Symptom Persistence Across Selected Orofacial Conditions: Toward a Chronic Explanatory Profile

ABSTRACT

Background

Although diagnostically heterogeneous, several orofacial conditions share a problem: symptoms persist when the original source is absent, has resolved, or is no longer sufficient to account for the persisting burden.

Objective

To compare burning mouth syndrome, persistent dentoalveolar pain, persistent idiopathic facial pain, occlusal dysesthesia, chronic myogenous orofacial pain and chronic joint‐related temporomandibular disorder in terms of their chronic explanatory profile: the pattern of factors that may help account for persistence once current peripheral findings are insufficient.

Methods

This theory‐driven narrative review selected publications across classification, consensus, review and empirical literature addressing diagnostic definition, peripheral or somatosensory findings, central or sensory processing, psychological modulation, behavioural factors, clinical management and persistence. The synthesis compared the retained conditions across shared maintenance domains rather than prevalence.

Results

The retained conditions remained clinically distinct but could be organized around a shared persistence problem. Shared maintenance domains included insufficient current peripheral explanation, altered sensory or central processing, attentional and affective salience, behavioural responses and clinical embedding. Evidence levels differed across conditions and mechanisms. Occlusal dysesthesia was especially informative because persistence may concern a perceptual symptom rather than pain amplification. Myogenous orofacial pain and joint‐related temporomandibular disorder served as contrast conditions because muscle and joint anchors may remain clinically meaningful.

Conclusion

The chronic explanatory profile is proposed as a hypothesis‐generating account of maintenance domains, not a new classification, etiological explanation or single mechanism. It identifies domains through which persistent orofacial symptoms can be compared, operationalized and studied as a basis for future mechanistic research.

This review compares selected persistent orofacial conditions at the level of symptom persistence. It proposes a chronic explanatory profile to organize maintenance domains—altered sensory or central processing, symptom salience, behavioural responses, clinical embedding and vulnerability modifiers—when current peripheral findings are insufficient to explain persisting symptom burden. The framework is hypothesis‐generating and intended for comparison, operationalization and future research, not as a new classification or single mechanism.

1. Introduction

Persistent orofacial conditions without sufficient current peripheral explanation present a clinical challenge because they encompass complaints that differ in location, symptom quality, anatomical anchor and presumed mechanism. The phrase indicates that persisting symptom burden is not sufficiently explained by current local tissue, dental, mucosal, occlusal, muscular or joint findings. This focus is situated within the broader clinical field of chronic orofacial pain [1].

The major classification systems approach this field from different perspectives. The International Classification of Orofacial Pain (ICOP) is specifically designed for orofacial pain and distinguishes source‐related, neuropathic, headache‐like and idiopathic orofacial pain categories, while also including psychosocial assessment [2]. The International Classification of Diseases, 11th Revision (ICD‐11) offers a broader chronic‐pain framework, distinguishing chronic primary pain, chronic secondary pain, chronic musculoskeletal pain and chronic neuropathic pain, and coding selected orofacial conditions under different headings [3]. These classifications are clinically appropriate for diagnosis and communication, but they also show why persistence is difficult to compare across conditions: some are defined by the absence of a sufficient local cause, others retain a clearer muscle or joint anchor, and occlusal dysesthesia remains difficult to place because it is primarily a persistent occlusal percept rather than a pain condition. This raises the question addressed in the present review: can diagnostically distinct orofacial symptom forms be compared at the level of persistence once current peripheral findings no longer provide a sufficient explanation?

The conditions compared here were selected because they make this question clinically visible. In burning mouth syndrome (BMS), burning or dysesthesia persists without adequate mucosal or systemic explanation [4]. In persistent dentoalveolar pain (PDAP), dentoalveolar pain persists despite insufficient current odontogenic pathology [5]. In persistent idiopathic facial pain (PIFP), facial or orofacial pain persists without a stable local or structural explanation [6]. In occlusal dysesthesia (OD), an abnormal bite percept persists despite insufficient occlusal explanation [7]. Myalgia and myofascial pain provide muscle‐related contrast conditions, while chronic arthrogenous temporomandibular disorder provides a joint‐related contrast condition. Their muscle or joint anchors may remain clinically visible, but in chronic or high‐burden presentations local findings may no longer fully account for symptom burden.

The target phenomenon is therefore not the symptom form itself, but its persistence without sufficient current peripheral explanation. The symptom form remains clinically important because it preserves diagnostic specificity: burning oral sensation, dentoalveolar pain, diffuse orofacial pain, abnormal bite perception, myogenous pain, and joint‐related pain or dysfunction are not the same complaint. What requires explanation is why such a recognizable symptom form remains clinically active after the original trigger, lesion or functional disturbance no longer provides a sufficient explanation.

In this review, myogenous orofacial pain (MOP) refers to chronic myalgia and myofascial orofacial pain, and joint‐related temporomandibular disorder (TMD‐J) refers to chronic arthrogenous temporomandibular pain and dysfunction. For readability, the abbreviations MOP and TMD‐J are used throughout, but they refer only to chronic or persistent presentations. The objective is to compare BMS, PDAP, PIFP, OD, MOP and TMD‐J in terms of chronic explanatory profile, defined here as the pattern of factors that may help account for persistence once current peripheral findings are insufficient. This profile does not denote a new diagnostic category or a single shared mechanism. Rather, the review asks whether separately classified orofacial conditions show convergence once symptoms become persistent, and whether this convergence can be described across shared maintenance domains, including reduced proportionality to current peripheral findings, altered sensory or central processing, psychological modulation, behavioural responses and clinical embedding.

