Symptoms in different severity degrees of bruxism: a cross-sectional study

Objective: The aim of the present study was to evaluate symptoms of the muscle pain, sleep quality, oral health, anxiety, stress and depression in individuals with different severity degrees of bruxism. Methods: Seventy-two individuals with bruxism were enrolled in the study, classified into: moderate (n=25) and severe (n=47) bruxism. Pain intensity was assessed using the Visual Analogical Scale, pain threshold with algometer, sleep quality by the Pittsburgh Sleep Quality Index, oral health by the Oral Health Impact Profile, anxiety by the State-Trait Anxiety Inventory, stress by the Perceived Stress Scale and depression using the Beck Depression Inventory. The significance level considered was 5%. Results: The results showed that individuals with severe bruxism presented greater muscle pain intensity, sleep disorder, worse oral health, high anxiety level and dysphoria with statistically significant differences (pObjetivo: Avaliar sintomas de dor muscular, qualidade de sono, saúde bucal, ansiedade, estresse e depressão em indivíduos com diferentes graus de severidade do bruxismo. Métodos: Setenta e dois indivíduos com bruxismo participaram do estudo e foram classificados com bruxismo moderado (n=25) e severo (n=47). A intensidade da dor foi avaliada pela Escala Visual Analógica, limiar de dor com o algômetro, qualidade de sono pelo Índice de Qualidade de Sono de Pittsburgh, saúde bucal pelo Perfil de Impacto de Saúde Bucal, ansiedade pelo Inventário de Ansiedade Traço-Estado, estresse pela Escala de Estresse Percebido e depressão pelo Inventário de Depressão de Beck. O nível de significância considerado foi 5%. Resultados: Os resultados demonstraram que indivíduos com bruxismo severo apresentaram maior intensidade de dor muscular, distúrbio do sono, pior qualidade de saúde bucal, elevado grau de ansiedade e disforia, com diferenças estatisticamente significantes (p;0,05). Conclusão: Os dados sugerem que indivíduos com bruxismo severo tem sintomas mais intensos. Eles apresentam maior intensidade de dor muscular, alterações na qualidade do sono e saúde bucal, ansiedade e depressão do que indivíduos com bruxismo moderado. Porém, ambos apresentam similaridade no estresse.Objetivo: Evaluar los síntomas dolor muscular, calidad de sueño, salud bucal, ansiedad, estrés y depresión en sujetos con diferentes niveles de gravedad del bruxismo. Método: Participaron del estudio 72 personas con bruxismo, clasificado según los niveles moderado (n=25) y grave (n=47). Se evaluaron la intensidad del dolor mediante la Escala Visual Analógica, umbral de dolor con algómetro, la calidad de sueño por el Índice de Calidad de Sueño de Pittsburgh, la salud bucal mediante el Perfil del Impacto de Salud Bucal, la ansiedad por el Inventario de Ansiedad Rasgo-Estado, el estrés mediante la Escala de Estrés Percibido y la depresión por el Inventario de Depresión de Beck. Se consideró el nivel de significación de 5%. Resultados: Los sujetos con bruxismo grave presentaron más intensamente dolor muscular, trastorno de sueño, peor calidad de salud bucal, alto grado de ansiedad y disforia, con diferencias estadísticamente significativas (p;0,05). Conclusión: Los datos mostraron que los sujetos con bruxismo grave sufren síntomas más intensos. A pesar de sufrir síntomas más intensos de dolor muscular, calidad de sueño y salud bucal alterada, ansiedad y depresión que los sujetos con bruxismo moderado, el estrés está presente en los dos niveles de bruxismo

