Department of Anatomy, Christian-Albrechts University of Kiel, Kiel, Germany.
Neurogastroenterol Motil. 2010 Apr;22(4):407-14, e93-4. doi: 10.1111/j.1365-2982.2009.01445.x. Epub 2009 Dec 23.
The pathogenesis of diverticular disease (DD) is attributed to several aetiological factors (e.g. age, diet, connective tissue disorders) but also includes distinct intestinal motor abnormalities. Although the enteric nervous system (ENS) is the key-regulator of intestinal motility, data on neuropathological alterations are limited. The study aimed to investigate the ENS by a systematic morphometric analysis.
Full-thickness sigmoid specimens obtained from patients with symptomatic DD (n = 27) and controls (n = 27) were processed for conventional histology and immunohistochemistry using anti-HuC/D as pan-neuronal marker. Enteric ganglia, nerve and glial cells were quantified separately in the myenteric, external and internal submucosal plexus compartments.
Compared to controls, patients with DD showed significantly (P < 0.05) (i) reduced neuronal density in all enteric nerve plexus, (ii) decrease of ganglionic nerve cell content in the myenteric plexus, (iii) decreased ganglionic density in the internal submucosal plexus, (iv) reduced glial cell density in the myenteric plexus, (v) decrease of ganglionic glial cell content in the myenteric plexus and increase in submucosal plexus compartments, (vi) increased glia index in all enteric nerve plexus. About 44.4% of patients with DD exhibited myenteric ganglia displaying enteric gliosis.
CONCLUSIONS & INFERENCES: Patients with DD show substantial structural alterations of the ENS mainly characterized by myenteric and submucosal oligo-neuronal hypoganglionosis which may account for intestinal motor abnormalities reported in DD. The morphometric data give evidence that DD is associated with structural alterations of the ENS which may complement established pathogenetic concepts.
憩室病(DD)的发病机制归因于多种病因因素(例如年龄、饮食、结缔组织疾病),但也包括明显的肠道运动异常。尽管肠神经系统(ENS)是肠道运动的关键调节者,但有关神经病理学改变的数据有限。本研究旨在通过系统形态计量学分析来研究 ENS。
从有症状的 DD 患者(n=27)和对照者(n=27)获得全层乙状结肠标本,分别用抗 HuC/D 作为神经元标志物进行常规组织学和免疫组织化学处理。分别在肌间、外和内黏膜下神经丛中对肠神经节、神经和神经胶质细胞进行定量。
与对照者相比,DD 患者的所有肠神经丛中的神经元密度显著降低(P < 0.05),(i)肌间神经丛中的神经节神经细胞含量减少,(ii)内黏膜下神经丛中的神经节密度降低,(iii)肌间神经丛中的神经胶质细胞密度降低,(iv)肌间神经丛中的神经节神经胶质细胞含量减少,(v)黏膜下神经丛中的神经节神经胶质细胞含量增加,(vi)所有肠神经丛中的神经胶质细胞指数增加。约 44.4%的 DD 患者的肌间神经节显示肠神经胶质增生。
DD 患者的 ENS 存在明显的结构改变,主要表现为肌间和黏膜下少神经节性低神经节症,这可能是 DD 报道的肠道运动异常的原因。形态计量学数据表明,DD 与 ENS 的结构改变有关,这可能补充已建立的发病机制概念。