Reply to Wasserman et al.: Elucidating the “Triggers” versus “Maintenance” in burning mouth syndrome/oral dysaesthetic and perceptual disorder

Dear Editor,

We are sincerely grateful to Wasserman et al. (1) for their valuable clinical perspectives on our proposed diagnostic framework for burning mouth syndrome (BMS) and the fruitful discussions that followed (2,3). Their letter provides a compelling and much-needed reinforcement of the rationale for a broader diagnostic framework, substantiated by specific and powerful clinical observations that resonate deeply with our own.

The contribution from Wasserman et al. (1) adds a critical layer to the complex “map” of BMS and oral dysaesthetic and perceptual disorder (ODPD) that we are collectively trying to chart. If our initial proposal sketched the general contours of this territory and the commentary by Musella et al. (3) clarified its major topography, the present letter illuminates the very “headwaters” of the symptomatic experience – the triggers from which the river of symptoms begins to flow, as well as the underlying “geology” of the maintenance mechanisms that keep it flowing.

Of particular interest is their observation of “instantaneous onset” following psychologically significant events, such as those in a sexual context or involving chemical exposures, which they posit suggests a powerful psychogenic component. We would further emphasize the notable overlap between such psychogenic triggers and other common initiating events, such as dental procedures. It is not uncommon for symptoms to begin immediately following a dental procedure, which can act as both physical and psychological stressors. This addition reinforces the concept that a variety of significant, localized events can initiate the complex cascade of symptoms we classify as BMS/ODPD. Furthermore, we consider that this phenomenon forces us to confront a fundamental etiological question in BMS/ODPD, akin to the classic chicken-and-egg problem (4).

Specifically, one can ask whether the precipitating psychophysical event merely acts as a “trigger” that unmasks a pre-existing neurobiological or psychological vulnerability, or instead induces persistent neuroplastic changes, resulting in a functional reorganization of central and peripheral neural circuits, capable of generating an autonomously maintained neuropathological state (“hardware” alteration).

Experimental data demonstrate that BMS/ODPD symptoms may fluctuate based on attentional and cognitive demands, as shown by Wasserman et al. (1), suggesting central sensitization mechanisms with dysfunction in frontoparietal and limbic networks responsible for top-down control of nociceptive processing (5,6). This dynamic interplay between “software” (emotional state, executive control, attentional gating) and “hardware” (nociceptive pathways, synaptic plasticity, microstructural white-matter changes) likely constitutes the core pathophysiology of BMS/ODPD.

From this perspective, the four revisions proposed by Wasserman et al. (1) are not only logical, but also essential for the future of the ICHD-4 and ICOP classifications. We explicitly endorse their suggestions:

Instantaneous onset: We fully support waiving the three-month duration criterion when a clear, precipitating event is identified. This would align the diagnosis more closely with the clinical reality for a significant subset of patients.

Intermittent presentation: Incorporating symptomatic variability into the diagnostic criteria is crucial for acknowledging that this condition is a dynamic process, not a static entity.

Expanded location: The inclusion of the vermilion border is a pragmatic and necessary step, prioritizing the patient's holistic symptomatic experience over rigid anatomical demarcations.

Broader symptom expression: The proposal to include presentations like “restless mouth syndrome” within the ODPD spectrum perfectly aligns with our goal of creating a more comprehensive and inclusive framework (7).

The letter from Wasserman et al. (1) powerfully reinforces our conviction that BMS/ODPD should be conceptualized not as an idiopathic “burning” of the mucosa, but as a dynamic neuropsychiatric condition involving a complex interplay of triggers, perceptual distortion, and central nervous system modulation.

We are confident that this vibrant and constructive dialogue will lead to a better future for the patient populations who have long been underserved by overly restrictive definitions. We thank our colleagues again for their insightful contribution.