Activation of satellite glial cells in trigeminal ganglion following dental injury and inflammation

Liu, Haichao; Zhao, Lei; Gu, Wen-Zhen; Liu, Qin; Gao, Zhixiong; Zhu, Xiao; Wu, Zhi-Fu; He, Hongwen; Huang, Fang; Fan, Wenguo

doi:10.1007/s10735-018-9765-4

Cited by 27 publications

(26 citation statements)

References 31 publications

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“…Similar to our data, Hawkins showed that secondary traumatic stress increases GFAP and leads to trigeminal sensitization, and dental injuries can lead to GFAP activation through ocular inflammation . As GFAP is directly associated with neural damage, inflammation in any structure related to the trigeminal ganglion seems to lead to neuroinflammation and altered behavior due to discomfort in the head and neck region and the blockage of TNF‐α pathway was important to attenuates GFAP overexpression, neuroinflammation, and oral discomfort in this ODI experimental model.…”

Section: Discussionsupporting

confidence: 88%

Tumor necrosis factor alpha mediates orofacial discomfort in an occlusal dental interference model in rats: The role of trigeminal ganglion inflammation

Silva

Martins

Neto

et al. 2019

J Oral Pathology Medicine

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Background: Tumor necrosis factor alpha (TNF-α) is a proinflammatory cytokine that plays an important role in the early stages of inflammation. In this study, we investigated its role in orofacial discomfort in rats subjected to occlusal dental interference (ODI). Methods:Female Wistar rats (180-200 g) were divided in three groups (n = 30/group):sham group, without ODI, and two experimental groups with ODI pre-treated with 0.1 mL/kg saline (ODI + SAL) or 5 mg/kg infliximab (ODI + INF) and treated every 3 days. The animals were euthanized after 1, 3, and 7 days. The number of bites and scratches and grimace scale scores were determined daily, and the bilateral trigeminal ganglion was histomorphometrically (neuronal body area) analyzed and submitted for immunohistochemistry for TNF-α, nitric oxide synthesis (NOS) neuronal (nNOS) and inducible (iNOS), peroxisome proliferator-activated receptors (PPAR) y (PPARy) and δ/β (PPARδ/β), and glial fibrillary acidic protein (GFAP). One-way/two-way ANOVA/ Bonferroni tests were used (P < .05, GraphPad Prism 5.0). Results:ODI + SAL showed a large number of bites (P = .002), scratches (P = .002), and grimace scores (P < .001) in the firsts days, and ODI + INF partially reduced these parameters. The contralateral and ipsilateral neuronal body area was significantly reduced on day 1 in ODI + SAL, but returned to the basal size on days 3 and 7, by increase in TNF-α, nNOS, PPARy, PPARδ/β, and GFAP immunostaining. The infliximab treatment attenuated these alterations (P < .05). There was no iNOS immunostaining. Conclusion:Occlusal dental interference induced transitory orofacial discomfort by trigeminal inflammatory mediator overexpression, and TNF-α blockage attenuated these processes.

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Section: Discussionsupporting

confidence: 88%

Tumor necrosis factor alpha mediates orofacial discomfort in an occlusal dental interference model in rats: The role of trigeminal ganglion inflammation

Silva

Martins

Neto

et al. 2019

J Oral Pathology Medicine

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“…Also, there was an increase in the number of neurons enrolled by GFAP-immunopositive satellite cells, after the extraction of right maxillary first and second molars in rats, for up to 10 days [ 39 ]. Corroborating our data, Liu et al 2018 demonstrated a time-related increase of GFAP-positive SGC surrounding the TG, peaking at 28 days after tooth pulp exposure [ 54 ].…”

Section: Discussionsupporting

confidence: 86%

Activation of trigeminal ganglion satellite glial cells in CFA-induced tooth pulp pain in rats

et al. 2018

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This study further investigated the mechanisms underlying the rat model of tooth pulp inflammatory pain elicited by complete Freund’s adjuvant (CFA), in comparison to other pulpitis models. Pulps of the left maxillary first molars were accessed. In the CFA group, the pulps were exposed, and CFA application was followed by dental sealing. In the open group, the pulps were left exposed to the oral cavity. For the closed group, the pulps were exposed, and the teeth were immediately sealed. Naïve rats were used as negative controls. Several parameters were evaluated at 1, 2, 3 and 8 days. There was no statistical significant difference among the groups when body weight variation, food or water consumption were compared. Analysis of serum cytokines (IL-1β, TNF or IL-6) or differential blood cell counts did not reveal any evidence of systemic inflammation. The CFA group displayed a significant reduction in the locomotor activity (at 1 and 3 days), associated with an increased activation of satellite glial cells in the ipsilateral trigeminal ganglion (TG; for up to 8 days). Amygdala astrocyte activation was unaffected in any experimental groups. We provide novel evidence indicating that CFA-induced pulp inflammation impaired the locomotor activity, with persistent activation of ipsilateral TG satellite cells surrounding sensory neurons, without any evidence of systemic inflammation or amygdala astrogliosis.

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“…In our study, we observed microglial and astrocytes activation in the Vc on days 21 and 28 in a time-dependent manner, similar to previous research that has reported that DPI markedly increases microglial activation in the Vc, beginning at 14 days and peaking at 21 days [11]. Moreover, previous literature has reported that DPI-induced activation of satellite glial cells in the trigeminal ganglion between days 7 and 28 [30]. In our study, despite the recovery in pain-related behaviors between days 14 and 21, there was glial activation in Vc at 21 days and continued up to day 28 after DPI (Figure 3).…”

Section: Neuroinflammatory Profile After Pulp Exposuresupporting

confidence: 91%

Analgesic and Neuroprotective Effects of Electroacupuncture in a Dental Pulp Injury Model—A Basic Research

Romero

Lee

Fuh

et al. 2020

IJMS

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Irreversible pulpitis is an extremely painful condition and its consequence in the central nervous system (CNS) remains unclear. A mouse model of dental pulp injury (DPI) resembles the irreversible pulpitis profile in humans. This study sought to determine whether pain induced by DPI activates microglia and astrocytes in the trigeminal subnucleus caudalis (Vc), as well as increases levels of proinflammatory cytokines, and whether electroacupuncture (EA) can be a potential analgesic and neuroprotective therapy following DPI. Pain behavior was measured via head-withdrawal threshold (HWT) and burrowing behavior at days 1, 3, 7, 14 and 21 after DPI. A marked decrease in HWT and burrowing activity was observed from day 1 to 14 after DPI and no changes were seen on day 21. Microglial and astrocytes activation; along with high cytokine (TNFα, IL-1β, and IL-6) levels, were observed in the Vc at 21 days after DPI. These effects were attenuated by verum (local and distal) EA, as well as oral ibuprofen administration. The results suggest that DPI-induced pain and glial activations in the Vc and EA exert analgesic efficacy at both local and distal acupoints. Furthermore, verum (local and distal) EA might be associated with the modulations of microglial and astrocytes activation.

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Activation of satellite glial cells in trigeminal ganglion following dental injury and inflammation

Cited by 27 publications

References 31 publications

Tumor necrosis factor alpha mediates orofacial discomfort in an occlusal dental interference model in rats: The role of trigeminal ganglion inflammation

Tumor necrosis factor alpha mediates orofacial discomfort in an occlusal dental interference model in rats: The role of trigeminal ganglion inflammation

Activation of trigeminal ganglion satellite glial cells in CFA-induced tooth pulp pain in rats

Analgesic and Neuroprotective Effects of Electroacupuncture in a Dental Pulp Injury Model—A Basic Research

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