Mechanisms Underlying Burning Mouth Syndrome and Occlusal Dysesthesia: Shared and Distinct Pathways of Oral Sensory Dysregulation

ABSTRACT

Background

Burning mouth syndrome (BMS) and occlusal dysesthesia (OD) are chronic oral sensory disorders that present without evident local pathology yet frequently cause substantial diagnostic and therapeutic challenges in oral medicine practice. Although both conditions may clinically overlap, their mechanistic relationship remains poorly understood.

Objective

To compare the pathophysiological mechanisms of BMS and OD, examine their potential overlap, and propose a hypothesis‐generating conceptual framework of oral sensory dysregulation.

Methods

Relevant literature was identified through searches of PubMed, Scopus, and Google Scholar using combinations of the terms “burning mouth syndrome,” “occlusal dysesthesia,” “phantom bite syndrome,” “central sensitization,” and “small fibre neuropathy.” Additional studies were identified through manual review of reference lists. Priority was given to clinically and mechanistically relevant neuroimaging, psychophysical, and pharmacological studies. This review was conducted as a narrative synthesis rather than a systematic review.

Results

Current evidence suggests that BMS involves trigeminal small‐fibre dysfunction with subsequent central nociceptive amplification, whereas OD predominantly reflects maladaptive central processing of otherwise intact periodontal mechanoreceptive input. Despite these mechanistic differences, both conditions demonstrate overlapping features including affective comorbidity, sensory hypervigilance, altered prefrontal and frontostriatal involvement, and responsiveness to centrally acting pharmacological agents. Clinical overlap between BMS and OD has also been reported, particularly in treatment‐refractory presentations.

Conclusion

BMS and OD may represent distinct but partially overlapping phenotypes within a broader framework of oral sensory dysregulation. Recognition of shared and divergent mechanisms may improve differential diagnosis, support mechanism‐informed pharmacological management, and guide future hypothesis‐driven research in oral medicine.

Oral sensory dysregulation framework. Burning mouth syndrome and occlusal dysesthesia are presented as distinct but partially overlapping oral sensory dysregulation phenotypes. Their divergent pathways—bottom‐up nociceptive amplification and top‐down modulatory failure—may converge through shared frontostriatal, affective, and hypervigilance‐related vulnerability mechanisms.

1. Introduction

Burning mouth syndrome (BMS) and occlusal dysesthesia (OD) are among the most diagnostically and therapeutically challenging conditions encountered in oral medicine practice. BMS is defined as idiopathic orofacial pain characterized by a daily intraoral burning or dysesthetic sensation recurring for more than 2 h per day over more than 3 months, in the absence of clinically evident causative lesions or systemic conditions sufficient to explain the symptoms [1]. OD, historically described as phantom bite syndrome, is characterized by a persistent perception that the occlusion feels uncomfortable, unstable, or “wrong” despite the absence of objectively verifiable occlusal discrepancy [2]. Both conditions are associated with substantial psychological distress, prolonged diagnostic delay, repeated consultations across multiple dental specialties, and a considerable risk of iatrogenic harm resulting from repeated irreversible dental interventions [2, 3].

Despite these clinical parallels, BMS and OD have largely been investigated as distinct entities. Research on BMS has predominantly focused on neuropathic pain mechanisms, trigeminal small‐fibre dysfunction, and central sensitization [4, 5], whereas OD literature has emphasized maladaptive oral somatosensory processing, occlusal hypervigilance, and impaired central modulation of periodontal mechanoreceptive input [2, 6]. Direct comparison between the two conditions is notably lacking. To date, no study has systematically compared their pathophysiological mechanisms, neurobiological overlap, or implications for pharmacological management within a unified conceptual framework.

This gap is clinically relevant because patients encountered in oral medicine practice may present with symptom profiles spanning both disorders. Direct clinical co‐occurrence of BMS and OD appears uncommon and has been reported only sparsely. In a retrospective cohort of 606 patients with oral somatic delusions/oral cenesthopathy, BMS was recorded as a comorbid psychosomatic dental symptom in 159 patients (26.24%), whereas phantom bite syndrome was recorded in 27 patients (4.46%) [7, 8]. These figures do not represent the prevalence of BMS among patients with OD, nor the frequency of direct BMS–OD overlap. The aim of the present review, however, is not to estimate comorbidity frequency, but to compare partially convergent peripheral and central mechanisms that may contribute to chronic medically unexplained oral sensory symptoms. These observations raise the possibility that at least a subset of patients with chronic oral sensory complaints may share overlapping central mechanisms despite differences in symptom expression.

Current evidence suggests that BMS may involve a combination of peripheral trigeminal small‐fibre dysfunction and altered central nociceptive processing, placing it within a mixed neuropathic–nociplastic pain framework [1, 4, 5]. By contrast, OD is increasingly conceptualized as a disorder of maladaptive central processing in which intact periodontal mechanoreceptive input may be inadequately suppressed or disproportionately weighted by central modulatory systems [2, 6]. Importantly, both disorders appear to involve altered prefrontal and frontostriatal network function, potentially implicating shared disturbances in sensory modulation, attentional weighting, and affective regulation [6, 9, 10, 11].

Rather than representing either identical disorders or entirely unrelated conditions, BMS and OD may therefore constitute distinct but partially overlapping phenotypes within a broader framework of oral sensory dysregulation. Within this framework, the primary difference may lie in the sensory modality predominantly affected—nociceptive and thermal dysesthesia in BMS versus proprioceptive and mechanosensory dysesthesia in OD—and whether dysregulation emerges primarily through bottom‐up or top‐down mechanisms.

