Xiong Xi-Xi, Ding Gao-Zhong, Zhao Wen-E, Li Xue, Ling Yu-Ting, Sun Li, Gong Qing-Li, Lu Yan
Dermatology Department, First Affiliated Hospital, Nanjing Medical University, #300 Guangzhou Road, Nanjing, Jiangsu, 210029, People's Republic of China.
Laboratory of Electron Microscopy, Department of Analysis and Testing Center, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, 210029, People's Republic of China.
Arch Dermatol Res. 2017 Jul;309(5):323-333. doi: 10.1007/s00403-017-1730-7. Epub 2017 Mar 17.
Skin color is determined by the number of melanin granules produced by melanocytes that are transferred to keratinocytes. Melanin synthesis and the distribution of melanosomes to keratinocytes within the epidermal melanin unit (EMU) within the skin of vitiligo patients have been poorly studied. The ultrastructure and distribution of melanosomes in melanocytes and surrounding keratinocytes in perilesional vitiligo and normal skin were investigated using transmission electron microscopy (TEM). Furthermore, we performed a quantitative analysis of melanosome distribution within the EMUs with scatter plot. Melanosome count within keratinocytes increased significantly compared with melanocytes in perilesional stable vitiligo (P < 0.001), perilesional halo nevi (P < 0.01) and the controls (P < 0.01), but not in perilesional active vitiligo. Furthermore, melanosome counts within melanocytes and their surrounding keratinocytes in perilesional active vitiligo skin decreased significantly compared with the other groups. In addition, taking the means-standard error of melanosome count within melanocytes and keratinocytes in healthy controls as a normal lower limit, EMUs were graded into 3 stages (I-III). Perilesional active vitiligo presented a significantly different constitution in stages compared to other groups (P < 0.001). The distribution and constitution of melanosomes were normal in halo nevi. Impaired melanin synthesis and melanosome transfer are involved in the pathogenesis of vitiligo. Active vitiligo varies in stages and in stage II, EMUs are slightly impaired, but can be resuscitated, providing a golden opportunity with the potential to achieve desired repigmentation with an appropriate therapeutic choice. Adverse milieu may also contribute to the low melanosome count in keratinocytes.
肤色由黑素细胞产生并转移至角质形成细胞的黑素颗粒数量决定。白癜风患者皮肤中表皮黑素单元（EMU）内黑素合成及黑素小体向角质形成细胞的分布情况研究较少。采用透射电子显微镜（TEM）研究了白癜风皮损周围和正常皮肤中黑素细胞及周围角质形成细胞中黑素小体的超微结构和分布。此外，我们用散点图对EMU内黑素小体分布进行了定量分析。与皮损周围稳定期白癜风（P < 0.001）、皮损周围晕痣（P < 0.01）及对照组（P < 0.01）相比，皮损周围稳定期白癜风角质形成细胞内黑素小体计数显著增加，但皮损周围进展期白癜风未见增加。此外，与其他组相比，皮损周围进展期白癜风皮肤中黑素细胞及其周围角质形成细胞内黑素小体计数显著减少。另外，以健康对照者黑素细胞和角质形成细胞内黑素小体计数的均值-标准误作为正常下限，将EMU分为3个阶段（I-III）。与其他组相比，皮损周围进展期白癜风在阶段构成上有显著差异（P < 0.001）。晕痣中黑素小体的分布和构成正常。黑素合成和黑素小体转运受损参与了白癜风的发病机制。进展期白癜风存在阶段差异，在II期，EMU略有受损，但可恢复，这为通过适当的治疗选择实现理想的色素再生提供了黄金机会。不良环境也可能导致角质形成细胞中黑素小体数量减少。