2. Methods

This study was designed as a theory‐driven narrative review and conceptual synthesis. Its aim was to compare selected persistent orofacial conditions at the level of symptom maintenance. Conditions were selected when they represented either: persistent orofacial symptom forms in which the current peripheral explanation is typically insufficient by definition or clinical presentation—BMS, PDAP, PIFP and OD; or major musculoskeletal orofacial conditions in which a peripheral or functional anchor may remain visible, but chronicity may involve broader maintenance mechanisms—MOP and TMD‐J. MOP and TMD‐J were included only in their chronic or persistent presentations. Orofacial conditions primarily defined by a demonstrable lesion or disease of the somatosensory nervous system were not the primary focus. This exclusion does not imply that the retained conditions lack nervous‐system involvement; rather, they were selected because their persistent clinical burden is not sufficiently explained by current peripheral findings and because they are not primarily classified through such a lesion‐ or disease‐defined neuropathic mechanism. Constant unilateral facial pain with added attacks was not retained as a central condition because, although included under idiopathic orofacial pain in ICOP [2], it remains too narrowly described to support comparison across the maintenance domains used in this review.

Literature was identified through iterative searches in PubMed, APA PsycNet and Google Scholar and reference lists of key articles, reviews and classification documents. Searches combined condition‐specific terms with cross‐cutting terms related to persistence, chronicity, reduced proportionality, central sensitization, nociplastic pain, somatosensory processing, psychological modulation, behavioural factors, habituation and clinical management.

Publications were prioritized when they contributed to one or more review domains: diagnostic classification, peripheral or somatosensory anchor, proportionality between symptoms and current peripheral findings, central or sensory processing, altered sensory‐perceptual experience, psychological modulation, behavioural or clinical embedding, and persistence. Foundational papers, classification documents, reviews, consensus papers and relevant empirical studies were included. Searches were not restricted to a single publication type, because the review required classification papers, consensus statements, reviews and empirical mechanistic studies. Literature selection was continued until each condition could be represented across the predefined maintenance domains and further searches did not materially change the conceptual comparison.

The synthesis proceeded in two steps. First, each condition was summarized as a condition‐specific chronic explanatory profile. Second, the profiles were compared across six domains: symptom form and peripheral or somatosensory anchor, reduced proportionality to current peripheral findings, central or sensory processing, altered sensory‐perceptual experience, psychological modulation, and persistence or symptom maintenance. Reduced proportionality referred to the situation in which, after appropriate assessment, current peripheral findings no longer sufficiently accounted for symptom intensity, duration, distribution, disability or treatment resistance. It was treated as a clinical and analytical judgement after appropriate assessment, not as an automatic consequence of chronicity.

Because this was a narrative and theory‐driven review, no formal risk‐of‐bias assessment or meta‐analysis was performed. The review does not claim exhaustive coverage of all orofacial pain literature but uses selected literature to develop and evaluate a conceptual comparison across persistent orofacial conditions.

3. Results

3.1. Condition‐Specific Chronic Explanatory Profiles

The condition‐specific profiles were first examined to determine how each disorder expressed the target phenomenon of this review: a recognizable orofacial symptom form that persists despite insufficient current peripheral explanation. For each condition, the chronic explanatory profile was summarized by identifying the dominant clinical anchor, the degree to which current peripheral findings remained explanatory, and the sensory, central, psychological, behavioural or clinical factors implicated in persistence.

3.1.1. Burning Mouth Syndrome

BMS represents the persistent burning/dysesthetic oral sensory condition. Its defining feature is not ordinary oral burning but burning or dysesthesia that persists in the absence of clinically evident causative mucosal lesions or sufficient systemic explanation. The dominant clinical anchor is therefore an altered oral sensory field rather than a tooth, bite, muscle or joint [4].

The chronic explanatory profile of BMS is heterogeneous. The literature does not support a single local mucosal disease model, but instead points to interacting somatosensory, neuropathic/nociplastic, stress‐related, systemic, central and psychological dimensions. These mechanisms are best understood as candidate maintenance domains rather than as a single established cause [8]. This does not exclude peripheral or central nervous‐system involvement. In BMS, small‐fibre involvement, altered oral somatosensory function and central pain or salience‐network mechanisms have been reported, supporting the view that insufficient mucosal explanation should not be equated with absence of neurobiological mechanisms [4, 9].

BMS was therefore positioned as a persistent oral sensory‐burning state in which the symptom form remains recognizable, but current mucosal findings are insufficient. Its persistence is approached here as a maintenance profile involving altered oral sensation, central or sensory processing, stress‐related and systemic factors, and psychological modulation, rather than as unexplained mucosal pathology [10].

3.1.2. Persistent Dentoalveolar Pain

PDAP represents the tooth‐ or dentoalveolar‐bound persistent pain condition. Its defining feature is not ordinary toothache, but pain experienced as arising from a tooth, socket or dentoalveolar region despite insufficient current odontogenic pathology. The dominant clinical anchor is therefore a localized dentoalveolar pain source, while the current dental, pulpal, periodontal, apical or surgical explanation is insufficient [5].

The chronic explanatory profile of PDAP points to altered oral somatosensory processing rather than ongoing dental disease alone. Insufficient odontogenic pathology should therefore not be equated with absence of neurobiological involvement: somatosensory gain/loss phenomena, altered intraoral trigeminal processing, and cortical representation changes suggest peripheral and central somatosensory mechanisms in persistent dentoalveolar pain [5, 11]. These findings support a maintenance profile in which pain remains locally represented but is no longer adequately explained by current peripheral dental pathology.

