M. Uitto L. Biostimulation of wound healing by lasers: experimental approaches in animal models and in fibroblast cultures.Dermatol Surg Oncol. 1987; 13: 127-133Crossref PubMed Scopus (216) Google Scholar;Yu et al., 1994Yu W. Naim J.O. Lanzafame R.J. The effect of laser irradiation on the release of bFGF from 3T3 fibroblast.Photochem Photobiol. 1994; 59: 167-170Crossref PubMed Scopus (190) Google Scholar). He–Ne laser treatment stimulated interleukin-8 and interleukin-1α release from cultured keratinocytes and induced an increase in the rate of keratinocyte migration and proliferation (Haas et al., 1990Haas A.F. Isseroff R.R. Wheeland R.G. Rood P.A. Graves P.J. Low-energy helium–neon laser irradiation increases the motility of cultured human keratinocytes.J Invest Dermatol. 1990; 94: 822-826Abstract Full Text PDF PubMed Google Scholar;Yu et al., 1996Yu H.S. Chang K.L. Yu C.L. Chen J.W. Chen G.S. Low-energy helium–neon laser irradiation stimulates interleukin-1α and interkeukin-8 release from cultured human keratinocytes.J Invest Dermatol. 1996; 107: 593-596Crossref PubMed Scopus (148) Google Scholar). Functional melanocytes in patients with vitiligo vulgaris disappear from the involved skin by a mechanism(s) that has yet to be identified. Segmental-type vitiligo is associated with a dysfunction of the sympathetic nerves in the affected skin (Koga, 1977Koga M. Vitiligo: a new classification and therapy.Br J Dermatol. 1977; 97: 255-261Crossref PubMed Scopus (134) Google Scholar;Wu et al., 2000Wu C.S. Yu H.S. Chang H.R. Yu C.L. Wu B.N. Cutaneous blood flow and adrenoceptor response increase in segmental-type vitiligo lesions.J Dermatol Sci. 2000; 23: 53-62Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar). This type of vitiligo is relatively resistant to conventional therapies such as psoralens and ultraviolet-A (UVA) light (PUVA), UVB, and systemic and topical steroids (Moffy and Moffy, 1980Moffy A.M. Moffy M. Vitiligo: a symptom complex.Int J Dermatol. 1980; 19: 237-244Crossref PubMed Scopus (62) Google Scholar;Koga and Tango, 1988Koga M. Tango T. Clinical features and course of type A and type B vitiligo.Br J Dermatol. 1988; 118: 223-228Crossref PubMed Scopus (116) Google Scholar;Hann and Lee, 1996Hann S.K. Lee H.J. Segmental vitiligo: clinical findings in 208 patients.J Am Acad Dermatol. 1996; 35: 671-674Abstract Full Text PDF PubMed Scopus (180) Google Scholar). There is evidence that He–Ne laser irradiation leads to biologic effects such as an improvement in nerve injury (Rochkind et al., 1989Rochkind S. Rousso M. Nissan M. Villarreal M. Barr-Nea L. Rees D.G. Systemic effects of low-power laser irradiation on the peripheral and central nervous system, cutaneous wounds and burns.Lasers Surg Med. 1989; 9: 174-182Crossref PubMed Scopus (245) Google Scholar;Khullar et al., 1996Khullar S.M. Bordin P. Barkvoll P. Haanaes H.R. Preliminary study of low-level laser for treatment of longstanding sensory alternation in the inferior alveolar nerve.J Oral Maxillofac Surg. 1996; 54: 2-7Abstract Full Text PDF PubMed Scopus (86) Google Scholar). Furthermore, a report from Russia (Mandel, 1984Mandel A.S.H. Skin repigmentation after laser therapy (Russian).Vestn Dermatol Venerol. 1984; (September): 26-29PubMed Google Scholar) and a preliminary report from us (Yu, 2000Yu H.S. Treatment of vitiligo vulgaris with helium–neon laser.MB Derma. 