Spinal CCK1 Receptors Contribute to Somatic Pain Hypersensitivity Induced by Malocclusion via a Reciprocal Neuron-Glial Signaling Cascade

Xiang, Ting; Li, Jia-Heng; Su, Han-Yu; Bai, Kun-Hong; Wang, Shuang; Traub, Richard J.; Cao, Dong-Yuan

doi:10.1016/j.jpain.2022.05.009

Cited by 6 publications

(9 citation statements)

References 87 publications

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“…Systemic antagonism of TNF reverses mechanical hyperalgesia that has developed after colonic mustard oil ( 174 ), suggesting the role of circulating cytokines in trans-segmental sensitization. A recent study has reported a more sophisticated comorbid pain model: unilateral anterior cross bite in rats produces somatic pain hypersensitivity, which involves the cholecystokinin receptor-mediated descending facilitation system ( 175 ). Mechanistically, the gut microbiome was also proposed to be involved in TMJ pain ( 176 ).…”

Section: Preclinical Studies For Tmjoa and Pain From Tmjmentioning

confidence: 99%

The degeneration-pain relationship in the temporomandibular joint: Current understandings and rodent models

et al. 2023

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Temporomandibular disorders (TMD) represent a group of musculoskeletal conditions involving the temporomandibular joints (TMJ), the masticatory muscles and associated structures. Painful TMD are highly prevalent and conditions afflict 4% of US adults annually. TMD include heterogenous musculoskeletal pain conditions, such as myalgia, arthralgia, and myofascial pain. A subpopulations of TMD patients show structural changes in TMJ, including disc displacement or degenerative joint diseases (DJD). DJD is a slowly progressing, degenerative disease of the TMJ characterized by cartilage degradation and subchondral bone remodeling. Patients with DJD often develop pain (TMJ osteoarthritis; TMJ OA), but do not always have pain (TMJ osteoarthrosis). Therefore, pain symptoms are not always associated with altered TMJ structures, which suggests that a causal relationship between TMJ degeneration and pain is unclear. Multiple animal models have been developed for determining altered joint structure and pain phenotypes in response to various TMJ injuries. Rodent models of TMJOA and pain include injections to induce inflammation or cartilage destruction, sustained opening of the oral cavity, surgical resection of the articular disc, transgenic approaches to knockout or overexpress key genes, and an integrative approach with superimposed emotional stress or comorbidities. In rodents, TMJ pain and degeneration occur during partially overlapping time periods in these models, which suggests that common biological factors may mediate TMJ pain and degeneration over different time courses. While substances such as intra-articular pro-inflammatory cytokines commonly cause pain and joint degeneration, it remains unclear whether pain or nociceptive activities are causally associated with structural degeneration of TMJ and whether structural degeneration of TMJ is necessary for producing persistent pain. A thorough understanding of the determining factors of pain-structure relationships of TMJ during the onset, progression, and chronification by adopting novel approaches and models should improve the ability to simultaneously treat TMJ pain and TMJ degeneration.

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Section: Preclinical Studies For Tmjoa and Pain From Tmjmentioning

confidence: 99%

The degeneration-pain relationship in the temporomandibular joint: Current understandings and rodent models

et al. 2023

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“…A dysfunction of the temporomandibular joint (TMJ), and/or the presence of periodontitis can cause alterations of dental occlusion, i.e., a discrepancy in the relationship between the teeth of the upper and lower arches [ 28 , 29 ]. The same mandibular joint pain can negatively affect the occlusion, which condition of impaired joint use involves just under 19% of patients with FMS [ 30 ]. The main afferents from the TMJ project to the trigeminal subnuclei interpolaris/caudalis transition zones (Vi/Vc), which is an important arrival station of nociceptive information, which starts to manage nociception [ 30 , 31 ].…”

Section: Reviewmentioning

confidence: 99%

“…The same mandibular joint pain can negatively affect the occlusion, which condition of impaired joint use involves just under 19% of patients with FMS [ 30 ]. The main afferents from the TMJ project to the trigeminal subnuclei interpolaris/caudalis transition zones (Vi/Vc), which is an important arrival station of nociceptive information, which starts to manage nociception [ 30 , 31 ]. The same nociceptive afferents send information to the ventromedial rostral Vi/Vc area of the spinal cord (C1-2) [ 30 , 31 ].…”

Section: Reviewmentioning

confidence: 99%

“…The main afferents from the TMJ project to the trigeminal subnuclei interpolaris/caudalis transition zones (Vi/Vc), which is an important arrival station of nociceptive information, which starts to manage nociception [ 30 , 31 ]. The same nociceptive afferents send information to the ventromedial rostral Vi/Vc area of the spinal cord (C1-2) [ 30 , 31 ]. In an animal model, a malocclusion generates a lowering of the pain threshold, widening the hypersensitivity of somatic pain, typical of FMS [ 30 ].…”

Section: Reviewmentioning

confidence: 99%

“…The same nociceptive afferents send information to the ventromedial rostral Vi/Vc area of the spinal cord (C1-2) [ 30 , 31 ]. In an animal model, a malocclusion generates a lowering of the pain threshold, widening the hypersensitivity of somatic pain, typical of FMS [ 30 ]. A nociceptive increase causes an increase in cholecystokinin (CKK), a neuropeptide found in the central nervous system, which increases and stimulates the descending pain pathways from the periaqueductal gray (PAG) midbrain and ventromedial Vi/Vc-rostral spinal cord [ 30 ].…”

Section: Reviewmentioning

confidence: 99%

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Fibromyalgia syndrome (FMS) is a systemic and multifactorial disease of unknown etiology. There are many co-morbidities that the patient presents, making the clinical picture not immediate. Cognitive decline and emotional alteration (anxiety and depression) are found in fibromyalgic patients, as well as temporomandibular joint arthrokinematic disorders, dental malocclusion, and periodontitis. There seems to be a biunivocal relationship between oral and psychiatric dysfunctions in fibromyalgia. The article reviews the information regarding oral health alterations with respect to the patient's cognitive and emotional response, as the most recent information we have raises new hypotheses about the diagnosis of FMS.

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Spinal CCK1 Receptors Contribute to Somatic Pain Hypersensitivity Induced by Malocclusion via a Reciprocal Neuron-Glial Signaling Cascade

Cited by 6 publications

References 87 publications

The degeneration-pain relationship in the temporomandibular joint: Current understandings and rodent models

The degeneration-pain relationship in the temporomandibular joint: Current understandings and rodent models

The Cognitive and Emotional Aspect in Fibromyalgia: The Importance of the Orofacial Sphere

Valproate attenuates somatic hyperalgesia induced by orofacial inflammation combined with stress through inhibiting spinal IL-6 and STAT1 phosphorylation

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