Treatment history is clinically relevant because the pain remains tooth‐ or region‐bound. Repeated dental testing, endodontic retreatment, extraction or surgical exploration may appear logical when the symptom is experienced as dental but may fail to resolve the complaint when sufficient odontogenic pathology is absent and may reinforce dentoalveolar source attribution. PDAP was therefore positioned as a persistent dentoalveolar pain state maintained by altered somatosensory processing, cognitive‐affective modulation, diagnostic uncertainty and treatment history rather than by ongoing odontogenic pathology alone [12].

3.1.3. Persistent Idiopathic Facial Pain

PIFP represents the diffuse persistent facial or orofacial pain condition. Its defining feature is not orofacial pain in general, but pain that persists without a stable local, dental, structural or neurological source. The dominant clinical anchor is therefore less object‐bound than in PDAP or OD: the complaint remains facial or orofacial, but is typically diffuse, poorly localized, dull, aching or nagging rather than fixed to a tooth, bite, muscle or joint [13].

The chronic explanatory profile of PIFP points toward altered central trigeminal pain processing and cognitive‐affective maintenance rather than an ongoing peripheral lesion. Recent imaging and clinical literature support possible nociplastic involvement in a condition without a demonstrable nerve lesion or sufficient local cause. Psychological and cognitive‐affective factors, including depressive symptoms, catastrophizing, alexithymia, loneliness, and functional burden, appear relevant to persistence and disability without constituting a primary explanation of the pain [14].

PIFP was therefore positioned as the least object‐bound persistent pain condition in the comparison. Its symptom form remains recognizable as persistent facial/orofacial pain, but current local or structural findings are insufficient. Its persistence is approached here as a maintenance profile involving altered central trigeminal processing, cognitive‐affective burden, functional impact and diagnostic uncertainty rather than as unexplained facial pain alone.

3.1.4. Occlusal Dysesthesia

OD represents the object‐bound abnormal occlusal percept condition. Its defining feature is not an objectively wrong bite, but an abnormal bite perception that persists despite absent, minor or insufficient occlusal findings. The dominant clinical anchor is therefore the occlusion as experienced object: the bite feels wrong, excessive, premature, unstable or uncomfortable, while the current occlusal explanation remains insufficient [7].

The chronic explanatory profile of OD differs from the pain‐dominant conditions because the primary problem is perceptual rather than nociceptive. The literature frames OD as a mismatch between subjective occlusal experience and objective occlusal findings, with maladaptive signal processing, disturbed habituation, attentional salience, checking, correction‐seeking and avoidance of irreversible occlusal treatment as central themes. This makes OD the clearest example of a persistent symptom form that is organized around a specific oral object rather than a tissue lesion or pain source [15].

OD was therefore positioned as the clearest reduced‐proportionality condition in the comparison. The symptom form remains recognizable as an abnormal bite percept, but persistence is not explained by a correctable occlusal discrepancy. Its maintenance profile is approached here in terms of altered occlusal perception, failed habituation, attentional fixation, clinical uncertainty and correction‐seeking rather than unresolved occlusal pathology [7, 15].

3.1.5. Myogenous Orofacial Pain

MOP represents the muscle‐ and function‐related contrast condition. Its defining feature is pain anchored in the masticatory muscles and modified by jaw function, loading, palpation, parafunction, clenching or bracing. Within this broader myogenous category, local myalgia remains more confined to the involved muscle, whereas myofascial pain is characterized by spreading or referred pain beyond the palpated muscle region. Thus, MOP retains a clinically visible peripheral and functional anchor, but its myofascial forms already suggest a broader sensory field than purely local muscle pain [16].

The chronic explanatory profile of MOP is therefore different from the more strongly reduced‐proportionality conditions. Peripheral muscle input may remain relevant, but persistent or high‐burden cases are not fully explained by local muscle findings alone. Chronic MOP may involve referred pain, mechanical hyperalgesia, pressure‐pain sensitivity, central sensitization, altered pain modulation, oral behaviours, sleep disturbance and psychosocial burden. In this sense, chronicity may reflect a shift from a primarily local muscle‐pain condition toward a broader sensorimotor and biopsychosocial maintenance profile [17].

MOP was therefore positioned as a contrast condition: its symptom form remains musculoskeletal and function‐related, but chronic cases may still show partial reduced proportionality. Its persistence is approached here as a maintenance profile involving recurrent muscle input, referred/spreading pain, altered pain processing, jaw‐use behaviour, sensorimotor adaptation, psychological modulation and disability rather than ongoing local muscle pathology alone [18].

3.1.6. Joint‐Related Temporomandibular Disorder

TMD‐J represents the articular and function‐related contrast condition. Its defining feature is pain and/or dysfunction anchored in the temporomandibular joint region and modified by jaw movement, loading, palpation or provocation. In contrast to BMS, PDAP, PIFP and OD, TMD‐J often retains a clinically visible articular and functional anchor, especially when local joint pathology, disc displacement, inflammatory change, degenerative joint disease, locking, joint sounds or restricted movement are present [16].

The chronic explanatory profile of TMD‐J is only partly comparable to the stronger reduced‐proportionality conditions. Ongoing joint nociception, mechanical loading and dysfunction may remain relevant, but chronic or high‐burden cases are not necessarily explained by articular findings alone. Persistence may involve altered pain modulation, central sensitization, or nociplastic features, jaw‐use behaviour, protective motor patterns, fear or avoidance of movement, sleep disturbance, psychosocial burden and disability. Chronic TMD‐J therefore tests whether a condition with a clearer articular and dysfunction‐related anchor can still acquire broader maintenance mechanisms once local findings no longer fully account for symptom burden [18].

