Burning mouth syndrome is a rare disorder of a complex nature that significantly impairs the life quality of those affected. Its clinical features are characterized by oral burning sensation as well as xerostomia, dysgeusia, and halitosis. While various etiological factors have been proposed over the last few decades, recent studies have focused on understanding its pathophysiology as a neuropathic disorder that involves both peripheral and central neuropathy. In addition, other explanations of BMS pathology have also been proposed, including hormonal disturbances during and after menopause, immunological challenges, and psychological distress. Despite these research efforts, the etiology of BMS remains elusive, awaiting further investigations. The scope of this review includes the current understanding of BMS pathology and animal models developed for deciphering molecular mechanisms underlying the development and progression of BMS. The overview of recent research efforts and our knowledge of BMS pathology will provide an opportunity to evaluate the status of our understanding of BMS and its future perspective in improving the life quality of those affected by this rather intractable disorder.

The limitation of markers for chronic oral diseases such as oral lichen planus (OLP) and burning mouth syndrome (BMS) is a diagnostic challenge for clinicians. The pathogenesis of OLP and BMS is not yet fully understood. Therefore, diagnoses are mainly based on the observation of clinical features and history, rather than established markers. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are used to determine the state of inflammation; however, these markers have some limitations. Recently, a new inflammatory marker, pentraxin-3 (PTX3), has been identified in other systemic inflammatory diseases. PTX3 is a member of the pentraxin family and is classified as a long pentraxin. PTX3 is found in various human tissues, whereas the classical short pentraxin, CRP, is secreted only in the liver. PTX3 is a marker of autoimmune diseases and periodontitis. However, there are no studies on PTX3 in OLP and BMS; therefore, we sought to determine if PTX3 can be a diagnostic marker for OLP and BMS. PTX3 was found to be correlated with other inflammatory markers, suggesting its diagnostic value for inflammatory oral diseases. We also found that the PTX3 levels were lower in patients with OLP and BMS. ESR levels were elevated in the OLP and BMS groups, but CRP levels were not. Despite these associations, no correlation was found between PTX3 expression and other known clinical features of OLP and BMS. We suggest that PTX3 plays a role in the immunological and neurological pathways involved in the complex pathogenesis of OLP and BMS.

Background: The purpose of this study was to determine the bidirectional association between burning mouth syndrome (BMS) and depression disorders. Methods: A total of 854 pairs of BMS and 58 999 pairs of depression disorders matched 1:1 for age and sex were analyzed using conditional logistic regression models, which were adjusted for potential confounding factors. Results: Bidirectional analysis found that BMS was associated with depression disorders (odds ratio=4.64, P < 0.001) and depression disorders was also significantly associated with BMS (odds ratio=2.97, P < 0.001). Conclusion: These findings indicate a significant bidirectional association between BMS and depression disorders. The odds ratios suggest that BMS is a stronger predictor for incidence of depression disorders than depression disorders predicting incidence of BMS. Given this retrospective cohort design, the mechanisms underlying the association between BMS and depression disorders are not directly analyzed. Therefore, further investigation are needed to analyze the causality between BMS and depression disorders.