Burning mouth syndrome and oral dysaesthetic/perceptual symptoms: Toward clinically actionable boundaries

Dear Editor,

We read with great interest the editorial by Musella et al., which proposes oral dysaesthetic and perceptual disorder (ODPD) as a tentative multidimensional framework for patients with chronic idiopathic oral symptoms that are not adequately captured by the current burning-centred definition of burning mouth syndrome (BMS). ¹ We support this attempt to recognize patients with disabling oral dysaesthetic and perceptual symptoms who remain diagnostically underserved. However, we would frame ODPD as a descriptive research construct that complements, rather than replaces, established BMS terminology. This direction is consistent with our recent proposal that future BMS criteria should move from “burning” alone to “burning or dysaesthetic quality of pain,” thereby retaining BMS while reflecting the clinical reality of patients who describe persistent intraoral pain as stinging, tingling, rasping, or other dysaesthetic sensations. ²

An important distinction is needed here. Xerostomia, dysgeusia, and denture intolerance, the last of which resembles occlusal dysaesthesia, have long been recognized as associated features within glossodynia descriptions ³ ; their presence alone does not require a new diagnostic label. Musella et al. describe xerostomia and dysgeusia as part of broader clinical heterogeneity and the ODPD spectrum, not as mandatory criteria for BMS. ¹ Our proposal is also limited: we do not advocate adding non-painful symptoms to mandatory BMS criteria. Rather, if chronic intraoral pain remains the core complaint, BMS should be retained and its criteria modified by broadening the quality of the core painful symptom from burning alone to burning or dysaesthetic pain. ² ODPD may then be most useful for presentations dominated by non-burning dysaesthesia or perceptual distortion that cannot be accommodated by refined BMS criteria.

A second boundary concerns oral cenesthopathy (OC). In our clinical practice, patients frequently present with overlapping features of BMS and OC, and symptoms such as oral dysmorphism, phantom taste, and oral foreign-body sensation may reasonably be understood as distorted oral perception caused by altered central sensory processing. However, overlap should not be mistaken for diagnostic identity. BMS and OC seem to differ in treatment response and psychiatric comorbidity. For example, oral pain may be the chief complaint at the initial visit, whereas dysgeusia or foreign-body sensations may become more prominent after pharmacotherapy alleviates pain. This sequence suggests that symptom trajectories and treatment responses should be recorded to identify an OC component.

At the same time, caution is necessary regarding the breadth of ODPD. In particular, globus pharyngeus is clinically important and may share perceptual or sensory-processing features with other ODPD-related symptoms. ¹ However, in Japanese dental settings, it lies outside routine dental practice and is more commonly managed through otolaryngological or primary care pathways. We therefore suggest that globus pharyngeus may be best regarded as an adjacent or referral-related manifestation rather than a core dental ODPD phenotype, unless it co-occurs with prominent intraoral dysaesthetic or perceptual symptoms. Similar caution is needed for oral dyskinesia. Although Musella et al. include it within the perceptual dimension, ¹ its primary pathology is motor dysregulation rather than a perceptual disorder. Nevertheless, some patients with BMS or OC perform chewing-like oral movements as a coping behavior in response to oral discomfort. Careful differential assessment is critical before classifying such movements as either a movement disorder or a coping behavior associated with perceptual disturbance.

We agree with Musella et al. that distorted oral perception may reflect altered central processing of sensory inputs. ¹ This view is consistent with previous single-photon emission computed tomography (SPECT) findings in patients with OC, which suggest altered regional brain perfusion and support the hypothesis that cenesthopathic oral symptoms involve central sensory processing. ⁴ By contrast, our unpublished SPECT observations in patients with BMS have not shown comparably distinctive features and have instead shown marked heterogeneity. These findings have not yet been translated into clinically deployable diagnostic classifiers or treatment-selection tools. Therefore, ODPD should not become an undifferentiated umbrella for all unexplained oral complaints. Its value will be greatest if used to map dysaesthetic and perceptual dimensions while preserving BMS, OC, motor disorders, and psychiatric phenotypes as clinical categories.

Finally, structured instruments such as the Oral Dysesthesia Rating Scale may help operationalize symptom quality, functional impairment, and daily-life impact. ⁵ We therefore support ODPD as a hypothesis-generating framework, while emphasizing that future ICHD and ICOP revisions should first ask whether refined BMS criteria can adequately capture dysaesthetic oral pain and then define which residual presentations require a broader perceptual or cenesthopathic framework. The aim should be not only to name what patients feel, but to identify the most clinically appropriate diagnostic pathway and individualized treatment strategy for each phenotype.