2000; 35: 13-18Google Scholar) reveal that low-energy laser treatment induces repigmentation responses in patients with vitiligo. Therefore, the evidence of the He–Ne laser as a potentially useful instrument in the treatment of segmental-type vitiligo validated our project. The purposes of this study were to clarify the biologic basis of He–Ne laser effects on melanocyte growth and to confirm the effectiveness of He–Ne laser therapy on segmental-type vitiligo repigmentation. Healthy adult foreskins were the source of keratinocytes, fibroblasts, and melanocytes. Keratinocytes, fibroblasts, and melanocytes were isolated and cultured as previously described (Jones et al., 1990Jones G.E. Establishment, maintenance, and cloning of human primary cell strains.in: Pollard J.W. Walker J.M. Animal Cell Culture. Humana Press, New Jersey1990: 13-32Crossref Google Scholar;Yu et al., 1993Yu H.S. Kao C.H. Yu C.L. Coexistence and relationship of antikeratinocyte and antimelanocyte antibodies in patients with nonsegmental-type vitiligo.J Invest Dermatol. 1993; 100: 823-828Abstract Full Text PDF PubMed Google Scholar). Keratinocytes were maintained in keratinocyte-SFM complete medium, supplemented with 2 ng per ml of recombinant human epidermal growth factor and 25 μg per ml of bovine pituitary extract (Gibco BRL, Gaithersburg, MD). Fibroblasts were maintained in Dulbecco's minimal essential medium supplemented with 10% fetal bovine serum, 100 U per ml penicillin G, and 100 μg per ml streptomycin sulfate (Gibco). Melanocytes were maintained in melanocyte medium kit (Sigma, St. Louis, MO), which contains growth supplements. The second or third passage of these three cells were used in the following experiments. The method for He–Ne laser irradiation was described in our previous study (Yu et al., 1996Yu H.S. Chang K.L. Yu C.L. Chen J.W. Chen G.S. Low-energy helium–neon laser irradiation stimulates interleukin-1α and interkeukin-8 release from cultured human keratinocytes.J Invest Dermatol. 1996; 107: 593-596Crossref PubMed Scopus (148) Google Scholar). The He–Ne laser used (Lasotronic MED-1000, Lasotronic, Switzerland) had an output of 10 mW with a diverging lens that delivered 7.0 mW (as measured by a power meter, POW-105, Lasotronic) to a platform 17 cm under the lens where the dishes were placed. The cultured cells were rinsed with phosphate-buffered saline (PBS) and then irradiated in PBS to minimize the loss of laser energy through absorption by colored culture medium. All irradiation experiments were repeated in triplicate and all dishes within an experiment (including controls) were maintained in PBS at room temperature and atmosphere during the period of experimentation. Cultured keratinocytes and fibroblasts were seeded in dishes (3.5 cm in diameter) with a density of 5×105 cells and incubated overnight. The plating efficiency was higher than 90%. Then cells were irradiated with 0, 0.5, 1.0, or 1.5 J per cm2 of He–Ne laser radiation. Melanocyte mitogens and growth factors in the culture supernatant were assayed by commercially available enzyme-linked immunosorbent assay (ELISA) kits according to the manufacturer's specifications. The measurements included nerve growth factor (NGF) (Promega, Madison, WI), bFGF, stem cell factor (SCF), hepatocyte growth factor (HGF), and endothelin-1 (ET-1) (R&D Systems, Minneapolis, MN). Total RNA was extracted from keratinocytes or fibroblasts using the TRIzol method (Gibco) and processed as recommended by the manufacturer. Single-stranded cDNA was reverse transcribed from total cellular RNA using the BcaBEST RNA PCR kit (Takara Shuzo, Kyoto, Japan) (Frohman et al., 1988Frohman M.A. Dush M.K. Martin G.R. Rapid production of full length cDNAs from rare transcripts: amplification using a single gene-specific oligonucleotide primer.Proc Natl Acad Sci USA. 1988; 85: 8998-9002Crossref PubMed Scopus (4333) Google Scholar). For amplification of β-actin, NGF, and bFGF, the following primer pairs were synthesized: β-actin (sense) 5′-TCC TGT GGC ATC CAC GAA ACT-3′ and (antisense) 5′-GAA GCA TTT GCG GTG GAC GAT-3′; NGF (sense) 5′-GGT GGT GCT GCC CCC TTC AA-3′ and (antisense) 5′-CAA AGG TGT GAG TCG TGG TA-3′ (Nilsson et al., 1997Nilsson G. Gorsberg-Nilsson F. Xiang Z. Hallbook F. Nilsson K. Metcalfe D.D. Human mast cells express functional TrkA and are a source of nerve growth factor.Eur J Immunol. 