The crucial role of NR2A mediating the activation of satellite glial cells in the trigeminal ganglion contributes to orofacial inflammatory pain during TMJ inflammation.

Temporomandibular joint inflammatory diseases are a significant subtype of temporomandibular disorders (TMD) characterized by inflammatory pain in the orofacial area. The N-methyl-D-aspartate receptor (NMDAR), specifically the NR2A subtype, was crucial in neuropathic pain. However, the exact role of NR2A in inflammatory pain in the TMJ and the molecular and cellular mechanisms mediating peripheral sensitization in the trigeminal ganglion (TG) remain unclear.

Jaw relation recording and transferring: Using digital technology to augment its instruction in predoctoral prosthodontics.

Objectives: The study compared the learning effectiveness and teaching satisfaction of dental students from three teaching methods (traditional, digital, and combined pedagogy) for instructing jaw relation recording and transferring (JRRT).

Methods: Note that, 276 fourth-year undergraduate students from three classes were randomly divided into three groups to study JRRT in complete dentures using different teaching methods: traditional pedagogy group, digital pedagogy group, and combined digital and traditional pedagogy group. After the course, the learning effectiveness of basic knowledge and satisfaction questionnaire was administered to the three groups of participants using a quick response code for online answering.

Contribution of inwardly rectifying potassium channel 4.1 in orofacial neuropathic pain: Regulation of pannexin 3 via the reactive oxygen species-activated P38 MAPK signal pathway.

The involvement of inwardly rectifying potassium channel 4.1 (Kir4.1) in neuropathic pain has been established.

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.

Temporomandibular joint osteoarthritis (TMJOA) is a severe form of temporomandibular joint disorders (TMD), and orofacial inflammatory allodynia is one of its common symptoms which lacks effective treatment. N-methyl-D-aspartate receptor (NMDAR), particularly its subtypes GluN2A and GluN2B, along with gap junctions (GJs), are key players in the mediation of inflammatory pain. However, the precise regulatory mechanisms of GluN2A, GluN2B, and GJs in orofacial inflammatory allodynia during TMJ inflammation still remain unclear.

Precise tooth design using deep learning-based templates.

Objectives: In prosthodontic procedures, traditional computer-aided design (CAD) is often time-consuming and lacks accuracy in shape restoration. In this study, we combined implicit template and deep learning (DL) to construct a precise neural network for personalized tooth defect restoration.

Methods: Ninety models of right maxillary central incisor (80 for training, 10 for validation) were collected.

Influence of intraoral scanning coverage on the accuracy of digital implant impressions - An in vitro study.

Objectives: To evaluate the influence of intraoral scanning coverage (IOSC) on digital implant impression accuracy in various partially edentulous situations and predict the optimal IOSC.

Methods: Five types of resin models were fabricated, each simulating single or multiple tooth loss scenarios with inserted implants and scan bodies. IOSC was subgrouped to cover two, four, six, eight, ten, and twelve teeth, as well as full arch.

LncRNA Anxa10-203 enhances Mc1r mRNA stability to promote neuropathic pain by recruiting DHX30 in the trigeminal ganglion.

Background: Trigeminal nerve injury is one of the most serious complications in oral clinics, and the subsequent chronic orofacial pain is a consumptive disease. Increasing evidence demonstrates long non-coding RNAs (lncRNAs) play an important role in the pathological process of neuropathic pain. This study aims to explore the function and mechanism of LncRNA Anxa10-203 in the development of orofacial neuropathic pain.

Phosphorylation of the AMPARs regulated by protein kinase C (PKC) and protein interacting with C-kinase 1 (PICK1) contribute to orofacial neuropathic pain.

The α-amino-3-hydroxy-5-methylisoxazole-4-isoxazolepropionic acid receptor (AMPAR) has been recognized to play a vital role in the development of neuropathic pain. Recent studies have indicated that protein kinase C (PKC) and protein interacting with C-kinase 1 (PICK1) are involved in the phosphorylation of AMPARs. However, whether PKC and PICK1 were involved in the AMPAR phosphorylation in the trigeminal ganglion (TG) to participate in orofacial neuropathic pain remains enigmatic.

Metabotropic glutamate receptor 5-mediated inhibition of inward-rectifying K channel 4.1 contributes to orofacial ectopic mechanical allodynia following inferior alveolar nerve transection in male mice.

Inward-rectifying K channel 4.1 (Kir4.1), which regulates the electrophysiological properties of neurons and glia by affecting K homeostasis, plays a critical role in neuropathic pain.

NMDARs mediate peripheral and central sensitization contributing to chronic orofacial pain.

