Genetics Affecting the Prognosis of Dental Treatments.

Genetics plays a significant role in determining an individual's susceptibility to dental diseases, the response to dental treatments, and the overall prognosis of dental interventions. Here, the authors explore the various genetic factors affecting the prognosis of dental treatments focusing on dental caries, orthodontic treatment, oral cancer, prosthodontic treatment, periodontal disease, developmental disorders, pharmacogenetics, and genetic predisposition to faster wound healing. Understanding the genetic underpinnings of dental health can help personalize treatment plans, predict outcomes, and improve the overall quality of dental care.

Genetic contributions to pain modulation in sickle cell: A focus on single nucleotide polymorphisms.

Background: Despite recent advances in our knowledge of genetic contributions to the highly variable sickle cell disease (SCD) phenotype, our understanding of genetic factors associated with pain sensitivity in SCD remains limited. Previous studies investigated specific variants in single candidate genes and their association with SCD pain variability. The primary aim of the current study was to expand the genes and polymorphisms tested to discover new risk genes (polymorphisms) associated with central sensitization for individuals with SCD.

Post-Traumatic Trigeminal Neuropathy: Neurobiology and Pathophysiology.

Painful traumatic trigeminal neuropathy (PTTN) is a chronic neuropathic pain that may develop following injury to the trigeminal nerve. Etiologies include cranio-orofacial trauma that may result from dental, surgical, or anesthetic procedures or physical trauma, such as a motor vehicle accident. Following nerve injury, there are various mechanisms, including peripheral and central, as well as phenotypic changes and genetic predispositions that may contribute to the development of neuropathic pain.

A peptidomimetic modulator of the Ca2.2 N-type calcium channel for chronic pain.

Transmembrane Ca2.2 (N-type) voltage-gated calcium channels are genetically and pharmacologically validated, clinically relevant pain targets. Clinical block of Ca2.

Intranasal CRMP2-Ubc9 inhibitor regulates Na V 1.7 to alleviate trigeminal neuropathic pain.

Dysregulation of voltage-gated sodium Na V 1.7 channels in sensory neurons contributes to chronic pain conditions, including trigeminal neuropathic pain. We previously reported that chronic pain results in part from increased SUMOylation of collapsin response mediator protein 2 (CRMP2), leading to an increased CRMP2/Na V 1.

Time-Course Progression of Whole Transcriptome Expression Changes of Trigeminal Ganglia Compared to Dorsal Root Ganglia in Rats Exposed to Nerve Injury.

Mechanisms underlying neuropathic pain (NP) are complex with multiple genes, their interactions, environmental and epigenetic factors being implicated. Transcriptional changes in the trigeminal (TG) and dorsal root (DRG) ganglia have been implicated in the development and maintenance of NP. Despite efforts to unravel molecular mechanisms of NP, many remain unknown.

Intranasal CRMP2-Ubc9 Inhibitor Regulates Na 1.7 to Alleviate Trigeminal Neuropathic Pain.

Dysregulation of voltage-gated sodium Na 1.7 channels in sensory neurons contributes to chronic pain conditions, including trigeminal neuropathic pain. We previously reported that chronic pain results in part from increased SUMOylation of collapsin response mediator protein 2 (CRMP2), leading to an increased CRMP2/Na 1.

Association between medication-induced xerostomia and orofacial pain: a systematic review.

Objective: Xerostomia (or oral dryness) is most commonly caused by medications that affect saliva secretion, and is often accompanied by symptoms of orofacial pain. Medication-induced xerostomia may or may not be associated with objectively demonstrable hyposalivation. The present study attempted to systematically identify an association between medication-induced xerostomia and orofacial pain.

Effects of intra-nasal melanocortin-4 receptor antagonist on trigeminal neuropathic pain in male and female rats.

Treatment of chronic orofacial pain remains a major therapeutic challenge despite available medications. Melanocortins have been implicated in pathologic pain. Intrathecal administration of MC4R antagonists has been shown to alleviate neuropathic pain (NP) in male rats.

Pathophysiology of Post-Traumatic Trigeminal Neuropathic Pain.

Trigeminal nerve injury is one of the causes of chronic orofacial pain. Patients suffering from this condition have a significantly reduced quality of life. The currently available management modalities are associated with limited success.

Response profile in a rat model of exercise-induced hypoalgesia is associated with duloxetine, pregabalin and diclofenac effect on constriction-induced neuropathy.

Background: Exercise is a known trigger of the inhibitory pain modulation system and its analgesic effect is termed exercise-induced hypoalgesia (EIH). Previous studies have demonstrated that rats with deficient analgesic response following exercise develop more significant hypersensitivity following nerve injury compared to rats with substantial analgesic response following exercise.

Objectives: A rat model of EIH as an indicator of the pain inhibitory system's efficiency was used to explore the association between EIH profiles and the effect of pharmacotherapy on rat's neuropathic pain.

Potential differences in somatosensory function during premenopause and early and late postmenopause in patients with burning mouth syndrome: An observational case-control study.

Background/purpose: Burning mouth syndrome (BMS) is a chronic condition presenting as intraoral burning or dysesthesia, with a high preponderance in menopausal women. This study aimed to examine the association between somatosensory dysfunction and BMS in premenopausal, early postmenopausal, and late postmenopausal patients, using a standardized Quantitative Sensory Testing (QST) protocol, and to determine the predictive value of thermal or mechanical perception by QST for detecting BMS.

Materials And Methods: An observational case-control study was performed with 36 female participants with BMS (12 premenopausal, 10 early postmenopausal, and 14 late postmenopausal) and 42 age- and sex-matched healthy volunteers (21 premenopausal, 10 early postmenopausal, and 11 late postmenopausal).