The aim of this narrative review is to synthesize current evidence regarding the pathophysiology of BMS and OD, provide a structured mechanistic comparison between the two conditions, examine the clinical significance of their overlap, and propose a hypothesis‐generating conceptual framework that may guide future research and clinical management in oral medicine practice.

2. Literature Search Strategy

Relevant literature was identified through searches of PubMed, Scopus, and Google Scholar using combinations of the following keywords: “burning mouth syndrome,” “occlusal dysesthesia,” “phantom bite syndrome,” “central sensitization,” “small fibre neuropathy,” and “oral sensory disorders.” Additional articles were identified through manual review of reference lists from relevant publications. Priority was given to clinically and mechanistically relevant studies, including neuroimaging, psychophysical, and pharmacological investigations. This review was conducted as a narrative synthesis and did not follow systematic review methodology.

3. Pathophysiology of Burning Mouth Syndrome

3.1. Peripheral Mechanisms: Trigeminal Small‐Fibre Dysfunction

Current evidence suggests that peripheral trigeminal small‐fibre dysfunction plays an important role in the pathophysiology of BMS [4, 12]. Histopathological studies of tongue biopsy specimens have demonstrated reduced intraepithelial nerve fibre density and morphological abnormalities involving thinly myelinated Aδ fibres and unmyelinated C fibres in patients with BMS [12, 13]. These findings support the concept that at least a subset of BMS represents a form of trigeminal small‐fibre neuropathy.

In addition to structural alterations, molecular changes associated with peripheral sensitization have also been reported. Increased expression of transient receptor potential vanilloid‐1 (TRPV1), purinergic P2X3 receptors, and voltage‐gated sodium channels have been identified in peripheral nerve fibres of BMS patients [12, 14]. Such changes may contribute to enhanced nociceptor excitability and spontaneous burning pain despite the absence of clinically visible mucosal pathology.

Interestingly, peripheral structural loss appears to coexist with functional sensory amplification. Quantitative sensory testing (QST) studies have demonstrated abnormalities in thermal detection and pain thresholds in BMS patients, particularly involving cold detection and heat pain processing [15, 16]. These findings suggest a paradoxical sensory state characterized by partial deafferentation alongside hyperexcitability of residual nociceptive pathways.

However, peripheral neuropathic findings alone are insufficient to explain the full clinical phenotype of BMS. The severity of spontaneous burning pain frequently exceeds the degree of measurable peripheral dysfunction, and symptom fluctuation is strongly influenced by emotional stress, attention, and affective state [5, 17]. These observations have increasingly shifted attention toward central mechanisms involved in pain amplification and sensory modulation.

3.2. Central Mechanisms: Central Sensitization and Altered Pain Modulation

Beyond peripheral trigeminal dysfunction, accumulating evidence supports an important role for altered central nociceptive processing in BMS [5, 9, 17]. Functional and structural neuroimaging studies have demonstrated abnormalities involving regions associated with pain modulation, affective regulation, and salience processing, including the prefrontal cortex, anterior cingulate cortex, insula, thalamus, and basal ganglia [5, 9, 10].

Among these findings, alterations involving the ventromedial prefrontal cortex (vmPFC) have attracted particular attention. Reduced grey matter volume and altered functional connectivity between the vmPFC and limbic regions, including the amygdala, have been reported in patients with chronic BMS [9]. Because the vmPFC represents an important component of the descending pain modulatory system, these findings have been interpreted as potentially reflecting impaired top‐down regulation of nociceptive processing.

Psychophysical studies further support the presence of abnormal central pain modulation. Conditioned pain modulation (CPM), an experimental measure of descending inhibitory function, has shown inconsistent but frequently impaired responses in BMS patients [18]. In addition, several studies suggest that enhanced pain facilitation and temporal summation may contribute more prominently than simple inhibitory failure [18]. Together, these observations support the concept of amplified central nociceptive gain within trigeminal pain networks.

Dopaminergic dysfunction has also been implicated in BMS pathophysiology. Positron emission tomography (PET) studies have demonstrated altered dopamine D1 and D2 receptor binding within the basal ganglia of BMS patients [10]. Although the precise significance of these findings remains uncertain, they suggest that altered frontostriatal modulation may contribute not only to pain amplification but also to the affective and attentional dimensions of chronic oral dysesthesia.

3.3. BMS Within a Neuropathic‐Nociplastic Framework

The International Classification of Orofacial Pain (ICOP) currently classifies BMS as idiopathic orofacial pain with or without somatosensory changes [1]. Increasingly, however, BMS has been discussed within a mixed neuropathic–nociplastic framework [5, 17].

The neuropathic component is supported by evidence of trigeminal small‐fibre dysfunction, altered thermal sensory processing, and peripheral nociceptor sensitization [12, 13, 14, 15, 16]. Simultaneously, the nociplastic dimension is reflected by enhanced central pain facilitation, altered affective modulation, widespread sensory amplification, and the absence of a clear correlation between peripheral findings and symptom severity [5, 17, 18].

Importantly, this dual framework may help explain the considerable clinical heterogeneity observed in BMS. Some patients exhibit predominantly neuropathic characteristics with prominent thermal sensory abnormalities, whereas others demonstrate greater affective burden, somatic hypervigilance, and features suggestive of centrally mediated sensory amplification [5, 19]. Such heterogeneity may partially account for the inconsistent treatment responses reported across pharmacological studies and suggests that BMS is unlikely to represent a single mechanistically uniform disorder.

