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Abstract: Psychological stress plays an important role in the occurrence and development of temporomandibular joint disorder (TMD). The correlation between psychological factors and TMD has been clinically shown, but the influence of psychological stress on the temporomandibular joint (TMJ) structure still lacks direct evidence. Here, we used communication box to establish the rat model of psychological stress. The stress level of animals was estimated by the elevated plus maze (EPM) test and hormonal assays. The histomorphology and three-dimensional microstructure of the rat condyles were observed by hematoxylin–eosin (HE) staining and Micro-CT, respectively. Compared with control rats, the anxious state of the stressed rats was evidenced by higher plasma adrenocorticotropic hormone (ACTH) and corticosterone (CORT), as well as lower ratios of open arm entries and time and lower time spent in open arms after 1, 2, 3, 4 and 5week(s) post-exposure to psychological stimuli. HE staining and histomorphometric data analysis showed decreased thicknesses of the central and posterior condylar cartilages in stressed rats at weeks 3, 4 and 5, with the most obvious changes in the posterior part characterized by debonding and thinned fibrous layer, thickened proliferative layer, thinned mature layer and hypertrophic layer. Moreover, Micro-CT scanning revealed local lesion of the subchondral bone in the posterior condylar cartilages of stressed rats at week 5. Our findings indicate that pathologic changes of the histomorphology and three-dimensional microstructure occur in the condyles of stressed rats, hinting us a potential link between psychological factors and the pathogenesis or progression of TMD. [Copyright &y& Elsevier]

Abstract: Psychological stressors are generally associated with masseter muscle dysfunction and disorders in emotional response. In addition, oxidative states and HSP70 expression, which are involved in the physical and pathological changes of the masseter muscle, could be altered in the stressed tissues and organs. However, the link between psychological stress and the redox homeostasis or the expression of HSP70 in masseter muscles in rats has not been examined. Therefore, we used a communication box paradigm to induce psychological stress in rats. The successful establishment of the animal model was evidenced by an increase in plasma corticosterone and adrenocorticotropic hormone (ACTH). Meanwhile, the stressed rats showed a decrease in the number of entries on open arms, percentage of time spent in open arms, and distance moved in the elevated plus-maze test. The stressed rats also displayed a decrease in the time spent in the center zone, active velocity, and the distance moved in the open-field test. These results demonstrate affective-like behavioral changes in the stressed rats. Moreover, compared with the control rats, a decrease in SOD, GSH-Px and catalase activities and an increase in MDA content were observed in the masseter muscles in stressed rats after 3weeks and 5weeks, and the HSP70 expression was elevated in muscles in the rats exposed to stress for 5weeks. These results indicate that psychological stress induces oxidative damage and up-regulates the expression of HSP70 in masseter muscles in rats, which are associated with behavior resembling anxiety. [Copyright &y& Elsevier]

It is commonly accepted that psychological stress contributes to the development of chronic orofacial pain. However, the neural mechanism underlying this process has remained unclear. The present study was performed to determine the involvement of satellite glia cells (SGCs) in the trigeminal ganglion (TG) in stress-induced increases in masseter muscle allodynia in rats. Using a chronic restraint stress model, we found that exposure to a 14-day stress but not a 3-day stress (6 h/day) caused decreased body weight gain, behavioral changes and marked masseter allodynia in rats. SGCs were dramatically activated, and substance P (SP) expression was significantly increased in the TG. A further analysis was undertaken to investigate the contribution of SGCs; the expression of interleukin-1β (IL-1β) in SGCs and interleukin-1 receptor I (IL-1RI) in neurons was significantly increased after chronic restraint stress, whereas injection of L -α-aminoadipate (a SGC inhibitor, LAA) into the TG dramatically inhibited the overexpression of these proteins. In addition, LAA or interleukin-1 receptor antagonist (IL-1ra) administration into the TG could significantly attenuate the mechanical masseter allodynia and overexpression of SP in the TG induced by restraint stress. These results suggest that SGC activation in the TG may play a role in masseter allodynia induced by restraint stress. The over-release of IL-1β and excessive IL1-RI expressions have close relationship with the stress induced masseter allodynia. [ABSTRACT FROM AUTHOR]