TMD‐J was therefore positioned as the articular dysfunction contrast condition. Its symptom form remains joint‐ and function‐dependent, but chronic cases may show partial reduced proportionality. Its persistence is approached here as a maintenance profile involving joint nociception and loading, dysfunction, altered pain processing, jaw‐use behaviour, psychological modulation, functional limitation and treatment history rather than ongoing articular pathology alone [19].

3.2. Cross‐Condition Synthesis Across Mechanisms

The condition‐specific profiles and key supporting literature are summarized in Table 1. Building on this evidence base, the following synthesis compares the retained conditions across four domains: persistent clinical presentation, central or sensory processing, psychological modulation, and behavioural or clinical embedding.

TABLE 1.

Condition‐specific chronic explanatory profiles and key supporting literature.

Condition	Clinical presentation and peripheral anchor	Central, sensory or neurobiological processing	Psychological and behavioural modulation	Maintenance profile	Evidence status/interpretation
Burning mouth syndrome (BMS)	Persistent burning or dysesthetic oral sensory field without consistent local mucosal lesion or sufficient mucosal/systemic explanation; may include dysgeusia, xerostomia‐like sensation and altered oral somatosensation. Possible systemic, hormonal, stress‐related, somatosensory or dental‐treatment context [2, 4, 8, 10]	Altered oral sensory processing; central/salience networks; stress biology; possible neuropathic, nociplastic and dopaminergic mechanisms [8, 20, 21]	Stress, anxiety/depression, somatic symptom burden; stress biomarkers elevated [10, 22]	Persistence may be shaped by altered oral sensation, stress biology, central networks, systemic vulnerability, psychological modulation, repeated investigations and absence of a satisfying local explanation [8, 10, 20, 21]	Established clinical definition; heterogeneous evidence for peripheral small‐fibre, somatosensory, central and stress‐related contributions; nociplastic interpretation remains candidate/hypothesis‐generating
Persistent dentoalveolar pain (PDAP; PIDP in ICOP terminology)	Tooth‐ or dentoalveolar‐bound pain, sometimes after dental procedures, persisting despite insufficient pulpal, periodontal, apical, surgical or other current odontogenic explanation [2, 5, 12]	Altered intraoral trigeminal and dentoalveolar somatosensory processing; oral S1 cortical changes; possible nociplastic mechanisms [11, 23, 24]	Catastrophizing, anxiety/depression, treatment‐related distress; catastrophizing linked to oral S1 structure [11]	Maintenance may involve local pain attribution, diagnostic uncertainty, repeated dental testing or treatment‐seeking, altered somatosensory processing and central plasticity [11, 12, 23, 25]	Established clinical phenotype; empirical somatosensory and cortical evidence in subgroups; mechanisms remain heterogeneous and are not reducible to current odontogenic pathology
Persistent idiopathic facial pain (PIFP)	Persistent facial or orofacial pain without stable local, dental or neurological source; diffuse, poorly localized, dull/aching/nagging pain; not nerve‐territory‐bound [2, 13]	Altered central trigeminal pain processing; possible nociplastic involvement [13, 26]	Depressive symptoms, catastrophizing, alexithymia, loneliness, cognitive‐affective burden [27]	Maintenance may involve central trigeminal processing, cognitive‐affective burden, disability, diagnostic uncertainty and avoidance of invasive procedures [13, 27]	Established classification; central or nociplastic involvement remains emerging and hypothesis‐generating; cognitive‐affective burden is clinically relevant but not a primary explanation
Occlusal dysesthesia (OD; phantom bite syndrome)	Abnormal bite percept, often after dental treatment or trauma, persisting despite absent, minor or insufficient occlusal findings; experienced as wrong bite, premature contact, pressure, instability or occlusal hyperawareness [7, 15, 28]	Altered occlusal signal processing; disturbed habituation; altered occlusal sensory weighting; attentional salience; top‐down attention/gating mechanisms [7, 29, 30]	Attention to occlusion, hypervigilance, distress, uncertainty, perceived need for correction; psychiatric comorbidity may modulate but does not explain OD [7, 15, 28]	Checking/avoidance, clenching, correction‐seeking, repeated dental adjustments, clinical uncertainty and disturbed habituation may keep the bite foregrounded as a problem [7, 15]	Clinical consensus condition; altered occlusal perception and failed habituation are plausible maintenance concepts; nociplastic pain is not applied because the core symptom is perceptual rather than pain amplification
Myogenous orofacial pain (MOP)	Chronic myalgia and myofascial orofacial pain involving masticatory muscles, jaw use, loading, palpation and parafunction; myofascial forms include spreading or referred pain. In high‐burden cases, symptom severity, spread, disability or treatment resistance may exceed local muscle findings [16, 17, 18, 31]	Central sensitization, impaired modulation and possible nociplastic features in persistent/high‐burden cases; pressure pain, trigger points, referred pain, mechanical hyperalgesia, larger pain fields and sometimes widespread sensitivity [32, 33]	Catastrophizing, depression, anxiety, stress, sleep disturbance, somatic symptoms and perceived injustice [31, 34]	Recurrent muscle input, clenching/bracing, jaw overuse, sensorimotor adaptation, psychosocial burden and disability may contribute to persistence [18, 35]	Established TMD phenotype; evidence supports peripheral muscle input, central sensitization, pain modulation, and psychosocial or behavioural contributions in chronic/high‐burden cases
Joint‐related temporomandibular disorder (TMD‐J)	Chronic arthrogenous temporomandibular pain and/or dysfunction involving TMJ loading, jaw movement, joint provocation, locking, joint sounds, restricted movement or intra‐articular disorders. In high‐burden cases, symptom severity, disability or treatment resistance may exceed local articular findings [16, 18, 19]	Altered pain modulation, central sensitization or nociplastic features may contribute in persistent/high‐burden cases; local mechanical hyperalgesia, movement/loading pain, familiar pain on provocation and sometimes regional sensitivity [16, 17, 18]	Distress, depression/anxiety, catastrophizing, sleep disturbance, somatic symptom burden and avoidance [18, 19, 31]	Joint nociception/loading, protective motor behaviour, jaw overuse/parafunction, altered modulation, psychosocial burden, sleep disturbance, disability and treatment history may contribute to persistence [18, 19, 31]	Established TMD phenotype; peripheral joint or functional findings may remain relevant; broader central and psychosocial mechanisms may contribute in chronic/high‐burden cases