Furthermore, emerging concepts from predictive coding and salience processing models may provide an additional interpretive framework for BMS [20]. Within this perspective, persistent oral burning sensations may reflect maladaptive central assignment of salience to ongoing trigeminal sensory input, resulting in sustained attention toward otherwise non‐threatening oral sensations. Although still speculative, such models provide a conceptual bridge between neuropathic dysfunction, central sensitization, and affective amplification in chronic oral dysesthesia.

4. Pathophysiology of Occlusal Dysesthesia

4.1. Peripheral Substrate: Intact Mechanoreception and Altered Sensory Interpretation

In contrast to BMS, current evidence does not support consistent structural peripheral neuropathy as the primary mechanism underlying OD [2, 6]. Rather, OD appears to involve abnormal interpretation and modulation of otherwise physiologic periodontal mechanosensory input.

The periodontal ligament (PDL) contains highly specialized mechanoreceptors capable of detecting minimal occlusal interference and fine alterations in tooth loading [6]. Under normal conditions, these mechanosensory signals are continuously integrated and filtered within central sensorimotor networks, allowing stable perception of occlusion despite minor physiological variations in tooth contact [6].

Patients with OD, however, appear to assign excessive significance to otherwise clinically insignificant occlusal input. Munakata and colleagues demonstrated that although occlusal recognition thresholds were similar between OD patients and healthy controls, occlusal discomfort thresholds were significantly reduced in the OD group [21]. In other words, OD patients retained normal ability to detect interocclusal stimuli, but were substantially more likely to perceive these stimuli as uncomfortable or abnormal.

This distinction is mechanistically important. The findings suggest that the primary abnormality in OD may not lie in peripheral transduction itself, but rather in the central interpretation and affective weighting assigned to incoming mechanosensory signals. The peripheral input remains largely intact; what appears altered is the central system responsible for contextualizing and suppressing that input within the background of normal oral sensation.

The clinical behaviour of OD further supports this interpretation. Symptoms are often exacerbated by increased attention toward occlusion, repeated checking behaviours, tongue positioning against the teeth, or repeated dental interventions intended to “correct” the perceived discrepancy [2, 22]. Such observations are consistent with maladaptive amplification of oral somatosensory salience rather than with structural occlusal pathology itself.

4.2. Central Mechanisms: Maladaptive Sensory Processing and Impaired Top‐Down Modulation

Increasingly, OD is conceptualized as a disorder of maladaptive central sensory processing rather than as a primary occlusal abnormality [2, 6, 22]. Several authors have proposed that altered top‐down modulation, excessive sensory hypervigilance, and impaired suppression of periodontal mechanosensory input contribute to persistent occlusal discomfort despite objectively stable occlusion [2, 6, 22].

The most direct neurophysiological evidence supporting this concept comes from functional near‐infrared spectroscopy (fNIRS) studies. Ono and colleagues evaluated prefrontal cortical hemodynamic responses during experimentally induced minimal occlusal interference and demonstrated persistent prefrontal activation patterns in OD patients that were not observed in healthy controls [11]. Notably, changes in deoxygenated haemoglobin within the frontal pole region discriminated OD patients from controls with relatively high accuracy.

Although the interpretation of fNIRS findings remains preliminary, these observations suggest altered prefrontal involvement in the modulation and contextualization of oral mechanosensory input. The prefrontal cortex plays a central role in attentional regulation, salience assignment, and descending sensory modulation [23]. Persistent activation within these regions may therefore reflect impaired suppression of otherwise physiologic occlusal sensory signals.

Additional support for central involvement comes from functional imaging case reports demonstrating normalization of asymmetric frontal cerebral blood flow following successful pharmacological treatment of phantom bite syndrome [24]. Although such findings suggest central involvement, they should be interpreted with caution. Altered regional cerebral blood flow on SPECT cannot be regarded as direct evidence of dysfunction in a specific large‐scale network such as the salience network. These findings may instead reflect altered central sensory appraisal, attentional weighting, or contextual modulation of occlusal input rather than isolated abnormalities of dental occlusion itself.

From a predictive coding perspective, OD may also be conceptualized as a disorder of persistent sensory prediction error [20]. Under normal circumstances, minor discrepancies between expected and actual occlusal input are rapidly integrated and dismissed as clinically irrelevant. In OD, however, these small discrepancies may be repeatedly assigned excessive salience, resulting in persistent attention toward occlusion and an inability to achieve perceptual adaptation. While still hypothetical, this framework provides a potentially useful bridge between neurophysiological findings, hypervigilance, and the remarkable persistence of symptoms observed in OD patients.

4.3. Dopaminergic Modulation and Frontostriatal Involvement

Accumulating observations further suggest that frontostriatal dopaminergic dysfunction may contribute to symptom persistence in OD [21, 24]. Interest in this possibility has largely emerged from pharmacological observations involving aripiprazole and related centrally acting agents.

Several case reports and small clinical series have described symptomatic improvement in OD following treatment with combinations including aripiprazole, mirtazapine, or serotonergic antidepressants [21, 24]. Although such evidence remains low in quality, the repeated observation that dopamine‐modulating agents may reduce occlusal discomfort has attracted increasing attention.

Importantly, the significance of aripiprazole in OD may extend beyond its conventional classification as an atypical antipsychotic. Aripiprazole acts as a partial dopamine D2/D3 receptor agonist while also modulating serotonergic transmission [25]. Similar pharmacological strategies have been employed in obsessive‐compulsive disorder (OCD), particularly in patients with intrusive cognitive fixation and repetitive checking behaviours resistant to serotonergic monotherapy [19].

