ReviewFrontiers in neuroscience2019
Peripheral and Central Mechanisms of Persistent Orofacial Pain.
Review in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 108 citations in OpenAlex.
- The Interaction Between the Central Nervous System and Dental Tissues: Hypothetical Dental Interoception Inferred From Skeletal Interoception.Journal of oral rehabilitation · 2026Review
- Muscle-Nerve Signaling and Neurogenic Inflammation in Temporomandibular Disorders: Potential Contributions of Occlusal Interference and Other Peripheral Triggers.Dentistry journal · 2026Review
- Topical Pregabalin in Burning Mouth Syndrome: A Real-World Study of Peripheral Neuromodulation.Medicina (Kaunas, Lithuania) · 2026Article
- Exploring Cognitive, Behavioral, and Psychological Dimensions in Persistent Idiopathic Facial Pain and Other Chronic Orofacial Pain Conditions.Brain and behavior · 2026Article
- Molecular landscape connecting complications of dry eye disease: mechanisms, therapeutic targets, biomarkers, and future innovations.International ophthalmology · 2026Review
- Schwann cell Lrp1 deletion drives trigeminal neuron sensitization and orofacial pain by modulating mitochondrial function and TRPV1/TRPA1 activity.The journal of headache and pain · 2025Article
- Burning mouth syndrome: updates on pathogenesis and diagnostic algorithms.Journal of oral & facial pain and headache · 2025Review
- Applicability of the theory of pain-sensorimotor interactions to orofacial pain and sensorimotor behavior, and implications for orofacial pain research and management.Journal of oral & facial pain and headache · 2025Review
- Review
- Corneal Sensory Receptors and Pharmacological Therapies to Modulate Ocular Pain.International journal of molecular sciences · 2025Review
- Article
- Obsessive-compulsive symptoms and traits in patients with burning mouth syndrome: a cross-sectional multicentric analysis.Clinical oral investigations · 2025Article
- Mechanisms for Orofacial Pain: Roles of Immunomodulation, Metabolic Reprogramming, Oxidative Stress and Epigenetic Regulation.Biomedicines · 2025Review
- Cognitive profile in burning mouth syndrome versus mild cognitive impairment: A comparative study.Oral diseases · 2025Article
- Preclinical Insights into the Role of Kir4.1 in Chronic Pain and Depression: Mechanisms and Therapeutic Potential.Biomolecules · 2025Review
- N-methyl-D-aspartate Receptor Subunits 2A and 2B Mediate Connexins and Pannexins in the Trigeminal Ganglion Involved in Orofacial Inflammatory Allodynia during Temporomandibular Joint Inflammation.Molecular neurobiology · 2025Article
- Impaired modulation of the trigeminal caudal nucleus by the locus coeruleus in diabetic mice: the role of GABAergic and glycinergic neurons.Frontiers in neuroanatomy · 2025Article
- DNA methylation profiling of CpG islands in trigeminal ganglion of rats with orofacial pain induced by experimental tooth movement.BMC oral health · 2024Article
- Emerging Psychotropic Drug for the Treatment of Trigeminal Pain: Salvinorin A.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Distinct expression profile reveals glia involvement in the trigeminal system attributing to post-traumatic headache.The journal of headache and pain · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroplastic changes in the neuronal networks involving the trigeminal ganglion (TG), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (C1/C2) are considered the mechanisms underlying the ectopic orofacial hypersensitivity associated with trigeminal nerve injury or orofacial inflammation. It has been reported that peripheral nerve injury causes injury discharges in the TG neurons, and a barrage of action potentials is generated in TG neurons and conveyed to the Vc and C1/C2 after trigeminal nerve injury. Long after trigeminal nerve injury, various molecules are produced in the TG neurons, and these molecules are released from the soma of TG neurons and are transported to the central and peripheral terminals of TG neurons. These changes within the TG cause neuroplastic changes in TG neurons and they become sensitized. The neuronal activity of TG neurons is further accelerated, and Vc and C1/C2 neurons are also sensitized. In addition to this cascade, non-neuronal glial cells are also involved in the enhancement of the neuronal activity of TG, Vc, and C1/C2 neurons. Satellite glial cells and macrophages are activated in the TG after trigeminal nerve injury and orofacial inflammation. Microglial cells and astrocytes are also activated in the Vc and C1/C2 regions. It is considered that functional interaction between non-neuronal cells and neurons in the TG, Vc, and C1/C2 regions is a key mechanism involved in the enhancement of neuronal excitability after nerve injury or inflammation. In this article, the detailed mechanisms underlying ectopic orofacial hyperalgesia associated with trigeminal nerve injury and orofacial inflammation are addressed.
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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 OpenQuestion graph.