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首页> 外文期刊>Dermatopathology >Keratinocytic Malfunction as a Trigger for the Development of Solar Lentigines
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Keratinocytic Malfunction as a Trigger for the Development of Solar Lentigines

机译：角化细胞功能失调引发太阳扁豆素的发展

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Introduction: Solar lentigines (SL) affect chronically UV-radiated skin. Treatment is often refractory. Deeper knowledge on its pathogenesis might improve therapeutic effects. Material and Methods: Morphological characterization of 190 SL was performed and epidermal thickness, pigment distribution, dendricity, and cornification grade were measured. Immunoreactivity was investigated using Melan A, Tyrosinase, MITF, p53, and CD20, as well as Notch1 using immunofluorescence. Results: We found 2 groups of histological patterns, i.e., either acanthotic or atrophic epidermis. Lesions with basket-woven cornification and atrophic epidermis were observed in 6 out of 9 and 14 out of 16 cases from the face, respectively. Consistency of areas with a high pigmentation was observed in 96–97% of the cases. Hyperpigmentation grade and acanthosis or cornification disorders correlated positively in 88.5% of the cases. Overexpressed of p53 was found in 19 out of 20 lesions, presenting in a scattered distribution. A significant correlation of p53 and acanthosis (p = 0.003) and cornification grade (p = 0.0008) was observed. Notch1 was expressed in all SL, with the highest immunoreactivity in atrophic facial lesions. Lesions from the hands expressed Notch1 mainly in acanthotic areas with elongated rete ridges and less compact cornification. Discussion: We suggest that Notch1-dependent keratinocytic malfunction causes the development of SL. Consequently, hyperpigmentation would be a result and not the primary cause of the pathogenesis. Confirmation of these findings might have clinical implications as hitherto treatment has mainly focused on melanocytes and pigmentation and not on the proliferation/differentiation balance of keratinocytes.
机译：简介：太阳发光素（SL）影响慢性紫外线辐射的皮肤。治疗通常是难治的。更深入地了解其发病机理可能会改善治疗效果。材料与方法：对190 SL进行形态表征，并测量表皮厚度，色素分布，树突度和角质化等级。使用Melan A，酪氨酸酶，MITF，p53和CD20以及Notch1使用免疫荧光法研究了免疫反应性。结果：我们发现了两组组织学模式，即棘皮表皮或萎缩表皮。面部分别有9例中的6例和16例中的14例观察到带有篮编织角质层和萎缩表皮的病变。 96–97％的病例观察到高色素沉着区域的一致性。 88.5％的病例中色素沉着过度和棘皮症或角质病呈正相关。在20个病变中有19个发现p53过表达，呈散布分布。观察到p53和棘皮症（p = 0.003）与角质化等级（p = 0.0008）显着相关。 Notch1在所有SL中均有表达，在萎缩性面部病变中具有最高的免疫反应性。手上的病变主要在棘突长而网纹少的棘皮区域表达Notch1。讨论：我们建议Notch1依赖性角化细胞功能障碍引起SL的发展。因此，色素沉着过多将是发病的结果，而不是主要原因。这些发现的确认可能具有临床意义，因为迄今为止的治疗主要集中在黑素细胞和色素沉着上，而不是在角质形成细胞的增殖/分化平衡上。

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