OD shares certain phenomenological features with these hypervigilant and repetitive cognitive states, including persistent attentional fixation on occlusion, repeated monitoring of tooth contact, and difficulty disengaging from oral sensory perception [22, 26]. Importantly, this comparison should not be interpreted as implying that OD is simply a psychiatric disorder or an odontological variant of OCD. Rather, it raises the possibility that partially overlapping frontostriatal mechanisms involved in salience attribution, attentional fixation, and sensory modulation may contribute to symptom persistence across multiple conditions.

Interestingly, altered dopaminergic signalling has also been independently implicated in BMS through PET studies demonstrating abnormal dopamine receptor binding within basal ganglia circuits [10]. Taken together, these observations raise the possibility that frontostriatal dysfunction and altered dopaminergic modulation may represent one potential convergence point between BMS and OD, particularly in patients with prominent sensory hypervigilance, affective burden, or treatment‐refractory symptoms.

5. Comparative Analysis and the Proposed Conceptual Framework

5.1. Shared Features and Mechanistic Divergence

When considered side by side, BMS and OD reveal a striking combination of clinical overlap and mechanistic divergence. Both conditions involve persistent oral sensory complaints occurring in the absence of clinically identifiable dental or mucosal pathology sufficient to explain symptom severity [1, 2]. Both are associated with substantial psychological distress, prolonged diagnostic delay, repeated healthcare utilization, and risk of iatrogenic worsening through unnecessary or repeated interventions [2]. Furthermore, both conditions appear to involve altered central modulation of trigeminal sensory processing [5, 6, 9, 22].

Despite these similarities, the dominant sensory modality and direction of dysregulatory processing differ considerably between the two disorders. The major mechanistic similarities and differences between BMS and OD are summarized in Table 1.

TABLE 1.

Proposed mechanistic comparison between burning mouth syndrome and occlusal dysesthesia.

Feature	Burning mouth syndrome (BMS)	Occlusal dysesthesia (OD)
Primary symptom	Burning oral pain	Persistent occlusal discomfort
Dominant sensory modality	Nociceptive/thermal dysesthesia	Mechanosensory/proprioceptive dysesthesia
Peripheral findings	Small‐fibre dysfunction	Largely preserved periodontal mechanoreception
Proposed central mechanism	Nociceptive amplification	Impaired top‐down sensory suppression
Directionality model	Bottom‐up nociceptive amplification	Impaired top‐down modulation
Neurobiological regions implicated	Pain matrix, vmPFC, basal ganglia	Prefrontal cortex, frontostriatal circuits
Behavioural features	Pain amplification, affective distress	Occlusal hypervigilance, repetitive checking
Proposed pharmacological focus	Peripheral and central nociceptive modulation	Central sensory weighting and dopaminergic modulation

Abbreviation: vmPFC, ventromedial prefrontal cortex.

In BMS, current evidence supports a model involving peripheral trigeminal small‐fibre dysfunction accompanied by amplification of nociceptive processing within central pain networks [4, 12, 17]. Partial deafferentation, peripheral sensitization, and enhanced central facilitation together contribute to persistent burning pain and thermal dysesthesia. Within this framework, BMS may be conceptualized primarily as a disorder of nociceptive amplification.

In OD, by contrast, peripheral periodontal mechanoreception appears relatively preserved [11]. The primary disturbance instead appears to involve maladaptive interpretation and insufficient suppression of otherwise physiologic mechanosensory input [2, 6, 22]. OD may therefore be conceptualized primarily as a disorder of altered proprioceptive or mechanosensory processing.

Importantly, both disorders may involve dysfunction within prefrontal and frontostriatal modulatory networks [9, 10, 11, 21, 24]. In BMS, altered connectivity within pain‐modulatory and affective networks may contribute to enhanced nociceptive gain [5, 9, 10]. In OD, abnormal prefrontal activation patterns may reflect impaired contextual modulation and excessive salience assignment toward occlusal sensation [11, 23]. Thus, although the sensory domains differ, both conditions may involve disturbance within broader systems responsible for sensory filtering, salience attribution, and affective modulation.

The mechanistic distinction proposed here should not be interpreted as indicating mutually exclusive processes. Rather, the primary difference may reflect which sensory system bears the predominant burden of dysregulation and how the central nervous system responds to incoming trigeminal sensory information.

5.2. Clinical Overlap and Related Oral Sensory Disorders

Although BMS and OD are traditionally treated as distinct disorders, direct clinical overlap between them has been reported only sparsely and appears uncommon in routine practice. As noted above, the previously cited 26% figure refers to BMS recorded as a comorbid psychosomatic dental symptom within a cohort of patients with oral somatic delusions/oral cenesthopathy and does not represent BMS prevalence among OD patients or the frequency of direct BMS–OD overlap [7, 8]. The present review therefore treats direct BMS–OD overlap as uncommon and insufficiently characterized, rather than as a common comorbid presentation.

This overlap is clinically meaningful. Patients presenting with both burning dysesthesia and persistent occlusal discomfort are frequently among the most diagnostically challenging cases encountered in oral medicine practice. Such patients often exhibit prolonged symptom duration, high levels of anxiety and somatic hypervigilance, repeated unsuccessful dental treatment histories, and limited response to single‐modality pharmacotherapy [7, 19].

The coexistence of BMS and OD raises several important mechanistic questions. One possibility is that shared vulnerability factors—including affective dysregulation, altered salience processing, anxiety‐related sensory hypervigilance, and frontostriatal dysfunction—predispose certain individuals to develop dysregulation across multiple oral sensory domains simultaneously [10, 20, 23]. Under this model, burning pain and occlusal discomfort would represent different phenotypic expressions of partially overlapping central dysfunction.