1997; 27: 2295-2301Crossref PubMed Scopus (182) Google Scholar); and bFGF (sense) 5′-AGA GAG AGG AGT TGT GCT-3′ and (antisense) 5′-GGT CCT GTT TTG GAT CCA-3′ (Tripathi et al., 1996Tripathi R.C. Li J.P. Chalam K.V. Tripathi B.J. Expression of growth factor mRNAs by human tendon's capsule fibroblasts.Exp Eye Res. 1996; 63: 339-346Crossref PubMed Scopus (34) Google Scholar). The annealing temperatures for the above-mentioned primer pairs were 60°C, 55°C, and 50°C, respectively. The profile of the amplification cycle was as follows: 30 s melting at 94°C, 45 s at annealing temperature, and 60 s extending at 72°C. PCR products were titrated to establish standard curves for documenting linearity and permitting semiquantitative analysis of density. The preliminary test for conditioning PCR cycle number determined that the PCR product reached the saturation point after 33 cycles. Therefore, 30 cycles was chosen for gene amplification. The sizes of the amplified fragments were 314 bp for β-actin, 302 bp for NGF, and 222 bp for bFGF. The PCR products were electrophoresed through 1.8% agarose gels, stained with ethidium bromide, and further visualized by UV illumination. The visualized gels were recorded and analyzed on a digital imaging system (Alpha Imager 2000, Alpha Innotech, San Leandro, CA). Levels of gene expression were expressed as the integrated density value of PCR products normalized to that of the β-actin in the same sample. CELLocate (Eppendorf, Hamburg, Germany) slips were coated with 10 μg per ml collagen type I (Roche, Mannheim, Germany) and incubated at 37°C for 1 h. Melanocytes were seeded on CELLocate slips in a 24-well culture plate at a density of 1×104 cells and incubated for 2 h until attachment. The cells were irradiated with He–Ne laser (1.0 J per cm2) or treated with supernatant (10% in final concentration) derived from He–Ne laser (1.0 J per cm2) irradiated keratinocytes. For the blocking test, 1 μg per ml of neutralizing antibody against bFGF (Ab-3, Oncogene Research Products, Boston, MA) or NGF (Chemicon, Temecula, NJ) was added to the supernatants to clarify the functional importance of these released growth factors in melanocyte migration. Then microphotographs were taken at indicated time points within 24 h and 15–20 cells for each group were selected to measure the migrating distances (Horikawa et al., 1995Horikawa T. Norris D.A. Yohn J.J. Zekman T. Travers J.B. Morelli J.G. Melanocyte mitogens induce both melanocyte chemokinesis and chemotaxis.J Invest Dermatol. 1995; 104: 256-259Crossref PubMed Scopus (90) Google Scholar). Melanocytes were seeded in 24-well plates with a density of 4×104 cells per well and cultured for 24 h as previously described. Melanocytes were treated either by He–Ne laser (1.0 J per cm2) irradiation or with keratinocyte medium obtained from He–Ne laser (1.0 J per cm2) irradiated or sham-irradiated keratinocytes (10% in final concentration). Forty-eight hours later, the cells were labeled with 1.0 μCi [methyl-3H]thymidine (Amersham Pharmacia Biotech, Buckinghamshire, U.K.) per ml for 6 h. After washing three times with PBS, the cells were lyzed with 2 N NaOH and then neutralized with 2 N HCl. Acid-insoluble material was precipitated with four volumes of 10% trichloroacetic acid, collected on glass filters, washed three times with 10% trichloroacetic acid and once with ethanol, and then dried. The radioactivity on the filters was determined in a liquid scintillation counter (Imokawa et al., 1992Imokawa G. Yada Y. Miyagishi M. Endothelins secreted from human keratinocytes are intrinsic mitogens for human melanocytes.J Biol Chem. 1992; 267: 24675-24680Abstract Full Text PDF PubMed Google Scholar). Melanocytes (1×106 cell) were plated in a 6 cm dish and incubated overnight. Then the cells were treated with He–Ne laser irradiation or cultured with irradiated conditioned medium (10% in final concentration) as described previously for 72 h. The treated cells were detached by trypsin–ethylenediamine tetraacetic acid solution. Cell suspension was centrifuged, and the pellet was dissolved in 1 N NaOH. Melanin concentration was assessed by spectrophotometry (Hu et al., 1995Hu D.N. Mccormick S.A. Orlow S.J. Rosemblat S. Lin A.Y. Wo K. Melanogenesis by human uveal melanocytes in vitro.Invest Ophthalmol Vis Sci. 1995; 36: 931-938PubMed Google Scholar). Optical density (OD) at 475 nm was measured and compared with a standard curve obtained from synthetic melanin (Sigma). Melanin content was expressed as picograms per cell. A colorimetric method for determining the activity of mitochondrial enzymes was used to detect melanocyte proliferation. The CellTiter cell proliferation assay kit was purchased from Promega. Melanocytes were seeded on 96-well plates with a density of 3×103 cells per well and incubated overnight. Then melanocyte growth supplements were deprived of culture medium for 24 h. The cells were treated with He–Ne laser (1.0 J per cm2) irradiation or keratinocyte conditioned medium collected from laser-irradiated or nonirradiated keratinocytes (10% in final concentration) and incubated for 48 h. Ten microliters of CellTiter reagent containing tetrazolium compound and electron coupling reagents were added into each well to be catalyzed by mitochondrial dehydrogenase enzymes in metabolically active melanocytes. The plates were incubated for 4 h and the colorimetric absorbance was recorded at 490 nm by microtiter plate reader (MRX-II, Dynex Technology, Chantilly, VA) (Scudiero et al., 1988Scudiero D.A. Shoemaker R.H. Paull K.D. et al.Evaluation of a soluble tetrazolium/formazan assay for cell growth and drug sensitivity in culture using human and other tumor cell lines.Cancer Res. 1988; 48: 4827-4833PubMed Google Scholar). Thirty patients with segmental-type vitiligo over the head and neck were recruited in this study. Their background, treatment course, and response are shown in Table I. There were 11 female and 19 male patients, aged 8–43 y with mean age 22±11 y. The lesions occurred in eight cases when the patients were children (<13 y old), in seven cases when adolescent (13–18 y old), and in 15 cases when adult (>19 y old). The duration of vitiligo ranged from 0.5 to 30 y (average 4.6±6.1 y). Twenty-six patients were in a stable stage of the disease (lesion without active progression in the previous 3 mo) (Moellmann et al., 1982Moellmann G. Klein-Angfrer S. Scollay D.A. Nordlund J.J. Lerner A.B. Extracellular granular material and degeneration of keratinocytes in the normally pigmented epidermis of patients with vitiligo.J Invest Dermatol. 1982; 79: 321-330Crossref PubMed Scopus (180) Google Scholar), two patients were in an active stage (lesion displaying progression in the previous 3 mo), and another two patients were in an unstable stage (lesion changed from stable to active stage during the course of treatment). As for lesional locations, there were 15 patients with the vitiliginous lesions on the cheek (eight left side and seven right side), five patients on the neck (two left side and three right side), seven on the chin (three left side and four right side), and three on the left frontal area. Leukotrichia was noticed on lesions in the case of 11 