ACC Plasticity Maintains Masseter Hyperalgesia Caused by Occlusal Interference

Xu, Xiaoxiang; Cao, Ye; Mo, Shanyan; Liu, Y; Xie, Qing

doi:10.1177/0022034519827590

Cited by 10 publications

(10 citation statements)

References 36 publications

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“…These human data provide an excellent starting point for reverse translational approaches to determine detailed neural circuit mechanisms of craniofacial muscle pain in the brains of experimental animals. For example, a recent study showed that enhanced synaptic transmission in ACC, as evaluated by stimulating the medial thalamus, was shown to maintain long-lasting masseter hyperalgesia induced by occlusal interference in rats (Xu et al 2019).…”

Section: Maladaptive Changes Of Pain Circuits In the Brainmentioning

confidence: 99%

Neural Pathways of Craniofacial Muscle Pain: Implications for Novel Treatments

et al. 2020

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Craniofacial muscle pain is highly prevalent in temporomandibular disorders but is difficult to treat. Enhanced understanding of neurobiology unique to craniofacial muscle pain should lead to the development of novel mechanism-based treatments. Herein, we review recent studies to summarize neural pathways of craniofacial muscle pain. Nociceptive afferents in craniofacial muscles are predominantly peptidergic afferents enriched with TRPV1. Signals from peripheral glutamate receptors converge onto TRPV1, leading to mechanical hyperalgesia. Further studies are needed to clarify whether hyperalgesic priming in nonpeptidergic afferents or repeated acid injections also affect craniofacial muscle pain. Within trigeminal ganglia, afferents innervating craniofacial muscles interact with surrounding satellite glia, which enhances the sensitivity of the inflamed neurons as well as nearby uninjured afferents, resulting in hyperalgesia and ectopic pain originating from adjacent orofacial tissues. Craniofacial muscle afferents project to a wide area within the trigeminal nucleus complex, and central sensitization of medullary dorsal horn neurons is a critical factor in muscle hyperalgesia related to ectopic pain and emotional stress. Second-order neurons project rostrally to pathways associated with affective pain, such as parabrachial nucleus and medial thalamic nucleus, as well as sensory-discriminative pain, such as ventral posteromedial thalamic nuclei. Abnormal endogenous pain modulation can also contribute to chronic muscle pain. Descending serotonergic circuits from the rostral ventromedial medulla facilitate activation of second-order neurons in the trigeminal nucleus complex, which leads to the maintenance of mechanical hyperalgesia of inflamed masseter muscle. Patients with temporomandibular disorders exhibit altered brain networks in widespread cortical and subcortical regions. Recent development of methods for neural circuit manipulation allows silencing of specific hyperactive neural circuits. Chemogenetic silencing of TRPV1-expressing afferents or rostral ventromedial medulla neurons attenuates hyperalgesia during masseter inflammation. It is likely, therefore, that further delineation of neural circuits mediating craniofacial muscle hyperalgesia potentially enhances treatment of chronic muscle pain conditions.

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Section: Maladaptive Changes Of Pain Circuits In the Brainmentioning

confidence: 99%

Neural Pathways of Craniofacial Muscle Pain: Implications for Novel Treatments

et al. 2020

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“…Increased medial thalamus (MT) stimulation steadily elicited gradually enhanced local field potential (LTP) amplitudes in the ACC of control and EOI rats. Rats that received EOI for 14 and 21 d exhibited dramatically enhanced LFP in the ACC in response to MT stimulation, in comparison with control rats and rats that received EOI for 7 d. The results suggest that MT‐ACC synaptic transmission was potentiated since 14 d after EOI application 68 …”

Section: Introductionmentioning

confidence: 77%

Occlusal disharmony and chronic oro‐facial pain: from clinical observation to animal study

Cao

2021

J of Oral Rehabilitation

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Background Occlusion can be viewed as the most sensitive susceptor of the central nervous system in the oro‐facial region. Its inalienable relationships to the temporomandibular joint, the muscles, the stomatognathic system and even the central nervous system are self‐evident. Almost all the dental treatments inevitably change the occlusion, potentially or actually, locally or extensively, and immediately or gradually. Objective The objective of this study was to present a narrative literature on occlusal disharmony and chronic oro‐facial pain. Methods Literature reviews focusing on clinical studies about the relationship between occlusal disharmony and myofascial oro‐facial pain, and related preclinical studies about the animal models of, as well as the peripheral and central mechanisms underlying this condition related to, occlusal disharmony were used as starting point and guidelines to describe the topics mentioned. A search of the PubMed database was performed mainly with the following search terms: “occlusion,” “occlusal interference,” “occlusal disharmony,” “occlusal change,” “oro‐facial pain” and “myofascial pain.” Results Relevant literature from the past 70 years until the present day was meticulously studied. The literature review together with three related characteristic clinical cases revealed an intimate association between occlusal disharmony and chronic oro‐facial pain, involving pathological changes, extending from the peripheral tissues to the central nervous system. The patients suffered from psychological distress, sleep disturbance and poor life quality. Conclusion Occlusal disharmony–related oro‐facial pain is a clinical problem that deserves attention, although there are no universally accepted clinical protocols. The existing literature provides some constructive suggestions, but further research is needed.