Peripheral and central sensitizations of the trigeminal nervous system are the main mechanisms to promote the development and maintenance of chronic orofacial pain characterized by allodynia, hyperalgesia, and ectopic pain after trigeminal nerve injury or inflammation. Although the pathomechanisms of chronic orofacial pain are complex and not well known, sufficient clinical and preclinical evidence supports the contribution of the N-methyl-D-aspartate receptors (NMDARs, a subclass of ionotropic glutamate receptors) to the trigeminal nociceptive signal processing pathway under various pathological conditions. NMDARs not only have been implicated as a potential mediator of pain-related neuroplasticity in the peripheral nervous system (PNS) but also mediate excitatory synaptic transmission and synaptic plasticity in the central nervous system (CNS).

Interactions Among Non-Coding RNAs and mRNAs in the Trigeminal Ganglion Associated with Neuropathic Pain.

Background: Recent studies have demonstrated the contribution of non-coding RNAs (ncRNAs) to neuropathic pain. However, the expression profile of ncRNAs in the trigeminal ganglion (TG) and their functional mechanism underlying trigeminal neuropathic pain are still unclear.

Methods: In the present study, the trigeminal neuropathic pain model induced by chronic constriction injury of the infraorbital nerve (CCI-ION) was used to study the expression profile and potential regulatory mechanism of miRNAs, lncRNAs, circRNAs, and mRNAs in the TG by RNA-sequencing (RNA-seq) and bioinformatics analysis.

Differential roles of NMDAR subunits 2A and 2B in mediating peripheral and central sensitization contributing to orofacial neuropathic pain.

The spinal N-methyl-d-aspartate receptor (NMDAR), particularly their subtypes NR2A and NR2B, plays pivotal roles in neuropathic and inflammatory pain. However, the roles of NR2A and NR2B in orofacial pain and the exact molecular and cellular mechanisms mediating nervous system sensitization are still poorly understood. Here, we exhaustively assessed the regulatory effect of NMDAR in mediating peripheral and central sensitization in orofacial neuropathic pain.

Activation of the N-methyl-D-aspartate receptor contributes to orofacial neuropathic and inflammatory allodynia by facilitating calcium-calmodulin-dependent protein kinase II phosphorylation in mice.

Neuropathic and inflammatory pain are major clinical challenges due to their ambiguous mechanisms and limited treatment approaches. N-methyl-D-aspartate receptor (NMDAR) and calcium-calmodulin-dependent protein kinase II (CaMKII) are responsible for nerve system sensation and are required for the induction and maintenance of pain. However, the roles of NMDAR and CaMKII in regulating orofacial pain are still less well known.

Guideline for Quality Control of Powered Polymerisation Activators for Chairside Use.

The irradiance of powered polymerisation activators for chairside use affects composite resin adhesive curing during the restorative process, whereas radiant accumulated temperature rise relates to clinical safety. Irradiance reduction and high radiant accumulated temperature will compromise the treatment results as there is a lack of curing output efficacy and safety awareness for powered polymerisation activators. Insufficient attention has been paid to the activator's quality control, irradiance attenuation and radiant accumulated temperature excessive temperature rise during its lifetime.

The influence of crown coverage on the accuracy of static guided implant surgery in partially edentulous models: An in vitro study.

Objective: To evaluate the influence of crown coverage of surgical guides on the accuracy of static computer-assisted implant surgeries (sCAISs) in different partially edentulous situations.

Methods: Acrylic models with five types of partially edentulous situations were fabricated in this study. In coDiagnostiX software (Dental Wings, Montreal, Canada), surgical templates were designed and fabricated with reduced crown coverage (RCC), standard crown coverage (SCC) and extended crown coverage (ECC).

C-X-C motif chemokine ligand 1 and its receptor C-X-C motif chemokine receptor 2 in trigeminal ganglion contribute to nerve injury-induced orofacial mechanical allodynia.

Background: Orofacial ectopic pain induced by trigeminal nerve injury is a serious complication of dental treatment. C-X-C motif chemokine ligand 1 (CXCL1) and its primary receptor C-X-C motif chemokine receptor 2 (CXCR2) contribute to the development and maintenance of neuropathic pain in the spinal nervous system, but their roles in trigeminal neuropathic sensation are still poorly understood.

Objectives: This study aimed to investigate the exact role of CXCL1 and CXCR2 in the regulation of orofacial ectopic mechanical allodynia and their potential downstream mechanisms in the trigeminal ganglion (TG).