patients (36.7%). All the patients had been cleared of the possibility of autoimmune diseases, such as thyroid diseases (Hashimoto's thyroiditis and Graves' disease), Addison's disease, pernicious anemia, insulin-dependent diabetes mellitus, and alopecia areata. All of them were healthy except for one patient with acute nonlymphocytic leukemia for 1.5 y. None of the participants had received any medical treatment in the preceding 3 mo. The study was approved by the Ethics Committee of the Kaohsiung Medical University Hospital.Table IBackground data of patientsNo.Sex/AgeHistory of vitiligo (y)StageLocationDermatomal distributionLargest diameter of vitiliginous lesion (cm)LeucotrichiaaN, negative; Y, positive.First repigmentation% of repigmentationTotal treatmentsessions1F/281StableL ChinV3bV, the fifth cranial nerve; C, the cervical branch of the vertebral column.2N8100202F/300.6StableL CheekV22N7100243M/420.5StableR CheekV21N6100164M/391.5ActiveR FrontalV1, V22.5N40901425M/135StableL CheekV1, V24.5Y16781326M/308StableR ChinV3, C3bV, the fifth cranial nerve; C, the cervical branch of the vertebral column.3N18781377F/301StableR ChinV3, C34N28721488M/1612StableL CheekV24Y871849M/122StableR ChinV3, C33.5N106513910M/154StableL FrontalV14Y156212011F/195StableL CheekV22.5N146113012M/162StableL NeckC2, C34Y8585813M/257StableR NeckV3, C22Y2055130cDiscontinued the treatment due to schoolwork.14F/81StableL CheekV21N85423cDiscontinued the treatment due to schoolwork.15M/208StableL NeckC34Y165311616F/120.5StableL CheekV21N18526417F/163StableR CheekV22Y345213418M/131StableR CheekV31.5N10514319M/420.8UnstableL CheekV1, V22.5Y2035122dDiscontinued the treatment due to busy job.20M/124UnstableR CheekV1, V24N483518021F/122StableL ChinV32.5N12337422M/120.5StableR ChinV32N6333223M/128StableL FrontalV14Y73039cDiscontinued the treatment due to schoolwork.24M/103StableL FrontalV12.5N20305425F/257StableR NeckV3, C33N1430105dDiscontinued the treatment due to busy job.26F/212StableR CheekV2, V32N16243727F/170.5StableR NeckV3, C22N1523100cDiscontinued the treatment due to schoolwork.,eDiscontinued the treatment due to distant residence.28M/4330StableR CheekV25Y068dDiscontinued the treatment due to busy job.,fDiscontinued the treatment due to poor treatment response.29M/320.5ActiveL CheekV24N042fDiscontinued the treatment due to poor treatment response.,gDiscontinued the treatment for other compelling reasons.30M/4016StableL ChinV33.5Y050eDiscontinued the treatment due to distant residence.,fDiscontinued the treatment due to poor treatment response.a N, negative; Y, positive.b V, the fifth cranial nerve; C, the cervical branch of the vertebral column.c Discontinued the treatment due to schoolwork.d Discontinued the treatment due to busy job.e Discontinued the treatment due to distant residence.f Discontinued the treatment due to poor treatment response.g Discontinued the treatment for other compelling reasons. Open table in a new tab A continuous wave He–Ne laser (OMNIPROBE™ Laser Biostimulation System, Physio Technology, Topeka, KS) with an average 1.0 mW power output was used for treatment. It was designed for point stimulation, i.e., irradiation point by point on the skin (Pöntinen and Pötinen, 1992bPöntinen P.J. Technique of LLLT.in: Pötinen P.J. Low Level Laser Therapy as a Medical Treatment Modality. Art Urpo Ltd, Tampere1992: 56-98Google Scholar;Allendorf et al., 1997Allendorf J.D.F. Bessler M. Huang J. et al.Helium–neon laser irradiation at fluences of 1, 2, and 4 J/cm2 failed to accelerate wound healing as assessed by both wound contracture rate and tensile strength.Lasers Surg Med. 1997; 20: 340-345Crossref PubMed Scopus (86) Google Scholar). When the He–Ne laser was used for the treatment of vitiligo, the