Note: Entries reflect the dominant literature‐based profile of each condition and are presented as comparative descriptors rather than quantitative scores, diagnostic criteria or evidence of a single shared mechanism. The evidence‐status/interpretation column distinguishes established clinical features from plausible, emerging or hypothesis‐generating maintenance mechanisms.

3.2.1. Persistent Clinical Presentation

Across the retained conditions, persistence was not treated as a minor temporal qualifier but as a central feature of the clinical presentation. The exact threshold differed across the literature and classifications: chronic pain is often defined by duration criteria, whereas chronic orofacial pain and headache classifications also use frequency and daily‐duration criteria, such as symptoms recurring for hours per day over at least 3 months [1, 36]. OD is defined less by pain chronicity than by a persistent abnormal bite perception, commonly described over a longer time frame such as 6 months [7].

These formal differences did not alter the shared clinical pattern identified in this review. The symptom remained repeatedly or continuously present, clinically salient, and no longer sufficiently explained by current findings. In BMS, PDAP, PIFP and OD, this pattern was clearest because the current mucosal, odontogenic, local structural or occlusal explanation was insufficient by definition or core presentation. In MOP and TMD‐J, the pattern was more partial: muscle or joint findings could remain clinically meaningful, but in chronic or high‐burden cases they could become insufficient to explain symptom severity, spread, disability or treatment resistance.

Thus, the difference lay mainly in the clinical form in which persistence appeared; the commonality lay in the continued clinical relevance of a recognizable symptom form after current findings had become insufficient. This preserved diagnostic specificity while allowing comparison at the level of persistence.

3.2.2. Central or Sensory Processing

Central or sensory processing became relevant when current peripheral findings no longer sufficiently explained symptom burden. In BMS, this concerned altered oral sensory processing, stress‐related modulation, possible neuropathic or nociplastic mechanisms, and central salience or pain‐network involvement. In PDAP, the processing profile was more dentoalveolar and somatosensory: the tooth or region remained the experienced pain source despite insufficient current odontogenic pathology. In PIFP, the profile was less object‐bound and may involve altered central trigeminal pain processing, with possible nociplastic features.

OD differed from the pain‐dominant conditions: its central or sensory component is better framed in terms of altered occlusal signal processing, disturbed habituation, attentional salience or sensory weighting.

In MOP and TMD‐J, central sensitization, impaired modulation or nociplastic features may contribute to chronic or high‐burden cases, but they do not replace the muscle or joint diagnosis. This preserves the peripheral and functional relevance of these conditions while recognizing that chronicity may involve broader sensory and central processing mechanisms.

3.2.3. Psychological Modulation

Psychological modulation recurred across conditions, but it did not function as a primary explanation of the symptom. Rather, distress, anxiety, depression, catastrophizing, stress, somatic symptom burden, sleep disturbance, uncertainty, perceived injustice, or fear‐avoidance could modulate symptom salience, coping, disability and treatment response.

The form of this modulation varied by condition. In BMS, stress biology, affective symptoms and somatic symptom burden may amplify oral sensory distress. In PDAP, catastrophizing, anxiety, treatment‐related distress and diagnostic uncertainty may reinforce the perceived dental significance of pain. In PIFP, depressive symptoms, loneliness, alexithymia and cognitive‐affective burden may contribute to disability and persistence. In OD, attention to occlusion, hypervigilance, distress, uncertainty and perceived need for correction may keep the bite experience clinically foregrounded. In MOP and TMD‐J, stress, sleep disturbance, anxiety, depression, catastrophizing, somatic symptoms and perceived injustice may interact with pain, jaw use, oral behaviours and disability.

Across conditions, psychological factors were therefore best understood as modulators of persistence and burden, not as evidence that the symptom is psychological in origin.

3.2.4. Behavioural and Clinical Embedding

Behavioural and clinical embedding described how symptoms became organized through action, avoidance, treatment history and clinical interpretation. In PDAP, the tooth‐ or region‐bound quality of pain could make repeated dental testing, endodontic retreatment, extraction or surgical exploration appear clinically logical, even when current odontogenic pathology was insufficient. In OD, checking, avoidance, clenching, repeated bite testing, correction‐seeking and occlusal adjustment could keep the bite percept foregrounded as a problem.

In BMS and PIFP, embedding was less tied to a correctable object but still clinically important. Repeated investigations, uncertainty, unsuccessful treatments and the absence of a satisfying explanation could maintain threat and symptom monitoring. In MOP and TMD‐J, embedding was more closely related to jaw function: clenching or bracing, parafunction, avoidance, protective motor behaviour, altered loading, sleep disturbance, treatment history and disability could help maintain the complaint.