Influence of Short-Term Glucocorticoid Therapy on Regulatory T Cells In Vivo

Background: Pre- and early clinical studies on patients with autoimmune diseases suggested that induction of regulatory T(Treg) cells may contribute to the immunosuppressive effects of glucocorticoids(GCs). Objective: We readdressed the influence of GC therapy on Treg cells in immunocompetent human subjects and naı¨ve mice. Methods: Mice were treated with increasing doses of intravenous dexamethasone followed by oral taper, and Treg cells in spleen and blood were analyzed by FACS. Sixteen patients with sudden hearing loss but without an inflammatory disease received high-dose intravenous prednisolone followed by stepwise dose reduction to low oral prednisolone. Peripheral blood Treg cells were analyzed prior and after a 14 day GC therapy based on different markers. Results: Repeated GC administration to mice for three days dose-dependently decreased the absolute numbers of Treg cells in blood (100 mg dexamethasone/kg body weight: 2.861.86104 cells/ml vs. 336116104 in control mice) and spleen (dexamethasone: 2.861.96105/spleen vs. 956226105/spleen in control mice), which slowly recovered after 14 days taper in spleen but not in blood. The relative frequency of FOXP3+ Treg cells amongst the CD4+ T cells also decreased in a dose dependent manner with the effect being more pronounced in blood than in spleen. The suppressive capacity of Treg cells was unaltered by GC treatment in vitro. In immunocompetent humans, GCs induced mild T cell lymphocytosis. However, it did not change the relative frequency of circulating Treg cells in a relevant manner, although there was some variation depending on the definition of the Treg cells (FOXP3+: 4.061.5% vs 3.461.5%*; AITR+: 0.660.4 vs 0.560.3%, CD127low: 4.061.3 vs 5.063.0%* and CTLA4+: 13.8611.5 vs 15.6612.5%; * p,0.05). Conclusion: Short-term GC therapy does not induce the hitherto supposed increase in circulating Treg cell frequency, neither in immunocompetent humans nor in mice. Thus, it is questionable that the clinical efficacy of GCs is achieved by modulating Treg cell numbers

Molecular cloning and sequencing of partial cDNA of tumor necrosis factor and p75 tumor necrosis factor receptor of Syrian golden hamster (Mesocricetus auratus) with the use of universal primers.

In this study we cloned and analysed partial cDNA of tumor necrosis factor (TNF) and p75 TNF-R receptor of Syrian golden hamster (Mesocricetus auratus). We obtained a 382-bp sequence of TNF and a 148-bp sequence coding for p75 TNF-R. The primers used for the cloning were designed on the basis of inter-species homology, thus presumably can be used for cloning and analysis of TNF and p75 TNF-R genes of other mammals

Molecular cloning and sequencing of partial cDNA of tumor necrosis factor and p75 tumor necrosis factor receptor of Syrian golden hamster (Mesocricetus auratus) with the use of universal primers.

In this study we cloned and analysed partial cDNA of tumor necrosis factor (TNF) and p75 TNF-R receptor of Syrian golden hamster (Mesocricetus auratus). We obtained a 382-bp sequence of TNF and a 148-bp sequence coding for p75 TNF-R. The primers used for the cloning were designed on the basis of inter-species homology, thus presumably can be used for cloning and analysis of TNF and p75 TNF-R genes of other mammals

T regulatory cells and the control of alloimmunity: from characterisation to clinical application.

T regulatory cells (Treg) play an important role in the induction and maintenance of immunological tolerance. Recent findings in experimental transplant models combined with the development of functional reporter mice have opened new avenues to study Treg biology and their therapeutic potential. In particular, recent advances in understanding Treg function and lineage stability revealed unexpected plasticity of this lineage. Nevertheless, pre-clinical and pilot clinical trials using Treg cells as cellular therapies have been initiated suggesting the safety and feasibility of such treatment

