Compilato Domenico, Campisi Giuseppina, Pastore Luca, Carroccio Antonio
Department of Oral Sciences "G. Messina", Section of Oral Medicine, University Hospital of Palermo, Italy.
ScientificWorldJournal. 2010 Dec 14;10:2385-94. doi: 10.1100/tsw.2010.228.
Celiac disease (CD) is a lifelong, T cell-mediated enteropathy, triggered by the ingestion of gluten and related prolamins in genetically susceptible subjects, resulting in minor intestinal mucosal injury, including villous atrophy with crypt hyperplasia and intraepithelial lymphocytosis, and subsequent nutrient malabsorption. Although serological tests for antiendomysial (EMA) and anti-tissue transglutaminase (anti-tTG) autoantibodies are used to screen and follow up on patients with CD, diagnostic confirmation is still based on the histological examination of the small intestinal mucosa. Although the small intestinal mucosa is the main site of the gut involved in CD, other mucosal surfaces (such as gastric, rectal, ileal, and esophageal) belonging to the gastrointestinal tract and the gut-associated lymphoid tissue (GALT) can also be involved. A site that could be studied less invasively is the mouth, as it is the first part of the gastrointestinal system and a part of the GALT. Indeed, not only have various oral ailments been reported as possible atypical aspects of CD, but it has been also demonstrated that inflammatory changes occur after oral supramucosal application and a submucosal injection of gliadin into the oral mucosa of CD patients. However, to date, only two studies have assessed the capacity of the oral mucosa of untreated CD patients to EMA and anti-tTG antibodies. In this paper, we will review studies that evaluate the capacity of the oral mucosa to produce specific CD autoantibodies. Discrepancies in sensitivity from the two studies have revealed that biopsy is still not an adequate procedure for the routine diagnostic purposes of CD patients, and a more in-depth evaluation on a larger sample size with standardized collection and analysis methods is merited. However, the demonstration of immunological reactivity to the gluten ingestion of the oral mucosa of CD, in terms of IgA EMA and anti-tTG production, needs to be further evaluated in order to verify whether the oral mucosa is colonized by lymphocytes activated in the intestine or if gluten could stimulate naïve lymphocytes directly in the oral mucosa. This would have important implications for the pathogenesis, diagnosis, and treatment of CD.
乳糜泻（CD）是一种由遗传易感性个体摄入麸质及相关醇溶蛋白引发的终身性、T细胞介导的肠病，会导致小肠黏膜损伤，包括绒毛萎缩伴隐窝增生和上皮内淋巴细胞增多，进而引起营养物质吸收不良。尽管抗肌内膜（EMA）和抗组织转谷氨酰胺酶（抗tTG）自身抗体的血清学检测用于筛查和随访CD患者，但诊断仍需基于小肠黏膜的组织学检查。虽然小肠黏膜是CD累及肠道的主要部位，但胃肠道的其他黏膜表面（如胃、直肠、回肠和食管）以及肠道相关淋巴组织（GALT）也可能受累。口腔作为胃肠道系统的起始部位和GALT的一部分，是一个可以采用侵入性较小的方式进行研究的部位。事实上，不仅有多种口腔疾病被报道为CD可能的非典型表现，而且还证实，在CD患者的口腔黏膜进行黏膜上应用和黏膜下注射麦醇溶蛋白后会出现炎症变化。然而，迄今为止，仅有两项研究评估了未经治疗的CD患者口腔黏膜对EMA和抗tTG抗体的反应能力。在本文中，我们将回顾评估口腔黏膜产生特异性CD自身抗体能力的研究。两项研究在敏感性上的差异表明，活检对于CD患者的常规诊断目的而言仍非充分手段，值得采用标准化的采集和分析方法，对更大样本量进行更深入的评估。然而，关于CD患者口腔黏膜对摄入麸质产生免疫反应性，即产生IgA EMA和抗tTG方面，仍需进一步评估，以确定口腔黏膜是被肠道中激活的淋巴细胞定植，还是麸质能直接刺激口腔黏膜中的幼稚淋巴细胞。这将对CD的发病机制、诊断和治疗产生重要影响。