Embedding therefore did not mean that the symptom was produced by care or behaviour alone. It meant that, once current findings were insufficient, the symptom could remain organized through the interaction of sensation, attention, interpretation, behaviour, and clinical response.

3.3. Synthesis

Across the retained conditions, the main difference was the clinical form in which persistence appeared. The convergence lay in the persistence of recognizable symptom forms without a sufficient current peripheral explanation. This did not erase diagnostic specificity or imply a single mechanism but suggested a chronic explanatory profile involving insufficient current peripheral explanation, altered central or sensory processing, psychological modulation, behavioural responses and clinical embedding.

4. Discussion

4.1. Principal Finding

The main finding of this review is that persistence provides a useful level of comparison across selected orofacial conditions. The retained conditions differ in symptom form and clinical anchor, but their persistent forms show partial convergence once current peripheral findings no longer sufficiently explain symptom burden. This does not mean that the conditions should be merged diagnostically. A burning mouth, a painful dentoalveolar region, an abnormal bite percept, myogenous pain and joint‐related dysfunction remain clinically different. The point is that, once these symptom forms remain active despite insufficient current peripheral explanation, the relevant question is no longer only where the complaint originally came from, but whether current findings still explain the persisting burden and what may keep it active.

The central contribution of the review is therefore to formulate persistence itself as the comparative problem. Diagnostic labels preserve clinical specificity, whereas the chronic explanatory profile describes the domains through which a recognizable symptom form may remain clinically active. In this sense, the review shifts the emphasis from classifying persistent conditions to examining persistence as a phenomenon requiring its own explanatory approach.

4.2. Reduced Proportionality as the Clinical Hinge

Once persistence is treated as the comparative problem, the next question is whether current peripheral findings still sufficiently explain the persisting burden. Here, reduced proportionality refers to the situation in which, after appropriate assessment, current findings no longer adequately account for the intensity, duration, disability, spread, clinical salience or treatment resistance of the complaint.

This distinction is essential in orofacial care, where symptoms are often mapped onto highly localizable and modifiable structures. Teeth can be tested or treated, occlusion can be marked or adjusted, mucosa can be inspected, muscles can be palpated and joints can be imaged. These possibilities remain diagnostically necessary when findings are proportionate to the complaint. However, when current findings are insufficient, further localization or correction may no longer clarify the problem and may instead keep attention fixed on the presumed local source.

Two clinical errors should therefore be avoided. The first is to keep treating the symptom as evidence of an undetected local defect. This may seem cautious, but it can become counterproductive: repeated testing, correction or reassurance‐seeking may keep attention fixed on the tooth, bite, mucosa, muscle or joint, increase monitoring, and reinforce the expectation that a hidden local problem must still be present. This concern is illustrated in PIFP, where patients are often overinvestigated and may undergo irreversible dental treatment, and in OD, where repeated occlusal adjustment may reinforce occlusal source attribution or even intensify the syndrome [7, 37].

The second error is to interpret the lack of sufficient findings as evidence that the symptom is primarily psychological. This does not solve the explanatory problem. Psychological distress, anxiety, depression, catastrophizing or hypervigilance may modulate symptom burden and disability, but they do not by themselves explain why the symptom takes a specific orofacial form. More broadly, the biopsychosocial model can help organize relevant biological, psychological and social factors, but it should not be treated as an explanatory model that by itself establishes causal relationships [27, 38].

The more useful clinical question is what keeps the symptom active once current local findings are insufficient. That question directs attention to maintenance factors such as altered sensory processing, central modulation, attentional salience, affective threat, checking or avoidance behavior, treatment history and clinical embedding.

For the present review, reduced proportionality provides the practical criterion for comparison. It explains why BMS, PDAP, PIFP and OD can be compared despite different symptom forms, and why MOP and TMD‐J can be included as contrast conditions rather than excluded as purely musculoskeletal disorders. In all cases, the question is not whether the clinical anchor exists, but whether it remains sufficient to explain the persisting burden.

4.3. Brain‐Network Evidence and Its Limits

Brain‐network evidence provides a neurobiological context for some of the maintenance domains proposed here, but its relevance differs substantially across the retained conditions. Terms such as attentional salience, monitoring, symptom foregrounding and clinical relevance should therefore not be read as purely psychosocial descriptors. They refer to processes through which the nervous system may continue to treat a bodily signal as important, threatening or action‐relevant. Cognitive‐affective models of pain have long emphasized that pain interrupts ongoing activity and demands attention, particularly when it is intense, novel, unpredictable, threatening or difficult to explain [39]. Network models further specify how such interruption may be implemented: salient bodily signals may recruit anterior insula and anterior cingulate systems, biassing attention and control toward signals that are judged behaviourally relevant [40].

In chronic pain, altered functional behaviour of the default‐mode and salience networks has been repeatedly reported, particularly involving medial prefrontal, anterior insula and cingulate connectivity. This supports a link between pain, self‐relevance, threat appraisal, salience processing and attentional control [41].

Importantly, this does not mean that persistent symptoms are simply ‘produced by the brain’ or that brain‐network findings replace peripheral, trigeminal or musculoskeletal mechanisms. Rather, they suggest that local symptoms may remain clinically active when sensory input, affective value, attention, self‐relevance and action tendencies remain coupled around a specific symptom form. This perspective is relevant to the retained orofacial conditions, but the strength of evidence differs by condition. In painful TMD, altered brainstem pain‐modulation circuitry provides direct orofacial evidence that descending modulation and trigeminal relay systems may contribute to pain persistence [42]. Resting‐state work in temporomandibular disorder has also linked pain rumination to enhanced medial prefrontal‐default mode network connectivity, providing a direct orofacial example of how persistent pain may become embedded in self‐referential and repetitive cognitive processing [43]. In BMS, brain‐network studies and reviews have implicated central/salience‐network involvement, although mechanisms remain heterogeneous [21]. In PDAP and PIFP, evidence for altered trigeminal, somatosensory or cortical processing supports central involvement, but does not yet define a single network mechanism [11, 14]. For OD, neuroimaging evidence is more limited and should be interpreted cautiously; available studies suggest altered prefrontal engagement during occlusal discomfort or chewing, but OD should not be presented as a proven brain‐network disorder [29, 30].