It is commonly accepted that psychological stress contributes to the development of temporomandibular joint disorders, in which chronic orofacial pain is the main symptom. However, the central mechanism underlying the development of these disorders has remained unclear. The current study was performed to determine the involvement of the glia in the trigeminal spinal subnucleus caudalis in stress-induced increases in masseter muscle hyperalgesia in rats. After being subjected to chronic restraint stress, the animals showed decreased body weight gain, behavioral changes and marked masseter allodynia. We also found that astrocytes, but not microglia, in the trigeminal subnucleus caudalis (Vc) were dramatically activated. A further analysis was undertaken to investigate the contribution of the glia; we intrathecally injected l -α-aminoadipate (astrocyte-specific inhibitor) and/or minocycline (microglia-specific inhibitor) into the stressed rats. Our results showed that l -α-aminoadipate (LAA), but not minocycline, could significantly attenuate the mechanical masseter allodynia and behavioral changes induced by restraint stress. In addition, the expression of interleukin-1β (IL-1β) and phosphorylated N-methyl- d -aspartic acid receptor 1 (p-NR1) in the Vc was significantly increased after chronic restraint stress, whereas LAA dramatically inhibited the overexpression of IL-1β and p-NR1. Taken together, these results suggest that activated astrocytes in the Vc may be one of the most important factors in the pathophysiology of masseter hyperalgesia induced by restraint stress and the following overexpression of IL-1β and excessive NMDAR phosphorylation may ultimately contribute to masseter hyperalgesia. Thus, inhibiting spinal astrocytic activation may represent a novel therapeutic strategy for the treatment of orofacial pain induced by stress. [ABSTRACT FROM AUTHOR]

Experimental and non-experimental stress significantly increase masseter muscle tone, which has been linked to the symptoms and pathogenesis of several stomatognathic system diseases. Until now, the mechanism underlying this phenomenon has remained unclear. The current study was performed to determine the mechanism of the stress-induced increase in masseter muscle tone and to investigate the effect of lamotrigine on this change. Animals challenged by repeated restraint stress received either saline as a vehicle or lamotrigine in doses of 20, 30 or 40 mg/kg body weight, whereas control animals received saline without stress treatment. Masseter muscle tone was assessed using electromyography. The activity of glutamate-related metabolic enzymes (glutaminase and glutamine synthetase) in the trigeminal motor nucleus was also investigated. Our results showed an interesting phenomenon: masseter muscle activity increased concurrently with the upregulation of the glutamate concentration after stress treatment. The activities of glutaminase and glutamine synthetase in the trigeminal motor nucleus were also upregulated and downregulated, respectively, when the rats were challenged by prolonged stress. The animals treated with lamotrigine at moderate and high doses had significantly decreased masseter muscle tone compared with stressed animals treated with vehicle. These results suggested that increased glutaminase activity and decreased glutamine synthetase activity increased glutamate production and decreased glutamate decomposition, causing an increase in glutamate levels in the trigeminal motor nucleus and eventually increasing masseter muscle tone. The administration of lamotrigine at doses of 30 or 40 mg/kg body weight effectively mitigated the adverse effects of stress on masseter muscle tone via inhibition of glutamate release. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To investigate the correlation between psychological stress and masseter muscle (MM) alterations, and explore the therapeutic agents for restoring the impaired masticatory muscle. Design: We established a chronic unpredictable mild stress (CUMS) animal model and observed the changes of ultrastructure, redox homeostasis and energy metabolism in MM in rats with and without curcumin treatment. Results: The depressive-like behavior in stressed rats was confirmed by the evidences of altered behaviors in sucrose preference test and open field test; while these phenomena were eased by curcumin. Except for the pathological changes in ultrastructure, decreased SOD, GSH-Px, CAT, Na+-K+ATPase, and Ca2+-Mg2+ATPase activities as well as increased MDA and LD content and LDH activity were also observed in MM in stressed rats. However, curcumin was capable of reversing CUMS-induced MM disorder by improving the activities of the examined anti-oxidant enzymes and energy metabolism enzymes. Additionally, the increased MDA content, LD content, and LDH activity in stressed rats were reduced by curcumin. Conclusion: All the findings indicate the adverse effects of CUMS on MM function in rats, and raise the possibility of developing curcumin as a potential therapeutic agent for psychological stress-induced masseter dysfunction. [Copyright &y& Elsevier]