Chemogenetic inhibition of trigeminal ganglion neurons attenuates behavioural and neural pain responses in a model of trigeminal neuropathic pain.

Background: Nerve injury can lead to ectopic activation of injured nociceptorsand central sensitization characterized by allodynia and hyperalgesia. Reduction in the activity of primary afferent neurons has been shown to be sufficient in alleviating peripherally generated pain. The cell bodies of such trigeminal nociceptors are located in the trigeminal ganglia (TG) with central processes that terminate in the brainstem trigeminal nucleus caudalis (TNC).

Diagnostic Tool Using the Diagnostic Criteria for Temporomandibular Disorders: A Randomized Crossover-Controlled, Double-Blinded, Two-Center Study.

Aims: To assess the speed and accuracy of a checklist user interface for the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD).

Methods: A diagnostic tool formatted as a checklist was developed and compared to an existing diagnostic tool, the DC/TMD diagnsostic decision trees. Both types of tools use the DC/TMD and were tested by dental students, interns, and residents in the USA and Japan for diagnosis of hypothetical patients.

Exercise-Induced Hypoalgesia Profile in a Rat Neuropathic Pain Model Predicts Pain Severity Following Infraorbital Nerve Injury and Is Associated with Local Cytokine Levels, Systemic Endocannabinoids, and Endogenous Opioids.

Aims: To investigate the role of exercise-induced hypoalgesia (EIH) in the development of neuropathic pain (NP) following infraorbital nerve (ION) injury and to explore possible underlying mechanisms defining the differences between rats with high and low EIH.

Methods: EIH was evaluated by measuring the percentage of withdrawal responses to a series of 30 mechanical stimuli applied to the hind paw before and after 180 seconds of exercise on a rotating rod. The rats were assigned to low- and high-EIH groups based on reduction in the percent of withdrawal responses following exercise.

Genetic variation in catechol-O-methyltransferase is associated with individual differences in conditioned pain modulation in healthy subjects.

Background: Genetic variation in the catechol-O-methyltransferase (COMT) gene is associated with sensitivity to both acute experimental pain and chronic pain conditions. Four single nucleotide polymorphisms (SNPs) have traditionally been used to infer three common haplotypes designated as low, average and high pain sensitivity and are reported to affect both COMT enzymatic activity and pain sensitivity. One mechanism that may partly explain individual differences in sensitivity to pain is conditioned pain modulation (CPM).

Exercise induced hypoalgesia profile in rats is associated with IL-10 and IL-1 β levels and pain severity following nerve injury.

Background: Pain may undergo modulation in the central nervous system prior to reaching the primary somatosensory cortex and being perceived as pain. Faulty pain modulation mechanisms have been linked to various chronic pain conditions. Cytokines such as IL-10 and IL-1beta, are known to be involved in initiation and maintenance of neuropathic pain.

Effects of melanocortin-4 receptor (MC4R) antagonist on neuropathic pain hypersensitivity in rats - A systematic review and meta-analysis.

Melanocortin-4 receptor (MC4R) has been investigated as a potential drug target for the treatment of neuropathic pain. The objective of the study was to systematically identify the effects of MC4R antagonists on hypersensitivity in rat models of neuropathic pain. A systematic search was conducted using the following databases: WoS, PubMed, SCOPUS, and MEDLINE.

Postendodontic pain: a practical approach to diagnosis and management.

Objectives: Endodontic treatment is a routine procedure performed by general dental practitioners and endodontists on a daily basis. Fortunately, most patients undergoing endodontic therapy show a favorable outcome with uneventful healing. However, some patients develop pain following endodontic therapy.

Molecular mechanisms of painful traumatic trigeminal neuropathy-Evidence from animal research and clinical correlates.

Painful traumatic trigeminal neuropathy (PTTN) may occur following major craniofacial or oral trauma, or may be subsequent to relatively minor dental interventions. Following injury, pain may originate from a peripheral nerve, a ganglion, or from the central nervous system. In this review, we focus on molecular mechanisms of pain resulting from injury to the peripheral branch of the trigeminal nerve.

Differential gene expression changes in the dorsal root versus trigeminal ganglia following peripheral nerve injury in rats.

Background: The dorsal root (DRG) and trigeminal (TG) ganglia contain cell bodies of sensory neurons of spinal and trigeminal systems, respectively. They are homologs of each other; however, differences in how the two systems respond to injury exist. Trigeminal nerve injuries rarely result in chronic neuropathic pain (NP).

The Effect of Nonstrenuous Aerobic Exercise in Patients with Chronic Masticatory Myalgia.

Aims: To evaluate the effect of nonstrenuous aerobic exercise on chronic masticatory myalgia (CMM) patients and healthy controls (HC) by means of mechanical temporal summation (TS) and response to mechanical stimulation (RMS) performed on the dominant forearm.

Methods: A total of 30 patients diagnosed with CMM and 30 pain-free HCs were first evaluated for maximum number of steps (MNS) on a stepper machine for 1 minute. Additionally, they completed the Generalized Anxiety Disorder (GAD-7), Graded Chronic Pain Scale (GCPS), and Jaw Functional Limitation Scale (JFL) questionnaires.

Primary burning mouth syndrome: Literature review and preliminary findings suggesting possible association with pain modulation.

Primary burning mouth syndrome (BMS) is a chronic pain of a burning quality affecting the tongue and intraoral mucosa. Currently, there are no definite diagnostic criteria; therefore, the diagnosis is made by exclusion of potential local and systemic causes that could justify the burning sensation. The etiology behind primary BMS remains unclear; however, the most acceptable theories link primary BMS with neuropathic pain.