Brain‐network evidence therefore strengthens the biological plausibility of the chronic explanatory profile, but it does not convert it into a single neural mechanism. Its main value here is to show how local symptoms may remain salient, self‐relevant and behaviourally consequential when current peripheral findings are insufficient to explain the full clinical presentation.

4.4. Candidate Explanatory Frameworks

The preceding comparison identifies a persistence problem rather than a completed explanation. Several broader literatures may help contextualize this problem, but they should be treated as heuristic and hypothesis‐generating rather than as evidence for a single mechanism of persistent orofacial conditions. Their value lies in specifying different routes through which a clinically specific symptom may remain active when current peripheral findings are insufficient, including altered nociceptive modulation, increased central excitability, altered salience and threat appraisal, vulnerability modifiers, behavioural responses and clinical embedding.

First, descending pain‐modulation and brainstem pain‐control research shows that nociceptive input is not passively transmitted but can be inhibited or facilitated through brainstem and spinal or trigeminal relay systems [23]. This is relevant to persistent orofacial pain because trigeminal nociceptive input is regulated at the spinal trigeminal nucleus, where peripheral input, descending modulation and local relay processes may interact. Altered brainstem pain‐modulation circuitry has been described in chronic painful TMD, providing direct orofacial evidence that pain persistence can involve more than local tissue state alone [42]. This literature provides one possible mechanistic route by which pain burden may exceed current peripheral findings in pain‐dominant conditions, including chronic or high‐burden MOP and TMD‐J, through insufficient inhibition or enhanced facilitation of nociceptive processing.

Second, central sensitization, nociplastic pain and chronic primary pain frameworks help formulate hypotheses about why pain can become disproportionate to current tissue pathology, persist beyond expected healing, or involve broader hypersensitivity, disability, sleep disturbance, affective symptoms or widespread sensitivity [44, 45]. At the neurobiological level, repeated or sustained nociceptive input may increase excitability in spinal dorsal horn and trigeminal brainstem relay systems. Mechanisms such as NMDA‐receptor‐dependent wind‐up, central sensitization and altered inhibitory–facilitatory balance provide biological plausibility for pain persistence when peripheral findings are no longer proportionate to symptom burden [23, 46]. These mechanisms are most relevant to pain‐dominant presentations and should not be assumed for OD, where persistence concerns an abnormal occlusal percept rather than amplified nociceptive pain.

Third, vulnerability modifiers may help explain why some individuals are more susceptible to persistence, without providing condition‐specific explanations by themselves. Sex and gender‐related factors are relevant in this respect: female predominance has been reported in several retained conditions, including BMS, OD and TMD‐spectrum pain, although the strength and interpretation of this association differ across diagnoses [4, 7, 17]. Hormonal, affective, sleep‐related and psychosocial factors may interact with pain sensitivity, stress responsiveness and descending pain modulation [47]. In the present framework, such factors are best understood as vulnerability or amplification modifiers rather than as sufficient explanations for any retained condition.

Fourth, persistent physical symptom and symptom‐perception models help bridge pain and non‐pain conditions by focusing on how bodily signals may remain salient, threatening or action‐relevant through attention, expectation, uncertainty, behaviour and clinical interpretation. This is important because not all retained conditions are pain‐dominant. In PDAP, PIFP, MOP and TMD‐J, persistence primarily concerns pain, although the mechanisms and evidence base differ. BMS occupies an intermediate position because burning pain, dysesthesia, taste disturbance and dry‐mouth‐like sensations may coexist. OD is different again: its core symptom is not pain amplification but a persistent abnormal occlusal percept. Symptom‐perception models are therefore especially useful because they allow persistence to be considered across both pain and non‐pain symptom forms without reducing them to the same mechanism. Predictive‐processing accounts can be included within this broader family as modest heuristic models of active, embodied and context‐sensitive perception, but not as literal or complete explanations [48]. They help express how bodily perception depends not only on incoming sensory signals, but also on expectation, uncertainty, prior experience, attention and action. In this limited sense, they are relevant to persistent orofacial symptoms because a symptom may remain clinically compelling when the perceptual system continues to treat a local bodily signal as salient, unresolved or action‐relevant. This use should remain cautious, especially in view of broader critiques of overextended predictive‐processing or free‐energy claims [49].

In this review, these frameworks are therefore treated as candidate explanatory frameworks rather than established evidence that the retained conditions share a single mechanism or belong to one explanatory class, such as nociplastic pain, brain‐network dysfunction or a single predictive‐processing mechanism. Their relevance is strongest when matched to the dominant clinical problem: descending modulation and central sensitization are most relevant to pain‐dominant presentations; symptom‐perception and predictive‐processing models are useful for bridging pain, dysesthesia and perceptual symptoms; and sex, gender, affective and sleep‐related factors are best treated as vulnerability modifiers. This distinction is important because the retained conditions differ in the extent to which persistence concerns pain, dysesthesia or perception.