Abstract: The aim of this study was to construct a cell transplant method consisting of cell sheet fragments of periodontal ligament stem cells (PDLSCs) and platelet-rich fibrin (PRF) granules to enhance periodontal healing in avulsed tooth reimplantation. To test this concept in vitro, human PDLSCs were isolated and characterized by colony forming unit assay, cell surface marker characterizations, and their osteogenic/adipogenic differentiation potential. The biological effects of autologous PRF as a growth factor-enriched endogenous scaffold on human PDLSCs were then investigated and quantified for statistical analyses, including cell viability and proliferation, alkaline phosphatase (ALP) activity, and the gene expression of bone sialoprotein (BSP), osteocalcin (OCN), collagen I (Col-I), and cementum protein 23 (CP23). It was found that the PRF induced a significant and continuous stimulation of proliferation in human PDLSCs throughout the 7-day incubation period. Furthermore, the PRF suppressed the osteoblastic differentiation of PDLSCs by decreasing ALP activity and the gene expression of BSP and OCN while up-regulating the mRNA expression levels of Col-I and CP23 during the testing period. To assess the potential application of the PDLSCs/PRF construct in tooth reimplantation, 36 incisors were extracted from 6 dogs. The incisors then underwent 2 h of dry storage and were randomly divided into four groups receiving different strategies of reimplantation, where the avulsed teeth were reimplanted with the use of the autologous PDLSCs/PRF construct (cell sheet fragments in combination with PRF granules), with the use of autologous PDLSCs or PRF alone, or without adjuvant use of PRF or PDLSCs. Eight weeks post-reimplantation, the PDLSCs/PRF group achieved a more effective periodontal healing, characterized by the regeneration of PDL-like tissues and a reduction of ankylosis and inflammation, compared with the other testing groups. These overall results suggest that the PDLSCs/PRF construct may be a useful tool for alveolar surgery that has the potential to improve the clinical outcomes in future avulsed tooth reimplantations. [Copyright &y& Elsevier]

Abstract: Two glasses with different contents of fluorine were fabricated. A single phase, KMg3.25Si3.625O10F2, precipitated in both of the glass samples after heat treatment. Both the crystallization activation energy (En) and the frequency factor (ν) increased with increasing fluorine content. This means that the fluorine content has a dual effect on the crystallization of fluorosilicic mica glass; the effect on the frequency factor is predominant. The flexural strength of the as-cerammed glass ceramic containing more fluorine is larger than that containing less fluorine when heated to the same temperature. [Copyright &y& Elsevier]

Abstract: Jaw clenching (clenching) is the result of an isometric contraction of jaw closing muscles. Because of the location of working muscles and afferent information during tooth contact, the effect of clenching on the cerebral and systemic circulation might differ from that of isometric limb exercise. This study aimed to investigate the characteristic changes in cerebral and systemic circulation during jaw clenching by comparing those during handgrip exercise. Subjects were 17 right-handed men. Bilateral middle cerebral arterial blood flow velocity (MCAV), electromyography (EMG) of contracting muscles, heart rate (HR) and blood pressure (BP) were measured during unilateral handgrip exercise and clenching tasks. Autonomic nerve activity was evaluated by analyzing fluctuations in HR and BP. MCAV was significantly increased during the task with significantly higher values on the non-working than working side irrespective of unilateral handgrip or unilateral jaw clenching. Changes in HR during jaw clenching were lower than those during handgrip exercise, and changes in vaso-motor sympathetic nerve activity during left jaw clenching were lower than those during left handgrip exercise. The present results indicate that, compared with handgrip exercise, unilateral jaw clenching promotes bilateral activation of MCAV with smaller effects on cardiac output and sympathetic nervous system activity. [Copyright &y& Elsevier]