Review Article
* Acceptable secondary publication
* This article was published in the Medical Lasers.
* The authors have received approval from the editors of the Medical Lasers and the D&PS.
In the previous article, we provided a systematic literature review of studies on laser toning-induced hypopigmentation or dyspigmentation(LTID).1 Several literatures reported of mottled hypopigmentation occurring after laser toning (LT) therapy.2-6 Because they emphasized the risk of LT treatment and claimed that the incidence of hypopigmentation caused by LT was found to be about 10% in Asians, there were excessive concerns regarding LTID. However, in the last article, we discussed that such concerns are unnecessary as the new treatment techniques and parameters in LT are much safer and require only reasonable caution on the part of the doctor.1
In this article, we would like to examine the pathophysiology of LTID based on histological findings. Moreover, we will also discuss the treatment options that can be offered to patients with hypopigmentation (dyspigmentation) caused by LT.
1. Histopathologic findings of melasma and laser toning outcomes
Before we move on to our main topic, let us help the readers’ understanding by briefly discussing histopathological characteristics of melasma and the principles of LT. As in-depth discussions on this topic could fill a review article, we will keep our discussion brief.
Among many papers on histomorphologic and immunohistochemical characteristics of melasma, there are a few important studies that are most frequently cited.7-12 They have in common a report of melanin increase in all epidermal layers, basal hyperpigmentation, solar elastosis, and epidermal flattening.13 However, they disagree over immunohistochemistry of melanocytes. Some reported the number of melanocytes was increased in the melasma lesion,7-9 whereas others found hyperfunction of melanocytes without a significant increase in the number.10-12 Other noticeable findings are as follows: melanocytes in melasma lesions are larger and have more pronounced dendrites than those in the normal skin;7,10-12 melanocytes protrude into the dermis (pendulous melanocytes) due to damaged basement membrane.14,15 In addition, other noteworthy findings include dermal environmental changes such as evidence of ultraviolet(UV)-induced skin damage, increased inflammatory cytokines, and increased expression of melanogenesis-associated proteins. Dermal inflammation induced from chronic UV irradiation activates fibroblasts, leading to increased dermal stem cell factors and other cytokines stimulating melanogenesis.16 UV irradiation also activates matrix metalloproteinases which in turn damages the basement membrane.15 For these reasons, it was suggested that improving the altered dermal environment of the melasma lesion can correct aberrant signals between dermis and epidermis. Various long-pulsed lasers including the 1,064 nm long-pulsed neodymium-doped yttrium aluminum garnet (Nd:YAG) laser have also been used to treat melasma for skin rejuvenation and improvement of abnormal dermal environment, not for removal of melanin pigments.17,18
In 2011, the structural modifications of melanocytes and melanosomes after LT were reported by Mun et al. 19 who had published a study presenting the theory of ‘subcellular selective photothermolysis’ as theoretical principles of LT. 20 They used transmission electron microscopy, 3VIEW surface block face-scanning electron microscopy and 3D structure reconstruction to allow an in-depth analysis of changes in melanocytes and melanosomes after LT treatment19. As for melanosomes, their number (especially, stage IV melanosomes) significantly decreased and the structure was changed after the treatment. As for melanocytes, they were not destroyed but were reduced in volume and the number of dendrites.19 This study clearly explained the mechanism of LT in melasma and had an impact on following histopathological studies on LT.
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Kim et al.21 reported similar results in 2013. In addition, they found that LT treatment could down-regulate the expression of tyrosinase-related protein (TRP)-1, TRP-2, nerve growth factors, α-melanocyte-stimulating hormones, tyrosinase, and stem cell factors in melasma lesions.21 This investigation into the mechanism of LT also showed that LT in melasma removed melanosomes and damaged the dendrites of melanocytes without killing the cells, as well as down-regulated the expression of melanogenic proteins. Moreover, some authors pointed out that beyond the actions in melanin fragmentation and dispersion in the epidermis, LT might also promote destruction and migration of dermal melanophages to result in lightening effects.3 It may be due to the effect of LT on promoting lymphatic excretion of melanophages.
Reference
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-To be continued