Taken together, these literatures suggest that persistence should not be understood as duration alone. In the retained conditions, the symptom remains clinically specific in form, while its continued clinical relevance may be shaped by sensory or central processing, descending modulation, salience, behavioural responses and clinical embedding. The explanatory value of the chronic explanatory profile therefore lies not in proposing a new mechanism, but in organizing candidate maintenance processes that are otherwise discussed separately in pain modulation, nociplastic pain and symptom‐perception literatures.

4.5. Clinical and Therapeutic Implications: Embedding Without Psychologization

If persistence is the shared problem, treatment may need to shift from correcting the presumed symptom source to reducing the processes that keep the symptom clinically active. In BMS, PDAP, PIFP and OD, the absence of a sufficient current local explanation is not a late afterthought but part of the clinical definition or core presentation of the condition. At that point, the somatic clinician's role is mainly diagnostic and explanatory: to contain further source‐seeking, set boundaries, and prevent unnecessary local intervention. In MOP and TMD‐J, this shift is more partial because muscle and joint findings may remain clinically meaningful, and current TMD practice already incorporates physical diagnosis together with assessment of pain‐related disability, psychosocial distress, somatic symptoms and behavioural factors [50].

The active treatment target may then become persistence itself: symptom salience, threat value, monitoring, checking, avoidance, correction‐seeking, distress, sleep disturbance, coping, disability and the patient's understanding of the complaint. This points toward behavioural care, coordinated with the somatic clinician. The implication is therefore not uniform symptom treatment, but a possible shared persistence‐oriented approach: the local form of the symptom is respected, while treatment shifts toward reducing the conditions under which that symptom remains clinically relevant.

4.6. Limitations and Future Directions

Several limitations should be acknowledged. First, this review was narrative and theory‐driven rather than systematic. Its aim was not to estimate prevalence, effect sizes or treatment efficacy, but to define and compare a target phenomenon: persistent orofacial symptom forms without sufficient current peripheral explanation. The resulting chronic explanatory profile is therefore a comparative and hypothesis‐generating construct, not a validated diagnostic model.

Second, the evidence base was heterogeneous. The included conditions differ in classification history, terminology, study design, sample size and mechanistic maturity. The broader TMD field, particularly through the DC/TMD Axis I‐Axis II framework [16], has a comparatively stronger diagnostic and biopsychosocial framework, whereas OD and some persistent pain conditions rely more heavily on expert consensus, clinical series, narrative reviews, and emerging mechanistic studies. Sex‐ and gender‐related factors were not developed as a separate maintenance domain. Female predominance is reported across several retained conditions, including BMS, OD and TMD‐spectrum pain, and may represent a shared vulnerability context. However, this does not alter the focus of the present review: sex and gender may modify vulnerability, burden or treatment response, but they do not by themselves explain the specific symptom form or constitute a separate maintenance domain in the proposed chronic explanatory profile. Their role in shaping persistence should be examined in future research.

Third, the proposed maintenance domains remain preliminary and are not intended to provide a molecular or cellular model of persistence. Reduced proportionality, altered sensory weighting, psychological modulation, behavioural embedding and clinical interaction are useful comparative concepts, but they have not yet been operationalized as a single empirical framework. Similarly, predictive processing, central sensitization, nociplasticity and central or sensory amplification should be understood as candidate explanatory frameworks, not as established biomarkers, diagnostic labels or proof of a shared central mechanism. Because the retained conditions differ in the extent to which persistence concerns pain, dysesthesia or perception, nociplastic pain was not treated as applicable to all conditions and was not applied to OD, where persistence concerns an abnormal occlusal percept rather than pain amplification.

Fourth, reduced proportionality must not be used to dismiss peripheral assessment. This is especially relevant for MOP and TMD‐J, where peripheral nociceptive, functional and structural contributors may remain clinically meaningful. The proposed comparison is intended to identify when current findings no longer sufficiently explain symptom burden, not to deny the relevance of muscle, joint, dental, mucosal or neurological assessment.

Finally, the chronic explanatory profile requires empirical testing. Future studies should examine whether reduced proportionality, symptom salience, altered sensory weighting, behavioural embedding and clinical interaction can be measured reliably using condition‐appropriate indicators, including clinical findings, sensory testing, symptom‐salience or monitoring measures, behavioural indices of checking, avoidance or correction‐seeking, distress and sleep measures, and treatment‐history variables. Such studies should also test whether different combinations of these domains predict persistence, disability or treatment response, and whether interventions targeting these maintenance dimensions improve outcomes across BMS, PDAP, PIFP, OD, MOP and TMD‐J.

5. Conclusion

The selected orofacial conditions should not be merged into one diagnosis. BMS, PDAP, PIFP, OD, MOP and TMD‐J retain distinct clinical forms, but can be compared through one shared feature: persistence. This persistence may be shaped by interacting maintenance processes involving altered sensory or central processing, attentional and affective salience, behavioural responses and clinical embedding.

The clinical implication is that persistence itself may become a treatment target. Care may need to shift from correcting the presumed local source to reducing the conditions that keep the symptom clinically relevant, including salience, threat, monitoring, checking, avoidance, correction‐seeking, distress, sleep disturbance, coping, disability and the patient's understanding of the complaint.

The proposed chronic explanatory profile is therefore not a new classification or a single mechanism. It is a hypothesis‐generating framework that makes persistence available for comparison, operationalization and empirical study.

Author Contributions

Paul A. M. Versteegh: conceptualization, methodology, project administration, writing – review and editing, writing – original draft, visualization.

Funding

The author has nothing to report.

Conflicts of Interest

The author declares no conflicts of interest.

Data Availability Statement

The author has nothing to report.