Another possibility is temporal interaction between the two disorders. Chronic nociceptive amplification in BMS may progressively alter attentional and modulatory systems involved in oral sensory filtering, thereby lowering the threshold for development of persistent occlusal awareness. Conversely, chronic hypervigilance toward occlusion in OD may secondarily amplify sensory attention toward other oral sensations, including burning or dysesthetic symptoms. At present, however, longitudinal data addressing temporal sequencing between the two conditions remain entirely lacking.

Importantly, overlap between BMS and OD may also help explain treatment resistance in certain patients. Individuals with mixed symptom profiles may respond poorly to therapeutic strategies targeting only one mechanistic domain while leaving concurrent sensory dysregulation unaddressed.

5.3. Toward a Conceptual Framework of Oral Sensory Dysregulation

Taken together, current evidence raises the possibility that BMS and OD may represent distinct but partially overlapping phenotypes within a broader framework of oral sensory dysregulation (Figure 1), and the proposed mechanistic pathways underlying BMS and OD are illustrated in Figure 2.

FIGURE 1.

Proposed conceptual framework of oral sensory dysregulation. Burning mouth syndrome (BMS) and occlusal dysesthesia (OD) are conceptualized as distinct but partially overlapping phenotypes involving altered central trigeminal sensory modulation. BMS predominantly involves nociceptive and thermal dysesthesia associated with trigeminal small‐fibre dysfunction and central nociceptive amplification, whereas OD predominantly involves mechanosensory and proprioceptive dysesthesia associated with altered attentional weighting and impaired top‐down modulation of periodontal mechanoreceptive input. Shared abnormalities involving frontostriatal dysfunction, affective regulation, and sensory hypervigilance may contribute to overlap phenotypes and treatment‐refractory presentations. The figure is a schematic representation intended to illustrate a conceptual framework and is not intended as a definitive mechanistic model.

FIGURE 2.

Proposed mechanistic pathways underlying burning mouth syndrome (BMS) and occlusal dysesthesia (OD). In BMS, peripheral trigeminal small‐fibre dysfunction and sensitization may contribute to enhanced central nociceptive gain and burning dysesthesia. In OD, intact periodontal mechanoreceptive input may become disproportionately amplified through impaired contextual modulation, hypervigilance, and increased attentional weighting. Although the predominant pathways differ, both conditions may involve altered modulation within prefrontal and frontostriatal networks. BMS, burning mouth syndrome; OD, occlusal dysesthesia; PDL, periodontal ligament; vmPFC, ventromedial prefrontal cortex; TRPV1, transient receptor potential vanilloid 1; P2X3, purinergic receptor P2X3; fNIRS, functional near‐infrared spectroscopy; Aδ, A‐delta fibre; C, C fibre. Arrows (↑) indicate upregulation.

Within this proposed framework, the defining feature is not simply the presence of chronic oral symptoms, but dysfunction in the central processing, modulation, and contextualization of trigeminal sensory input in the absence of overt structural pathology sufficient to explain symptom severity. The primary difference between BMS and OD may therefore lie in the predominant sensory modality involved and whether dysregulation emerges primarily through bottom‐up or top‐down mechanisms.

In BMS, peripheral trigeminal dysfunction and partial deafferentation may contribute to increased central nociceptive gain, resulting predominantly in burning pain and thermal dysesthesia [4, 5, 12]. In OD, intact mechanoreceptive input may instead become excessively amplified through impaired top‐down modulation, abnormal salience assignment, and persistent attentional fixation toward occlusion [2, 6, 20, 22].

Importantly, these mechanisms are unlikely to exist in complete isolation. Shared abnormalities involving frontostriatal modulation, affective processing, and sensory hypervigilance may create a common neurobiological vulnerability upon which different oral sensory phenotypes emerge [10, 20, 23]. Under such a model, BMS and OD would not be considered identical disorders, but neither would they be viewed as entirely unrelated entities.

As illustrated conceptually in Figure 1, the proposed framework does not imply that BMS and OD represent a single disorder. Rather, it suggests partially overlapping disturbances in trigeminal sensory modulation expressed through different sensory modalities. BMS predominantly involves nociceptive and thermal dysesthesia associated with peripheral small‐fibre dysfunction and central nociceptive amplification, whereas OD predominantly involves mechanosensory and proprioceptive dysesthesia associated with impaired top‐down modulation and a putative alteration in the contextual weighting of occlusal input.

This framework should not be interpreted as implying that BMS and OD are the only relevant conditions, or that they represent proven endpoints of a single disease continuum. In psychosomatic dentistry, the broader category of medically unexplained oral symptoms/syndromes has been used to encompass conditions such as BMS, atypical odontalgia, phantom bite syndrome, oral cenesthopathy, and halitophobia [27]. The present framework builds on this broader concept and is not intended to replace it or to establish a new diagnostic category; rather, it offers a mechanism‐oriented comparison of two of its members. Persistent idiopathic dentoalveolar pain and persistent idiopathic facial pain may likewise be considered adjacent idiopathic orofacial pain conditions, rather than direct components of the category cited above, that could share partially overlapping peripheral and central mechanisms. The present review focuses on BMS and OD because they represent two clinically recognizable prototypes of oral sensory disturbance—burning pain and altered occlusal perception—while acknowledging that future work should clarify their relationship to these other idiopathic oral sensory and pain disorders.