probe was placed directly on the vitiliginous lesion. According to the manufacturer's instructions, the calculation formula for He–Ne laser point stimulation is used for a beam surface area of 0.01 cm2 (direct effect) and assumes only one application point per square centimeter of tissue. The balance of tissue is untreated directly but receives a peripheral effect, thus creating islands of biologically active tissue in the area (indirect effect) (Earle, 1985Earle V. Clinical treatment guidelines: He–Ne point stimulation energy densities.Instruction Manual of OMNIPROBE™Laser Biostimulation System. Physio Technology Ltd, Downsview, Ontario1985: 8Google Scholar). The number of treatment points depends on the size of the lesions. The power output was measured with a power meter (POW-105, Lasotronic). The irradiating flux for each treatment point in our patients was 3.0 J per cm2 with a stimulation time of 30 s (Kovacs, 1981Kovacs L. The stimulatory effect of laser on the physiological healing process of portio surface.Lasers Surg Med. 1981; 1: 241-252Crossref PubMed Scopus (25) Google Scholar;Yu et al., 1996Yu H.S. Chang K.L. Yu C.L. Chen J.W. Chen G.S. Low-energy helium–neon laser irradiation stimulates interleukin-1α and interkeukin-8 release from cultured human keratinocytes.J Invest Dermatol. 1996; 107: 593-596Crossref PubMed Scopus (148) Google Scholar). The calculation formula for treatment is Ta=(Ea/Pav)×At where Ta is the treatment time for a given area, Ea is the millijoules of energy required per square centimeter, Pav is the average laser power in milliwatts, and At is the area to be treated in square centimeters. It is 0.01 cm2 in point stimulation per centimeter of treatment area. All our vitiligo patients received He–Ne laser treatment once or twice a week. Vitiliginous lesions in all patients were traced and the square centimeters of involvement were counted on an overlaid grid; the lesions were recorded regularly by photography before, during, and after the He–Ne laser therapy. The percentage of repigmentation after He–Ne laser treatment was defined as follows: (area of repigmented skin±area of vitiliginous lesion prior to He–Ne laser therapy)×100% (Kao et al., 1995Kao C.H. Ko W.C. Ko S.S. Tsai R.Y. A comparative study on autologous graft for segmental vitiligo.Dermatol Sinica. 1995; 13: 65-74Google Scholar). The software of the SPSS system for Windows 10.0 version (SPSS, Chicago, IL) was used for statistical analysis. The results were expressed as mean±standard deviation (mean±SD). The Student's t test was also used for statistical evaluation between control and experimental groups in the in vitro study. The two-way ANOVA one factor repeated method was used to analyze the results of the cell migration assay. The Student's t test for unpaired observations was used to detect differences of sex and leukotrichia in the He–Ne laser treatment of segmental-type vitiligo patients. A p-value of <0.05 is considered to be statistically significant. The one-way ANOVA method for various independent groups was used to contrast the effects of age, age of onset, duration, stage, location, and the size of lesion in the He–Ne laser therapy of the segmental-type vitiligo patients (significant level <0.05). The assay for bFGF release from cells was performed 30 min after He–Ne" @default.
• W2068139504 created "2016-06-24" @default.
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• W2068139504 date "2003-01-01" @default.
• W2068139504 modified "2023-10-12" @default.
• W2068139504 title "Helium–Neon Laser Irradiation Stimulates Migration and Proliferation in Melanocytes and Induces Repigmentation in Segmental-Type Vitiligo" @default.
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