ReviewDentistry journal2026
Muscle-Nerve Signaling and Neurogenic Inflammation in Temporomandibular Disorders: Potential Contributions of Occlusal Interference and Other Peripheral Triggers.
Review in Dentistry journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
3 authors.
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Abstract
Temporomandibular disorders (TMD) comprise a heterogeneous group of pain and dysfunction conditions involving the temporomandibular joint, masticatory muscles, and related structures. Although occlusal interference has long been discussed in relation to TMD, current evidence does not support an occlusion-centered etiological model for most patients. Within the contemporary biopsychosocial framework embodied by the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD), occlusal interference is better regarded as one of several potential peripheral biomechanical inputs that may interact with individual pain susceptibility, parafunctional loading, inflammatory status, and psychosocial factors. This review synthesizes evidence on how peripheral biomechanical and inflammatory inputs may engage masticatory muscle-nerve signaling, trigeminal nociceptor activation, and neurogenic inflammation. We discuss altered masticatory muscle activity, proprioceptive and nociceptive afferent signaling, neuropeptide release, neurovascular and mast cell-nerve interactions, and glial activation within trigeminal pain pathways. Molecular mechanisms, including TRP channel and P2X3 receptor activation, voltage-gated ion channel dysregulation, MAPK, PI3K/Akt/mTOR, cAMP/PKA/CREB signaling, and epigenetic regulation, are reviewed as candidate pathways linking peripheral input to pain-related plasticity. These mechanisms are further considered in relation to hyperalgesia, mechanical allodynia, pain memory, emotional and cognitive modulation, and sex-related differences in pain processing. Finally, we evaluate translational implications, including mechanism-oriented animal models, exploratory biomarkers, human-derived experimental systems, and mechanism-informed interventions, while emphasizing their current limitations. Overall, this review proposes a cautious mechanistic framework in which peripheral inputs may contribute to TMD-related pain amplification in selected contexts, but clinical translation requires validated phenotyping, longitudinal evidence, and integration with conservative, reversible, and patient-centered standard-of-care management.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.