This framework may also help explain the considerable heterogeneity observed clinically within both conditions. Some patients may present with predominantly neuropathic or nociceptive features, whereas others exhibit stronger affective, hypervigilant, or obsessive‐ruminative characteristics. Still others may demonstrate mixed phenotypes involving both burning dysesthesia and persistent occlusal discomfort.

Although highly preliminary, the proposed framework generates several testable predictions. If BMS and OD share partially overlapping central mechanisms, future neuroimaging studies using standardized protocols may reveal graded rather than categorical differences across BMS‐only, OD‐only, and comorbid patient groups. Similarly, pharmacological responsiveness may correlate more closely with mechanistic phenotype than with traditional diagnostic labels alone.

At present, however, this framework should be regarded as a hypothesis‐generating conceptual model rather than an established pathophysiological mechanism. Prospective clinical characterization studies, multimodal neuroimaging investigations, and phenotype‐stratified treatment trials will be required to determine whether this proposed relationship reflects true shared neurobiology or merely superficial clinical overlap.

6. Clinical Implications for Oral Medicine Practice

6.1. Differential Diagnosis: Toward a Mechanism‐Informed Approach

The proposed framework has several practical implications for oral medicine clinicians. Traditionally, both BMS and OD have been diagnosed largely through exclusion, requiring the absence of identifiable dental, mucosal, systemic, or radiographic pathology sufficient to explain symptoms [1, 2]. While exclusion of secondary causes remains essential, the present framework suggests that a mechanism‐informed approach may provide greater clinical utility than diagnosis based solely on elimination.

Several clinical features may assist in distinguishing the predominant sensory phenotype. Key differential characteristics between BMS and OD are summarized in Table 2.

TABLE 2.

Differential clinical features between burning mouth syndrome and occlusal dysesthesia.

Clinical feature	Burning mouth syndrome (BMS)	Occlusal dysesthesia (OD)
Primary complaint	Burning oral pain	Persistent occlusal incongruity or discomfort
Main sensory domain	Thermal/nociceptive	Mechanosensory/proprioceptive
Typical location	Tongue, oral mucosa	Occlusion, tooth contact
Dysgeusia/xerostomia	Common	Not typically reported
Effect of eating	Often partially relieves symptoms	Often increases occlusal awareness
Occlusal fixation	Usually absent or secondary	Prominent
Repeated dental treatment history	Variable	Common
Behavioural characteristics	Pain‐related distress	Hypervigilance, repetitive checking
Peripheral findings	Small‐fibre dysfunction may be present	No consistent peripheral neuropathic findings

BMS most commonly presents with burning, scalding, tingling, or dysesthetic sensations involving the tongue, palate, or other oral mucosal surfaces [1]. Symptoms frequently fluctuate throughout the day and may partially improve during eating or oral function [1, 5]. Dysgeusia and xerostomia are also commonly reported [1, 5]. In contrast, OD is characterized primarily by a persistent perception of occlusal incongruity—a sense that the bite feels uncomfortable, unstable, or uneven—despite the absence of clinically meaningful occlusal discrepancy [2]. Symptoms are often intensified during chewing, tooth contact, tongue checking, or focused attention toward occlusion [2, 22].

Behavioural patterns may also provide clinically useful clues. Patients with OD frequently demonstrate repeated monitoring of tooth contact, requests for repeated occlusal adjustment, extensive prior dental treatment histories, or persistent dissatisfaction despite technically adequate restorative or orthodontic outcomes [2, 22]. By contrast, BMS patients more commonly emphasize spontaneous burning pain, mucosal discomfort, or sensory disturbance rather than mechanical occlusal concerns [5].

The present framework additionally highlights the importance of recognizing overlap presentations. Patients reporting both persistent oral burning and fixation on occlusal sensation may represent a clinically distinct subgroup characterized by heightened sensory hypervigilance, greater affective burden, and increased risk of treatment resistance [7, 19]. In such patients, strict categorization into either BMS or OD alone may oversimplify the clinical picture and inadvertently delay appropriate multidisciplinary management.

Where available, quantitative sensory testing (QST) and psychophysical assessment may further assist mechanistic characterization [11, 15, 16]. Thermal sensory abnormalities may support neuropathic involvement in BMS, whereas altered discomfort thresholds despite preserved recognition thresholds may support maladaptive sensory processing in OD [11]. However, such testing remains adjunctive rather than diagnostic and should be interpreted within the broader clinical context.

6.2. Pharmacological Implications

The mechanistic distinction between BMS and OD may also carry important implications for pharmacological management. Proposed treatment considerations based on predominant mechanistic phenotype are summarized in Table 3.

TABLE 3.

Proposed pharmacological considerations based on predominant mechanistic phenotype.

Predominant phenotype	Proposed mechanistic target	Potential therapeutic approaches a
Neuropathic‐predominant BMS	Peripheral sensitization and central nociceptive amplification	Topical clonazepam, SNRIs, TCAs, gabapentinoids b , alpha‐lipoic acid
Hypervigilant/affective BMS	Central pain modulation and affective amplification	SNRIs, TCAs, psychological interventions
OD with prominent sensory fixation	Central sensory weighting and descending modulation	SNRIs, mirtazapine
OD with obsessive‐ruminative features	Frontostriatal modulation	Aripiprazole augmentation strategies
Mixed BMS‐OD phenotype	Multidomain sensory dysregulation	Combined neuropathic and central modulation approaches

Abbreviations: BMS, burning mouth syndrome; OD, occlusal dysesthesia; SNRI, serotonin–norepinephrine reuptake inhibitor; TCA, tricyclic antidepressant.

