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Purpose of Review <p>Burning Mouth Syndrome has long been described as an idiopathic or neuropathic condition. However, emerging evidence indicates that immune and endocrine mechanisms play a significant role in its pathophysiology. This review aimed to integrate current findings on neuroimmune and hormonal interactions in BMS and to examine the influence of autoimmune conditions and sensory dysfunction on its contemporary understanding.</p> Recent Findings <p>A structured search was conducted in PubMed, Scopus, and Web of Science covering publications from 1985 to 2025. Studies addressing pathophysiology, diagnosis, and treatment related to immune, hormonal, and neuropathic mechanisms were critically analyzed. BMS has been increasingly associated with autoimmune diseases such as Sjögren’s syndrome, Hashimoto’s thyroiditis, and type 1 diabetes mellitus. Systemic autoantibodies and mast cell activation have been identified as potential contributors to disease mechanisms. Histopathological and sensory evidence supports the presence of small fiber neuropathy and neuroimmune interactions, including the upregulation of TRPV1 and P2X3 receptors. Hormonal disturbances, particularly thyroid dysfunction, may exacerbate sensory and gustatory alterations. These findings highlight the contribution of systemic and local immune endocrine interactions to chronic oral pain in BMS.</p> Summary <p>BMS has been increasingly associated with autoimmune diseases such as Sjögren’s syndrome, Hashimoto’s thyroiditis, and type 1 diabetes mellitus. Preliminary evidence suggests that systemic autoantibodies and mast cell activation may serve as contributors to disease mechanisms. Histopathological and sensory findings are consistent with small fiber neuropathy and neuroimmune interactions, including the upregulation of TRPV1 and P2X3 receptors.</p> Graphical Abstract <p></p>

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Neuroimmune and Endocrine Dimensions of Burning Mouth Syndrome: An Integrative Review of Autoimmunity, Sensory Dysfunction, and Systemic Influences

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月3日

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  • Lukas Mendes de Abreu,
  • Izabel Regina Fischer Rubira-Bullen,
  • Michele Di Benedetto,
  • Raquel Molina Sanches,
  • Mariel Ruivo Biancardi,
  • Ana Carolina Carneiro Cardoso,
  • Camila Lopes Cardoso,
  • Cássia Maria Fischer Rubira

摘要

Purpose of Review

Burning Mouth Syndrome has long been described as an idiopathic or neuropathic condition. However, emerging evidence indicates that immune and endocrine mechanisms play a significant role in its pathophysiology. This review aimed to integrate current findings on neuroimmune and hormonal interactions in BMS and to examine the influence of autoimmune conditions and sensory dysfunction on its contemporary understanding.

Recent Findings

A structured search was conducted in PubMed, Scopus, and Web of Science covering publications from 1985 to 2025. Studies addressing pathophysiology, diagnosis, and treatment related to immune, hormonal, and neuropathic mechanisms were critically analyzed. BMS has been increasingly associated with autoimmune diseases such as Sjögren’s syndrome, Hashimoto’s thyroiditis, and type 1 diabetes mellitus. Systemic autoantibodies and mast cell activation have been identified as potential contributors to disease mechanisms. Histopathological and sensory evidence supports the presence of small fiber neuropathy and neuroimmune interactions, including the upregulation of TRPV1 and P2X3 receptors. Hormonal disturbances, particularly thyroid dysfunction, may exacerbate sensory and gustatory alterations. These findings highlight the contribution of systemic and local immune endocrine interactions to chronic oral pain in BMS.

Summary

BMS has been increasingly associated with autoimmune diseases such as Sjögren’s syndrome, Hashimoto’s thyroiditis, and type 1 diabetes mellitus. Preliminary evidence suggests that systemic autoantibodies and mast cell activation may serve as contributors to disease mechanisms. Histopathological and sensory findings are consistent with small fiber neuropathy and neuroimmune interactions, including the upregulation of TRPV1 and P2X3 receptors.

Graphical Abstract