Lamel Sonia A, Rahvar Maral, Maibach Howard I
Department of Dermatology, School of Medicine, University of California-San Francisco, San Francisco, CA 94143, USA.
Cutan Ocul Toxicol. 2013 Mar;32(1):67-71. doi: 10.3109/15569527.2012.684419. Epub 2012 Jun 6.
Despite new technologies, few studies have quantified changes in melanocyte numbers associated with postinflammatory hyperpigmentation (PIH) secondary to exogenous causes.
This article aims to review what is known about the pathogenesis of PIH secondary to external insults and its relationship to the resultant degree of quantitative changes in melanocytes.
We performed a review of articles exploring PIH resulting from external cutaneous insults retrieved through database searching. We reviewed relevant articles for the pathogenesis, histopathology, and quantitative changes in melanocytes related to specific etiologies of PIH. Methodologies to quantify pigmentation changes in dermatologic conditions with clinical hyperpigmentation were also explored.
Significant increases in melanocyte counts of irritant affected skin is seen compared with melanocyte counts of unaffected skin. An increase in melanocyte counts was also found for spontaneous inflammatory dermatoses, even in the absence of clinical hyperpigmentation. Furthermore, changes in melanocyte density and appearance are also seen secondary to inflammation. In addition, increases in epidermal melanocytes are seen with cutaneous exposure to certain agents, and melanocyte increases vary by exposure agent.
The degree of hyperpigmentation related to the intensity and duration of exposure to the causative factors of PIH is essential to better understand the pathophysiology of the disease process. The application of new methodologies to determine quantitative changes in melanocytes elicited by specific causative inflammatory agents has implications to prevent PIH, add to knowledge about disease duration, to develop better treatments for PIH, and to aid our understanding of the biology of the melanocyte.
尽管有了新技术，但很少有研究对继发于外部原因的炎症后色素沉着（PIH）相关的黑素细胞数量变化进行量化。
本文旨在综述关于外部损伤继发的PIH发病机制及其与黑素细胞数量变化程度之间关系的已知情况。
我们对通过数据库检索获得的探讨外部皮肤损伤导致的PIH的文章进行了综述。我们回顾了相关文章中与PIH特定病因相关的发病机制、组织病理学以及黑素细胞的数量变化。还探讨了量化伴有临床色素沉着的皮肤病中色素沉着变化的方法。
与未受影响皮肤的黑素细胞计数相比，刺激性损伤皮肤的黑素细胞计数显著增加。在自发性炎症性皮肤病中也发现黑素细胞计数增加，即使在没有临床色素沉着的情况下也是如此。此外，炎症继发时黑素细胞密度和外观也会发生变化。另外，皮肤接触某些物质后表皮黑素细胞会增加，且黑素细胞增加因接触物质而异。
与PIH致病因素的暴露强度和持续时间相关的色素沉着程度对于更好地理解疾病过程的病理生理学至关重要。应用新方法来确定特定致病炎症因子引起的黑素细胞数量变化，对于预防PIH、增加对疾病持续时间的了解、开发更好的PIH治疗方法以及帮助我们理解黑素细胞生物学具有重要意义。
