Effects of trait anxiety,somatosensory amplification,and facial pain on self-reported oral behaviors

Objectives

Oral behaviors are activities, like gum chewing, teeth clenching, and biting of objects, that go beyond normal functioning demands and contribute to the onset of temporomandibular disorders (TMD). Somatosensory amplification refers to the tendency to experience somatic sensations as intense, noxious, and disturbing and is related to bodily hypervigilance. Clinical experience suggests that individuals with bodily hypervigilance also present with occlusal hypervigilance and continuously check their occlusion. This study aimed at investigating whether somatosensory amplification and trait anxiety, a characteristic correlated with hypervigilance, are associated with a greater incidence of oral behaviors, and verifying how self-reported facial TMD pain affect this relationship.

Materials and methods

The State-Trait Anxiety Inventory, the Somatosensory Amplification Scale, the Oral Behavior Checklist (OBC), and the TMD-Pain Screener Questionnaire were filled out by 255 University students with self-reported facial TMD pain (PAIN group; 47 subjects, 24.8 ± 4.2 years) and without pain (CTR group; 208 subjects, 26.0 ± 4.8 years) using a web survey.

Results

Trait anxiety, somatosensory amplification, and OBC scores were greater in the PAIN than CTR group (all p < 0.05). Trait anxiety and somatosensory amplification were positively associated with the frequency of oral behaviors, as measured with the OBC (all p < 0.05). A significant effect of the interaction study group*trait anxiety (p = 0.028) on OBC scores was found.

Conclusions

Individuals with greater trait anxiety and somatosensory amplification report more frequent oral behaviors. The relationship between anxiety and oral behaviors is affected by concurrent facial pain.

Clinical relevance

Individuals with increased trait anxiety and concurrent facial pain report more frequent oral behaviors than those without pain. Clinicians should evaluate patients’ anxiety and somatosensory amplification before starting dental treatment.

     

Selective Blockade of Dopamine D3 Receptors Enhances while D2 Receptor Antagonism Impairs Social Novelty Discrimination and Novel Object Recognition in Rats: A Key Role for the Prefrontal Cortex

Dopamine D₃ receptor antagonists exert pro-cognitive effects in both rodents and primates. Accordingly, this study compared the roles of dopamine D₃ vs D₂ receptors in social novelty discrimination (SND), which relies on olfactory cues, and novel object recognition (NOR), a visual-recognition task. The dopamine D₃ receptor antagonist, {"type":"entrez-protein","attrs":{"text":"S33084","term_id":"420474","term_text":"pir||S33084"}}S33084 (0.04–0.63 mg/kg), caused a dose-related reversal of delay-dependent impairment in both SND and NOR procedures in adult rats. Furthermore, mice genetically deficient in dopamine D₃ receptors displayed enhanced discrimination in the SND task compared with wild-type controls. In contrast, acute treatment with the preferential dopamine D₂ receptor antagonist, L741,626 (0.16–5.0 mg/kg), or with the dopamine D₃ agonist, PD128,907 (0.63–40 μg/kg), caused a dose-related impairment in performance in rats in both tasks after a short inter-trial delay. Bilateral microinjection of {"type":"entrez-protein","attrs":{"text":"S33084","term_id":"420474","term_text":"pir||S33084"}}S33084 (2.5 μg/side) into the prefrontal cortex (PFC) of rats increased SND and caused a dose-related (0.63–2.5 μg/side) improvement in NOR, while intra-striatal injection (2.5 μg/side) had no effect on either. In contrast, bilateral microinjection of L741,626 into the PFC (but not striatum) caused a dose-related (0.63–2.5 μg/side) impairment of NOR. These observations suggest that blockade of dopamine D₃ receptors enhances both SND and NOR, whereas D₃ receptor activation or antagonism of dopamine D₂ receptor impairs cognition in these paradigms. Furthermore, these actions are mediated, at least partly, by the PFC. These data have important implications for exploitation of dopaminergic mechanisms in the treatment of schizophrenia and other CNS disorders, and support the potential therapeutic utility of dopamine D₃ receptor antagonism.     

