Background: Psychological factors such as anxiety and depression have been recognized as the etiology of temporomandibular disorders. Objectives: The study aimed to evaluate the prevalence of temporomandibular disorders in dental students and describe the state of depression and anxiety and related factors in the students with the disorders. Materials and methods: 323 students at the Faculty of Odonto-Stomatology, Hue University of Medicine and Pharmacy, were examined to detect temporomandibular disorders, using the DC/TMD axis I. Then GAD-7 and PHQ-9 questionnaires were used to screen for anxiety and depression in the group with the disorders. Results: The proportion of students with temporomandibular disorders was 38.1%, intra-articular disorders accounted for the highest rate (80.5%). The percentages of depression and anxiety among students with the disorder were 28.4% and 55.3%, respectively. 41.5% of TMD students had mild anxiety and the same proportion of students had risk of depression. Risk factors associated with depression and anxiety were economic status and excercise, respectively (p < 0.05). Conclusions: The percentage of students with temporomandibular disorders is relatively high. The majority of students with the disorders are at risk for depression and low level of anxiety. There is a link between the economic status and depression, between exercise and anxiety.

The long belief that dental primary afferent (DPA) neurons are entirely composed of nociceptive neurons has been challenged by several anatomical and functional investigations. In order to characterize non-nociceptivepopulation among DPA neurons, retrograde transport fluorescent dye was placed in upper molars of rats and immunohistochemical detection of peripherin and neurofilament 200 in the labeled trigeminal ganglia was performed. As the results, majority ofDPA neurons were peripherin-expressing small-sized neurons, showing characteristic ofnociceptive C-fibers. However, 25.7% of DPA were stained with antibody against neurofilament 200, indicating significant portion of DPA neurons are related to large myelinated Abeta fibers. There were a small number of neurons thatexpressed both peripherin and neurofilament 200, suggestive of Adelta fibers. The possible transition of neurochemical properties by neuronal injury induced by retrograde labeling technique was ruled out by detection of minimal expression of neuronal injury marker, ATF-3. These results suggest that in addition to the large population of C-fiber-related nociceptive neurons, a subset of DPA neurons is myelinated large neurons, which is related to low-threshold mechanosensitive Abeta fibers. We suggest that these Abeta fiber-related neurons might play a role as mechanotransducers of fluid movement within dentinal tubules.
Animals ; Dentin ; Intermediate Filament Proteins ; Membrane Glycoproteins ; Molar ; Myelin Sheath ; Nerve Tissue Proteins ; Neurofilament Proteins ; Neurons ; Neurons, Afferent ; Nociceptors ; Rats ; Trigeminal Ganglion

Mitochondrial reactive oxygen species (mROS) that are overproduced by mitochondrial dysfunction are linked to pathological conditions including sensory abnormalities. Here, we explored whether mROS overproduction induces itch through transient receptor potential canonical 3 (TRPC3), which is sensitive to ROS. Intradermal injection of antimycin A (AA), a selective inhibitor of mitochondrial electron transport chain complex III for mROS overproduction, produced robust scratching behavior in naïve mice, which was suppressed by MitoTEMPO, a mitochondria-selective ROS scavenger, and Pyr10, a TRPC3-specific blocker, but not by blockers of TRPA1 or TRPV1. AA activated subsets of trigeminal ganglion neurons and also induced inward currents, which were blocked by MitoTEMPO and Pyr10. Besides, dry skin-induced chronic scratching was relieved by MitoTEMPO and Pyr10, and also by resveratrol, an antioxidant. Taken together, our results suggest that mROS elicit itch through TRPC3, which may underlie chronic itch, representing a potential therapeutic target for chronic itch.
Animals ; Antioxidants/pharmacology* ; Mice ; Mitochondria ; Pruritus/chemically induced* ; Reactive Oxygen Species/metabolism* ; TRPA1 Cation Channel