^a These approaches are illustrative and should be individualized; the evidence base, particularly for OD, remains limited and is largely derived from small studies and case reports.

^b Evidence supporting gabapentinoids in BMS remains limited and heterogeneous.

In BMS, pharmacological treatment has traditionally focused on neuropathic pain modulation and reduction of central nociceptive amplification [5, 28]. Topical clonazepam remains among the most consistently supported therapeutic approaches and may reduce peripheral and central sensory hyperexcitability [29]. Tricyclic antidepressants, serotonin‐norepinephrine reuptake inhibitors (SNRIs), gabapentinoids, and alpha‐lipoic acid have also demonstrated varying degrees of efficacy across studies [29].

Within the present framework, patients with prominent thermal sensory abnormalities, spontaneous burning pain, and widespread nociceptive amplification may represent a more neuropathic‐predominant BMS phenotype potentially responsive to neuropathic pain‐oriented strategies.

In OD, by contrast, pharmacological management may rely more heavily on modulation of central salience processing, affective hypervigilance, and descending sensory modulation [2, 6]. Several reports have described improvement with combinations involving SNRIs, mirtazapine, or aripiprazole [21, 24]. Although evidence remains limited to small series and case reports, these observations raise the possibility that certain OD phenotypes may respond preferentially to modulation of frontostriatal and attentional regulatory systems.

Importantly, this does not imply that OD should be regarded primarily as a psychiatric disorder. Rather, centrally acting pharmacological approaches may be effective because the dominant dysfunction appears to involve maladaptive sensory processing and salience attribution rather than structural occlusal abnormality itself.

The present framework may be particularly useful in treatment‐refractory overlap cases. Patients exhibiting both burning dysesthesia and persistent occlusal fixation may require broader modulation of sensory amplification, affective distress, and attentional hypervigilance simultaneously rather than sequential treatment directed toward only one symptom domain [7].

Equally important is recognition of what should be avoided. Repeated irreversible occlusal interventions—including extensive occlusal adjustment, repeated prosthodontic reconstruction, or unnecessary orthodontic retreatment—may reinforce maladaptive sensory attention and perpetuate symptom chronicity in OD [2, 6]. Avoidance of iatrogenic escalation therefore represents a central principle of management.

6.3. Implications for Multidisciplinary Care

Finally, the proposed framework reinforces the importance of multidisciplinary management in chronic oral sensory disorders. Both BMS and OD frequently exist at the intersection of oral medicine, pain medicine, neurology, psychiatry, psychology, and behavioural science [5].

Psychiatric referral should not be framed as dismissal of symptoms or reduction of the disorder to purely psychogenic causation. Rather, involvement of mental health professionals may assist in management of affective distress, maladaptive attentional fixation, sleep disturbance, anxiety, depressive symptoms, and cognitive hypervigilance that may contribute to symptom persistence across both conditions [19, 26].

Similarly, the framework emphasizes the importance of clinician communication. Patients with BMS and OD frequently report invalidation, repeated contradictory explanations, and escalating frustration after multiple unsuccessful dental interventions [2, 3]. A coherent mechanistic explanation acknowledging the reality of altered sensory processing while avoiding unnecessary structural intervention may itself reduce distress and improve therapeutic alliance.

Taken together, these observations suggest that chronic oral sensory disorders may benefit less from increasingly aggressive structural intervention and more from carefully integrated approaches targeting sensory modulation, affective processing, and maladaptive salience attribution simultaneously.

7. Discussion

The present review proposes that BMS and OD may be conceptualized as distinct but partially overlapping phenotypes within a broader framework of oral sensory dysregulation. Although traditionally investigated as separate conditions, both disorders share several striking clinical characteristics, including chronic oral sensory symptoms without sufficient structural pathology, substantial affective burden, prolonged diagnostic trajectories, and vulnerability to iatrogenic escalation [2, 3]. At the same time, the available evidence suggests important mechanistic distinctions involving sensory modality, peripheral contribution, and direction of central dysregulatory processing.

The proposed framework attempts to reconcile these similarities and differences without collapsing the two disorders into a single entity. BMS appears to involve a stronger peripheral neuropathic component, with trigeminal small‐fibre dysfunction contributing to enhanced central nociceptive gain and burning dysesthesia [4, 12, 17]. OD, by contrast, appears to involve maladaptive interpretation and insufficient suppression of otherwise physiologic mechanosensory input [2, 6, 22]. Within this model, BMS predominantly reflects dysregulation within nociceptive and thermal sensory domains, whereas OD predominantly involves proprioceptive and mechanosensory dysregulation.

Importantly, however, both disorders appear to involve abnormalities within broader systems responsible for salience attribution, sensory filtering, affective modulation, and attentional regulation [9, 10, 11, 20, 23]. This overlap may help explain why some patients exhibit mixed symptom profiles involving both burning dysesthesia and persistent occlusal discomfort [7]. It may also explain why treatment responses are often heterogeneous and incomplete when therapeutic approaches target only a single mechanistic domain.

The proposed framework additionally aligns with emerging concepts from predictive coding and salience‐processing theories of chronic pain [20]. Under predictive coding frameworks, symptom persistence may arise not solely from peripheral sensory input itself, but from maladaptive weighting of sensory prediction error and excessive attentional allocation toward bodily sensations. Within such a framework, BMS may involve persistent attribution of salience to ongoing nociceptive input despite limited peripheral pathology, whereas OD may involve failure to adapt to minor physiologic occlusal variation that would normally be filtered from conscious awareness.

