Abbvie Bioresearch Center, Worcester, MA, USA.
AbbVie Inc, North Chicago, IL, USA.
Exp Dermatol. 2021 Jun;30(6):820-830. doi: 10.1111/exd.14273. Epub 2021 Jan 20.
Since first recognized in 1839, the pathogenesis of acne inversa (AI) has undergone repeated revisions. Although there is agreement that AI involves occlusion of hair follicles with subsequent inflammation and the formation of tracts, the histologic progression of this disease still requires refinement. The objective of this study was to examine the histologic progression of AI based on the examination of a large cohort of punch biopsies and excisional samples that were examined first by hematoxylin and eosin staining. The most informative of these samples were step-sectioned and stained by immunohistochemistry for epithelial and inflammatory markers. Based on this examination, the following observations were made: 1) AI arises from the epithelium of the infundibulum of terminal and vellus hairs; 2) These form cysts and epithelial tendrils that extend into soft tissue; 3) Immunohistochemical staining demonstrates the epithelium of AI is disordered with infundibular and isthmic differentiation and de novo expression of stem cell markers; 4) The inflammatory response in AI is heterogeneous and largely due to cyst rupture. The conclusions of this investigation were that AI is an epithelial-driven disease caused by infiltrative, cyst forming tendrils and most of the inflammation is due to cyst rupture and release of cornified debris and bacteria. Cyst rupture often occurs below the depths of punch biopsy samples indicating their use for analysis may give an incomplete picture of the disease. Finally, our data suggest that unless therapies inhibit tendril development, it is unlikely they will cause prolonged treatment-induced remission in AI.
自 1839 年首次被认识以来，痤疮性逆向（AI）的发病机制已经反复修订。尽管人们一致认为 AI 涉及毛囊闭塞，随后发生炎症和形成管道，但这种疾病的组织学进展仍需要细化。本研究的目的是通过检查大量的打孔活检和切除样本，首先通过苏木精和伊红染色来检查 AI 的组织学进展。这些样本中最具信息性的样本通过免疫组织化学染色用于上皮和炎症标志物。基于此检查，观察到以下结果：1）AI 源于终末和毳毛漏斗部的上皮；2）这些形成囊肿和上皮卷须，延伸到软组织中；3）免疫组织化学染色显示 AI 的上皮排列紊乱，具有漏斗部和峡部分化以及新表达干细胞标志物；4）AI 中的炎症反应是异质的，主要是由于囊肿破裂。本研究的结论是，AI 是一种上皮驱动的疾病，由浸润性、囊肿形成的卷须引起，大多数炎症是由于囊肿破裂和角蛋白碎片和细菌的释放引起的。囊肿破裂通常发生在打孔活检样本的深度以下，这表明它们用于分析可能无法完整地反映疾病。最后，我们的数据表明，除非治疗方法抑制卷须的发展，否则它们不太可能导致 AI 治疗诱导的缓解持续时间延长。