Modulatory effect of the SLC9A3 gene on susceptibility to infections and pulmonary function in children with cystic fibrosis

In cystic fibrosis (CF), CFTR dysfunction leads to salt and water imbalance across airway epithelia, depleted surface liquid layer, and impaired mucociliary clearance. This provides optimal conditions for chronic bacterial infections leading to excessive inflammation and progressive obstructive lung disease. We hypothesized that other epithelial channels affecting salt balance across the airways may play a role in the susceptibility to bacterial infections and modulate severity of CF lung disease. The SLC9A3 gene encoding a Na⁺/H⁺ exchanger was demonstrated to be a modifier intestinal disease in a murine model of CF. We examined the potential role of SLC9A3 as a modifier of CF lung disease severity. We analyzed 11 SLC9A3 gene variants for association with age of first Pseudomonas aeruginosa infection and lung function in children with CF. The T allele of an intronic variant in the SLC9A3 gene (rs4957061) was significantly (P = 0.02) associated with earlier acquisition of Pseudomonas infection in a cohort of 1,004 pediatric patients. Analysis of lung function in a subset of these patients (752) revealed that patients homozygous for the T allele had substantially reduced lung function and accelerated rate of decline. Although the functional basis for the modulatory effects of this SLC9A3 variant on CF lung disease remains to be elucidated, altered function of the Na⁺/H⁺ exchanger may further deplete the airway liquid surface, thereby enhancing susceptibility to Pseudomonas infections and worsening the severity of lung disease. Pediatr Pulmonol. 2011; 46:385–392. © 2010 Wiley‐Liss, Inc.     

The role of PKA and PKCε pathways in prostaglandin E2-mediated hypernociception

Background and purpose:

Protein kinase (PK) A and the ε isoform of PKC (PKCε) are involved in the development of hypernociception (increased sensitivity to noxious or innocuous stimuli) in several animal models of acute and persistent inflammatory pain. The present study evaluated the contribution of PKA and PKCε to the development of prostaglandin E₂ (PGE₂)-induced mechanical hypernociception.

Experimental approach:

Prostaglandin E₂-induced mechanical hypernociception was assessed by constant pressure rat paw test. The activation of PKA or PKCε was evaluated by radioactive enzymic assay in the dorsal root ganglia (DRG) of sensory neurons from the hind paws.

Key results:

Hypernociception induced by PGE₂ (100 ng) by intraplantar (i.pl.) injection, was reduced by i.pl. treatment with inhibitors of PKA [A-kinase-anchoring protein St-Ht31 inhibitor peptide (AKAPI)], PKCε (PKCεI) or adenylyl cyclase. PKA activity was essential in the early phase of the induction of hypernociception, whereas PKC activity was involved in the maintenance of the later phase of hypernociception. In the DRG (L4-L5), activity of PKA increased at 30 min after injection of PGE₂ but PKC activity increased only after 180 min. Moreover, i.pl. injection of the catalytic subunit of PKA induced hypernociception which was markedly reduced by pretreatment with an inhibitor of PKCε, while the hypernociception induced by paw injection of PKCε agonist was not affected by an inhibitor of PKA (AKAPI).

Conclusions and implications:

Taken together, these findings are consistent with the suggestion that PKA activates PKCε, which is a novel mechanism of interaction between these kinases during the development of PGE₂-induced mechanical hypernociception.     

Multi-center transferability of a breath-hold T2 technique for myocardial iron assessment

Background

Cardiac iron overload is the leading cause of death in thalassemia major and is usually assessed using myocardial T2* measurements. Recently a cardiovascular magnetic resonance (CMR) breath-hold T2 sequence has been developed as a possible alternative. This cardiac T2 technique has good interstudy reproducibility, but its transferability to different centres has not yet been investigated.

Methods and Results

The breath-hold black blood spin echo T2 sequence was installed and validated on 1.5T Siemens MR scanners at 4 different centres across the world. Using this sequence, 5–10 thalassemia patients from each centre were scanned twice locally within a week for local interstudy reproducibility (n = 34) and all were rescanned within one month at the standardization centre in London (intersite reproducibility). The local interstudy reproducibility (coefficient of variance) and mean difference were 4.4% and -0.06 ms. The intersite reproducibility and mean difference between scanners were 5.2% and -0.07 ms.

Conclusion

The breath-hold myocardial T2 technique is transferable between Siemens scanners with good intersite and local interstudy reproducibility. This technique may have value in the diagnosis and management of patients with iron overload conditions such as thalassemia.