Importantly, the present review does not suggest that BMS or OD are “psychogenic” conditions in the traditional reductive sense. Rather, the available evidence increasingly supports the concept that sensory perception itself is dynamically shaped by interactions among peripheral input, affective state, attention, salience attribution, and central modulation [20, 23]. Psychological distress and hypervigilance may therefore contribute to symptom persistence without implying that symptoms are imagined or fabricated.

The present framework may also help contextualize the recurring observation that irreversible dental interventions frequently worsen OD [2, 6]. If the dominant abnormality involves maladaptive sensory salience and persistent monitoring of occlusal input, repeated structural alteration may unintentionally reinforce attentional fixation and perpetuate chronicity. Similar mechanisms may partially explain why some BMS patients undergo repeated dental treatment despite the absence of meaningful pathology [3].

Several limitations should nevertheless be acknowledged. First, much of the evidence underlying the proposed framework remains indirect and inferential. The literature on OD in particular remains limited, with many studies consisting of case reports, small observational series, or single‐center experiences [2, 3]. Neuroimaging evidence is heterogeneous, and direct mechanistic comparison between BMS and OD using standardized methodologies has not yet been performed.

Second, the proposed overlap between BMS and OD currently rests largely on limited observational clinical data. A frequently cited comorbidity estimate from a specialized referral setting refers to BMS recorded as a comorbid symptom within an oral somatic delusions cohort rather than to direct BMS–OD overlap [8], and direct co‐occurrence remains sparsely documented. Whether meaningful overlap exists across broader oral medicine populations remains uncertain. Prospective multicenter characterization studies will therefore be necessary to determine the true prevalence, phenotype distribution, and clinical significance of overlap presentations.

Third, the present framework remains conceptual rather than definitive. The distinction between “bottom‐up amplification” and “top‐down modulatory failure” should not be interpreted as an absolute dichotomy. In reality, peripheral sensitization, affective amplification, attentional fixation, salience attribution, and central sensory modulation likely interact dynamically across both disorders. The proposed model is therefore intended primarily as a heuristic framework to guide future investigation rather than as a finalized pathophysiological classification system.

Despite these limitations, the proposed framework generates several potentially testable hypotheses. Future neuroimaging studies comparing BMS‐only, OD‐only, and overlap patient groups using identical paradigms may clarify whether these conditions exhibit graded or distinct alterations within prefrontal and frontostriatal networks. Longitudinal cohort studies may determine whether chronic sensory amplification in one oral sensory domain predisposes patients to the development of dysregulation in another. Similarly, phenotype‐stratified pharmacological trials may help determine whether mechanistic features predict treatment responsiveness more effectively than traditional diagnostic labels alone.

Ultimately, the present review highlights the need to move beyond rigid structural models of chronic oral sensory complaints. BMS and OD may not simply represent isolated disorders confined to mucosa or occlusion, but rather manifestations of altered trigeminal sensory modulation expressed through different perceptual domains. Recognizing this possibility may improve both mechanistic understanding and clinical management of some of the most challenging conditions encountered in oral medicine practice.

8. Conclusion

Burning mouth syndrome and occlusal dysesthesia are traditionally regarded as distinct disorders within oral medicine. However, the current literature suggests that the relationship between the two conditions may be more complex than previously recognized. Although their predominant sensory manifestations differ—burning nociceptive dysesthesia in BMS and persistent mechanosensory dysesthesia in OD—both conditions appear to involve altered central modulation of trigeminal sensory processing in the absence of sufficient structural pathology to explain symptom severity.

Current evidence supports the view that BMS involves a combination of trigeminal small‐fibre dysfunction, peripheral sensitization, and enhanced central nociceptive amplification, whereas OD appears to involve maladaptive interpretation and insufficient suppression of otherwise physiologic periodontal mechanosensory input. Despite these mechanistic distinctions, both disorders may share abnormalities involving salience attribution, affective regulation, sensory hypervigilance, and frontostriatal modulation.

On the basis of these observations, this review proposes that BMS and OD may represent distinct but partially overlapping phenotypes within a broader framework of oral sensory dysregulation. This framework does not imply that the two conditions are identical or interchangeable. Rather, it suggests that chronic oral sensory symptoms may emerge through different interactions among peripheral input, central modulation, attentional processing, and affective amplification across multiple sensory domains.

Clinically, this perspective may encourage more integrated assessment of patients presenting with chronic oral sensory complaints, particularly those exhibiting mixed symptom profiles, treatment resistance, or repeated unsuccessful structural interventions. Recognition of overlapping mechanisms may also support more individualized and mechanism‐informed therapeutic strategies while reducing the risk of unnecessary irreversible dental treatment.

Importantly, the framework proposed here remains preliminary and requires prospective validation. Future studies integrating standardized neuroimaging, psychophysical assessment, and phenotype‐stratified clinical characterization will be essential to clarify the relationship between BMS and OD and to determine whether shared neurobiological mechanisms meaningfully contribute to symptom overlap.

Nevertheless, reconsidering BMS and OD within a broader framework of oral sensory dysregulation may provide a useful conceptual step toward improved understanding of chronic oral sensory disorders and more effective multidisciplinary management within oral medicine practice.

Author Contributions

Eunhye Choi: conceptualization, methodology, investigation, visualization, writing – original draft, writing – review and editing, project administration.

Ethics Statement

This manuscript is a narrative review based entirely on previously published literature. No original data were collected, no human participants or animals were involved, and therefore ethical approval was not required.

Conflicts of Interest

The author declares no conflicts of interest.

Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.