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Mechanical stimulation and estrogen have been proven to be two important factors in promoting mesenchymal stem cell activity, which is closely associated with bone formation, mass maintenance and remodeling. However, the superposition effects of mechanical stimulation and estrogen on stem cells remain unknown. It is also unclear if the estrogen receptor (ER) plays only a key role in estrogen signaling or if it is also involved in the mechanotransduction of stem cells. To investigate the role of estrogen and its receptors in the mechanobiological effects in bone mesenchymal stem cells (BMSCs), isolated mesenchymal stem cells from bone marrow were exposed to mechanical pressure under additional estrogen treatment or ER blockade. Cell proliferation was examined using an MTT assay and alkaline phosphatase (ALP) activity was determined by a modified enzyme kinetic method. Alignment of the cytoskeleton was observed by Coomassie brilliant blue staining and F-actin fluorescent staining. Cellular ultrastructure was observed under transmission electron microscope. Expression of ERα was investigated using Western blot analysis. Results indicated that mechanical pressure promoted cell proliferation, ALP activity, ERα expression and F-actin stress fiber formation. Overall, this effect was enhanced by the addition of estrogen and inhibited by ER blockade. We concluded that pressure stimulated proliferation and differentiation capability via F-actin transduction in BMSCs. The effects were enhanced by the addition of estrogen, and the ER plays an important role in regulating mechanobiological effects and the mechanotransduction processes of BMSCs. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

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]

Background A rodent occlusal hypofunction model has been widely established in jawbone-related studies. However, the effects of occlusal stimuli, with total elimination of molar contacts, and its rehabilitation on mandibular remodeling remain unclear. Materials and methods Forty-eight 5-wk-old Sprague–Dawley male rats were used. Twenty-four experimental rats underwent occlusal hypofunction by insertion of a bite-raising appliance. Twenty-four rats received no treatment (control group). Two weeks later, half the experimental rats (occlusal hypofunction group) were killed; the appliance was removed from the remaining experimental rats (recovery group) for two additional weeks before killing. Control animals were killed biweekly. Body weight and masseter muscle weight were measured, and the mandibles were subjected to micro-computed tomography to evaluate the mandibular morphology and cortical bone characteristics. The expressions of osteoblast- and osteoclast-related genes were evaluated with quantitative polymerase chain reaction. Results No significant body weight differences were observed between the experimental and control rats. However, lighter masseter muscle, shorter mandibular incisor crown, mandibular body and ramus, and higher mandibular alveolar process and first molar fossae were observed in the occlusal hypofunction group. Moreover, the cortical bone characteristics associated with the expression of osteoblast- and osteoclast-related genes were remarkably different in the central and posterior mandible in the occlusal hypofunction group. At the 2-wk recovery time point after occlusal stimuli, the altered parameters in the masseter and mandible returned to normal levels. Conclusions Mandibular remodeling via bone turnover is region specific for altered occlusal stimuli. Normal occlusion is an important determinant of the mandibular morphology and architecture. [ABSTRACT FROM AUTHOR]

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]

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]