12例口腔内刺激及接触性超敏反应的组织病理谱分析。

Head and neck pathology Pub Date : 2021-12-01 Epub Date: 2021-04-26 DOI:10.1007/s12105-021-01330-8
Diana Wang, Sook-Bin Woo
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引用次数: 4

摘要

背景:刺激性接触性口炎(ICS)和接触性超敏性口炎(CHS)通常是由酒精、调味剂和牙膏和食品中的添加剂以及高或低ph的接触物引起的。ICS公认的接触物是李斯特林™漱口水,而CHS的接触物是肉桂醛。然而,许多其他调味剂,甚至无烟烟草都是接触物,会导致完全可逆的粘膜损伤。本研究的目的是1)呈现具有明确接触史的ICS和CHS病例以及由此产生的病变的组织病理学特征,2)定义表征此类病变的组织病理学特征。方法:对12例已知接触者表现出明显的组织病理学特征的ICS和CHS病例进行分析。结果:ICS表现为三种类型,其严重程度依次为:1)浅表性脱屑,2)浅表性角化细胞水肿,3)角化细胞凝固性坏死伴/伴海绵状和微脓肿。CHS以两种模式为特征,即浆细胞性口炎伴强烈浆细胞浸润和淋巴组织细胞浸润伴或不伴非坏死性肉芽肿性炎症。后者有三种类型:(1)淋巴组织细胞浸润于界面,形成良好或松散聚集的非坏死性肉芽肿;(2)淋巴组织细胞浸润于血管周围和血管旁淋巴组织细胞结节;(3)淋巴组织细胞浸润于含有非坏死性肉芽肿的血管周围和血管旁淋巴组织细胞结节的界面。同一接触者可能诱发ICS和CHS,而不同的接触者可能引起同一种组织病理模式。结论:ICS与CHS具有明显的组织学特征。认识到这些模式是由接触者引起的,将有助于临床医生管理这种粘膜病变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Histopathologic Spectrum of Intraoral Irritant and Contact Hypersensitivity Reactions: A Series of 12 cases.

Histopathologic Spectrum of Intraoral Irritant and Contact Hypersensitivity Reactions: A Series of 12 cases.

Background: Irritant contact stomatitis (ICS) and contact hypersensitivity stomatitis (CHS) are often caused by alcohol, flavoring agents and additives in dentifrices and foods, and contactants with high or low pH. A well-recognized contactant for ICS is Listerine™ mouthwash, while that for CHS is cinnamic aldehyde. However, many other flavoring agents and even smokeless tobacco are contactants that cause mucosal lesions that are entirely reversible. The objective of this study is to 1) present cases of ICS and CHS with a clear history of a contactant at the site and the histopathologic features of the resulting lesion and 2) define the histopathologic features that characterize such lesions.

Methods: 12 cases of ICS and CHS with known contactants that exhibited distinct histopathologic patterns were identified.

Results: ICS are characterized by three patterns in increasing order of severity namely: 1) superficial desquamation, 2) superficial keratinocyte edema, and 3) keratinocyte coagulative necrosis with/out spongiosis and microabscesses. CHS is characterized by two patterns namely plasma cell stomatitis with an intense plasma cell infiltrate and a lymphohistiocytic infiltrate with or without non-necrotizing granulomatous inflammation. Three patterns of the latter are recognized: (1) lymphohistiocytic infiltrate at the interface with well-formed or loosely aggregated non-necrotizing granulomas; (2) lymphohistiocytic infiltrate at the interface with peri- and para-vascular lymphohistiocytic nodules; and (3) lymphohistiocytic infiltrate at the interface with peri- and para-vascular lymphohistiocytic nodules containing non-necrotizing granulomas. The same contactant may elicit ICS and CHS, while one histopathologic pattern may be brought on by various contactants.

Conclusion: ICS and CHS have distinct histologic patterns. Recognizing that these patterns are caused by contactants would help clinicians manage such mucosal lesions.

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