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“…9,46 Other CNS areas involved in the descending pain-modulatory systems such as the ACC may also have participated in the maintenance of pain on postoperative day 14 induced by PEOI although our earlier study suggests that the ACC may have not been involved in the maintenance of hyperalgesia following late EOI removal on postoperative day 8, which more likely involves mainly the descending facilitatory influence of RVM ON-cells. 10,11 Undoubtedly, there are complex interactions between EOI-related nociceptive inputs and the RVM as well as higher brain areas involved in descending modulation of nociceptive transmission, 12,13,15,18 and further studies are needed to unravel these interactions, including the role of glioplasticity as well as neuroplasticity in the RVM.…”

Section: On-and Off-cell Activity Following Reoi On Day 8 and Effect Of Cbxmentioning

confidence: 99%

“…The possible mechanisms underlying the PEOI-induced hyperalgesia were suggested to include neuronal and glial activation in the medullary dorsal horn (MDH) 9 and potentiation of synaptic transmission in the thalamus to the anterior cingulate cortex (ACC). 10 Also noteworthy are our recent findings that adaptive neuroplasticity of ON-and OFF-cells in the rostral ventromedial medulla (RVM) participated in the chronification, maintenance and inhibition of the PEOI-induced oro-facial hyperalgesia. 11 The RVM is part of the descending pain modulation system which exerts 'top-down' control on ascending nociceptive transmission.…”

Section: Introductionmentioning

confidence: 99%

Astrocytes in the rostral ventromedial medulla contribute to the maintenance of oro‐facial hyperalgesia induced by late removal of dental occlusal interference

Bai

et al. 2021

J of Oral Rehabilitation

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Background: Astrocytes in the rostral ventromedial medulla (RVM) contribute to descending pain modulation, but their role in oro-facial pain induced by persistent experimental dental occlusal interference (PEOI) or following EOI removal (REOI) is unknown.Objective: To explore the involvement of RVM astrocytes in PEOI-induced oro-facial hyperalgesia or its maintenance following REOI.Methods: Male rats were randomly assigned into five groups: sham-EOI, postoperative day 6 and 14 of PEOI (PEOI 6 d and PEOI 14 d), postoperative day 6 following REOI on day 3 (REOI 3 d) and postoperative day 14 following REOI on day 8 (REOI 8 d). The nociceptive head withdrawal threshold (HWT) and activities of RVM ON-or OFF-cells were recorded before and after intra-RVM astrocyte gap junction blocker carbenoxolone (CBX) microinjection. RVM astrocytes were labelled immunohistochemically with glial fibrillary acidic protein (GFAP) and analysed semi-quantitatively.Results: Persistent experimental dental occlusal interference-induced oro-facial hyperalgesia, as reflected in decreased HWTs, was partially inhibited by REOI at day 3 but not at day 8 after EOI placement. Increased GFAP-staining area occurred only in REOI 8 d group in which CBX could inhibit the maintained hyperalgesia; CBX was ineffective in inhibiting hyperalgesia in PEOI 14 d group. OFF-cell activities showed no change, but the spontaneous activity and responses of ON-cells were significantly enhanced that could be suppressed by CBX in REOI 8 d group. Conclusion:Rostral ventromedial medulla astrocytes may not participate in PEOIinduced oro-facial hyperalgesia or hyperalgesia inhibition by early REOI but are involved in the maintenance of oro-facial hyperalgesia by late REOI.

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ACC Plasticity Maintains Masseter Hyperalgesia Caused by Occlusal Interference

Cited by 10 publications

References 36 publications

Neural Pathways of Craniofacial Muscle Pain: Implications for Novel Treatments

Neural Pathways of Craniofacial Muscle Pain: Implications for Novel Treatments

Occlusal disharmony and chronic oro‐facial pain: from clinical observation to animal study

Astrocytes in the rostral ventromedial medulla contribute to the maintenance of oro‐facial hyperalgesia induced by late removal of dental occlusal interference

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