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脑网络在灼口综合征中的作用:一项叙述性综述。

Role of Brain Networks in Burning Mouth Syndrome: A Narrative Review.

作者信息

Nagamine Takahiko

机构信息

Department of Psychiatric Internal Medicine, Sunlight Brain Research Center, Hofu 747-0066, Japan.

Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Bunkyou 113-8510, Japan.

出版信息

Dent J (Basel). 2025 Jul 4;13(7):304. doi: 10.3390/dj13070304.

DOI:10.3390/dj13070304
PMID:40710149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12293904/
Abstract

: Burning mouth syndrome (BMS) is a chronic and often debilitating orofacial pain condition characterized by a burning sensation in the oral mucosa without clear abnormal lesions. While its etiology is considered multifactorial, the underlying pathophysiology remains unclear. This narrative review aims to synthesize existing functional magnetic resonance imaging (fMRI) studies to shed light on the central neural mechanisms contributing to BMS. : A focused electronic search was conducted across the PubMed and J-STAGE databases for relevant articles published in English from January 2000 to May 2025. The review prioritized studies investigating brain structure and function using fMRI in individuals with BMS. : Our synthesis of the literature consistently demonstrated that the brains of individuals with BMS exhibit augmented connectivity within the medial pain system and a diminished gray matter volume in the medial prefrontal cortex (mPFC). These findings suggest a crucial role for altered brain circuitry, particularly a reduction in the output of the basal ganglia dopamine system, in the experience of BMS pain. : The consistent fMRI findings strongly indicate that BMS involves significant functional and structural brain alterations. The observed changes in the mPFC and its connections to the basal ganglia dopamine system highlight this pathway as a potential target for both pharmacological and non-pharmacological neurological interventions for individuals with BMS.

摘要

灼口综合征(BMS)是一种慢性且常使人衰弱的口面部疼痛病症,其特征为口腔黏膜有烧灼感但无明显异常病变。虽然其病因被认为是多因素的,但其潜在的病理生理学仍不清楚。本叙述性综述旨在综合现有的功能磁共振成像(fMRI)研究,以阐明导致BMS的中枢神经机制。:在PubMed和J-STAGE数据库中进行了针对性的电子检索,以查找2000年1月至2025年5月以英文发表的相关文章。该综述优先考虑使用fMRI研究BMS患者脑结构和功能的研究。:我们对文献的综合分析一致表明,BMS患者的大脑在内侧疼痛系统内表现出增强的连通性,并且内侧前额叶皮质(mPFC)的灰质体积减少。这些发现表明,大脑回路改变,特别是基底神经节多巴胺系统输出减少,在BMS疼痛体验中起关键作用。:一致的fMRI研究结果强烈表明,BMS涉及大脑显著的功能和结构改变。mPFC及其与基底神经节多巴胺系统连接的观察变化突出了该通路作为BMS患者药物和非药物神经干预潜在靶点的地位。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42e9/12293904/ffe45f5824e8/dentistry-13-00304-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42e9/12293904/5607540ed8ab/dentistry-13-00304-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42e9/12293904/ffe45f5824e8/dentistry-13-00304-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42e9/12293904/5607540ed8ab/dentistry-13-00304-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42e9/12293904/ffe45f5824e8/dentistry-13-00304-g002.jpg

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本文引用的文献

1
Estrogen-Mediated Neural Mechanisms of Sex Differences in Burning Mouth Syndrome.灼口综合征性别差异的雌激素介导神经机制
Neurol Int. 2025 Apr 20;17(4):61. doi: 10.3390/neurolint17040061.
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Neuroplasticity in chronic pain: insights into diagnosis and treatment.慢性疼痛中的神经可塑性:对诊断和治疗的见解
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Pathogenesis of Orofacial Pain Based on Brain Circuits.基于脑回路的口面部疼痛发病机制
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The role of the salience network in cognitive and affective deficits.突显网络在认知和情感缺陷中的作用。
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White and Gray Matter Abnormality in Burning Mouth Syndrome Evaluated with Diffusion Tensor Imaging and Neurite Orientation Dispersion and Density Imaging.弥散张量成像和神经丝取向分散和密度成像评估灼口综合征的白质和灰质异常。
Magn Reson Med Sci. 2024 Apr 1;23(2):204-213. doi: 10.2463/mrms.mp.2022-0099. Epub 2023 Mar 29.
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Central sensitization in burning mouth syndrome: a practical approach using questionnaires.灼口综合征中的中枢敏化:使用问卷的实用方法。
Oral Surg Oral Med Oral Pathol Oral Radiol. 2022 Mar;133(3):292-300. doi: 10.1016/j.oooo.2021.10.010. Epub 2021 Oct 22.
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Structural connectivity changes in the cerebral pain matrix in burning mouth syndrome: a multi-shell, multi-tissue-constrained spherical deconvolution model analysis.大脑疼痛矩阵中结构性连接变化在灼口综合征中的表现:一种多壳层、多组织约束球谐反卷积模型分析。
Neuroradiology. 2021 Dec;63(12):2005-2012. doi: 10.1007/s00234-021-02732-9. Epub 2021 Jun 18.