NMDAR1-Src-Pannexin1 Signal Pathway in the Trigeminal Ganglion Contributed to Orofacial Ectopic Pain Following Inferior Alveolar Nerve Transection.

The N-methyl-d-aspartate receptor (NMDAR) is a glutamate-gated receptor channel that plays a role in peripheral neuropathic pain. Src, a protein tyrosine kinase, can regulate the activation of NMDARs in chronic pain conditions. Pannexin 1 (Panx1), a plasma membrane channel, plays an important role in neuropathic pain and functionally interacts with NMDARs in the pathological condition of epilepsy.

The α2δ-1-NMDAR1 interaction in the trigeminal ganglion contributes to orofacial ectopic pain following inferior alveolar nerve injury.

Orofacial ectopic pain can often arise following nerve injury. However, the exact mechanism responsible for orofacial ectopic pain induced by trigeminal nerve injury remains unknown. The α2δ-1 and glutamate N-methyl-d-aspartic acid receptor (NMDAR) interactions have been demonstrated to participate in neuropathic pain regulation in the spinal cord.

Activation of oxytocin receptor in the trigeminal ganglion attenuates orofacial ectopic pain attributed to inferior alveolar nerve injury.

This study explores the effects of oxytocin receptor (OXTR) in the trigeminal ganglion (TG) on orofacial neuropathic pain. We demonstrate that OXTR activation in the TG relieves the orofacial ectopic pain as well as inhibits the upregulated expression of calcitonin gene-related peptide (CGRP), IL-1β, and TNFα in the TG and spinal trigeminal nucleus caudalis (SpVc) of rats with inferior alveolar nerve transection. OXTR, a G protein-coupled receptor, has been demonstrated to play a significant role in analgesia after activation by its canonical agonist oxytocin (OXT) in the dorsal root ganglion.

Effects of trigeminal nerve injury on the expression of galanin and its receptors in the rat trigeminal ganglion.

In the spinal nervous system, the expression of galanin (GAL) and galanin receptors (GALRs) that play important roles in the transmission and modulation of nociceptive information can be affected by nerve injury. However, in the trigeminal nervous system, the effects of trigeminal nerve injury on the expression of GAL are controversy in the previous studies. Besides, little is known about the effects of trigeminal nerve injury on the expression of GALRs.

Activation of the RAS/B-RAF-MEK-ERK pathway in satellite glial cells contributes to substance p-mediated orofacial pain.

The cross talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs) is crucial for the regulation of inflammatory orofacial pain. Substance P (SP) plays an important role by activating neurokinin (NK)-I receptors in this cross talk. The activation of extracellular signal-regulated kinase (ERK) 1/2, protein kinase A (PKA) and protein kinase C (PKC) in neurons and SGCs of peripheral ganglions by peripheral inflammation is associated with inflammatory hypersensitivity.

The P2Y receptor in the trigeminal ganglion contributes to the maintenance of inflammatory pain.

P2Y purinergic receptors expressed in neurons and satellite glial cells (SGCs) of the trigeminal ganglion (TG) contribute to inflammatory and neuropathic pain. P2Y receptor expression is reported in the spinal cord, dorsal root ganglion (DRG), and TG. In present study, the role of P2Y receptor in the TG in inflammatory orofacial pain of Sprague-Dawley (SD) rats was investigated.

[Minimal invasive microscopic tooth preparation based on endodontic, periodontal and functional health].

Tooth preparation is the primary and core operation technique for dental esthetic restoration treatment, due to its effect of providing restoration space, bonding interfaces and marginal lines for dental rehabilitation after tooth tissue reduction. The concept of microscopic minimal invasive dentistry put forward the issue of conducting high-quality tooth preparation, conserve tooth-structure, protect vital pulp and periodontal tissue simultaneously. This study reviewed the concepts, physiology background, design and minimal invasive microscopic tooth preparation, and in the meantime, individualized strategies and the two core elements of tooth preparation (quantity and shape) are listed.

GABA receptor activation attenuates inflammatory orofacial pain by modulating interleukin-1β in satellite glial cells: Role of NF-κB and MAPK signaling pathways.

Orofacial inflammation could activate satellite glial cells (SGCs) in the trigeminal ganglion (TG) to produce interleukin 1β (IL-1β) which plays crucial roles in the development of inflammatory pain. Recent studies have shown that gamma-amino butyric acid-B (GABA) receptor could modulate the expression of inflammatory cytokines in microglia and astrocytes in the spinal cord. The objective of this study was to investigate whether GABA receptors in TG SGCs attenuate inflammatory facial pain via mediating IL-1β following inflammation and its mechanisms.