HUMAN REGULATORY T CELLS PREVENT ISLET ALLOGRAFT REJECTION

Background: Type 1 diabetes mellitus represents a significant burden on global healthcare. Pancreatic islet transplantation offers an effective means of controlling the disease, but shortage of donor tissue, graft thrombosis, and immunological rejection after transplantation remain obstacles that need to be overcome. Our aim was to assess the ability of ex vivo expanded human regulatory T cells (Treg) in modulating the rejection response against a human islet allograft in a clinically relevant model of human pancreatic islet transplantation. Methods: We studied the rejection response against allogeneic human islets in acohort of 32 immunodeficient mice which had been reconstituted with a functional human immune system. Thirteen subjects were transplanted with human islets without further immunological modification; graft survival was compared with that of thirteen subjects treated additionally with human regulatory T cells. Six controls were given a human islet transplant, but not reconstituted with human immune cells to demonstrate the functionality of the islet graft in the absence of immunological rejection. Graft function was assessed with serial blood glucose measurements, immunohistochemistry,immunoflourescence, and flow cytometry. Findings: Human islet allografts were rapidly rejected in subjects that did notreceive Treg. With Treg treatment, however, human islet allograft rejection was prevented (median survival time (MST) of > 45 days with Treg, as opposed to an MST of 23 days without Treg). Ex vivo expanded Treg homed to the lymphoid tissue draining the graft site where they suppressed the priming, activation, proliferation, and effector cytokine production of alloreactive T cells. Interpretation: These findings in a clinically relevant model of human pancreatic islet transplantation demonstrate the ability of ex vivo expanded human Treg to attenuate acute islet allograft rejection, and provide further support for their use in cellular immunotherapy

Effects of oestrogen deprivation on interleukin-6 production by peripheral blood mononuclear cells of postmenopausal women.

Various hormones can influence the expression of interleukin-6 (IL-6) and oestrogens are the most extensively studied. There is, however, controversy about the nature of the IL-6 secreted by human cells and its regulation by 17beta-oestradiol. The aim of this work was to clarify whether oestrogen deprivation after menopause may contribute to an enhanced IL-6 production by peripheral blood mononuclear cells (PBMC) in postmenopausal women. Twenty-two healthy postmenopausal women, age range 45-63 years, with clinical symptoms of oestrogen deficiency were enrolled in the study. The control group consisted of 16 healthy young women, age range 22-31 years, with regular menses and who were not taking oral contraceptives. Levels of IL-6 in the sera and PBMC culture supernatants were measured by the biological B9 cell-proliferation assay and expression of the IL-6 gene in non-stimulated PBMC was detected by RT-PCR. The effect of 17beta-oestradiol on spontaneous IL-6 production by the PBMC of postmenopausal women was also studied in vitro and in vivo. Seventeen out of the twenty-two postmenopausal women were given hormonal replacement therapy of 50 microg 17beta-oestradiol/day transdermally and the spontaneous production of IL-6 by the PBMC was analysed after 6 and 12 months of treatment. The postmenopausal women had significantly higher serum levels of IL-6 than the young controls. The spontaneous production of IL-6 by non-stimulated PBMC into the culture supernatants was also significantly higher in the postmenopausal women compared with the young. We also found that IL-6 gene expression was present in the non-stimulated PBMC isolated directly from the venous blood of the majority of the postmenopausal women. Women with IL-6 gene expression in the non-stimulated PBMC had significantly lower serum levels of 17beta-oestradiol compared with those where the IL-6 gene was not expressed in the PBMC. Our in vitro experiments showed that 17beta-oestradiol at concentrations of 10(-9) M and 10(-10) M decreased spontaneous IL-6 production by the PBMC of postmenopausal women. In vivo treatment with 17beta-oestradiol transdermally also significantly decreased spontaneous IL-6 production by the PBMC of postmenopausal women after 12 months of the therapy. Our results indicate that oestrogen deprivation after menopause may enhance IL-6 production by the PBMC of postmenopausal women. We suspect that the late complications of oestrogen deficiency, such as osteoporosis, coronary heart disease and Alzheimer's disease, may be mediated by an exaggerated production of IL-6 - a cytokine which seems to play a pivotal role in the pathogenesis of these age-related diseases

Interleukin-2 as a predictor of early postoperative atrial fibrillation after cardiopulmonary bypass graft (CABG).

Recently, inflammation has been considered as a risk factor of postoperative atrial fibrillation (PAF). The main purpose of this study was to estimate the connections between occurrence of PAF and cytokine release. Thirty-three patients who qualified for cardiopulmonary bypass graft (CABG) were included in the study. Blood was taken from all of them before CABG, then 3 h, 24 h, and 72 h afterwards. Cytokine (IL-6, IL-2, IL-4, IL-10, IFN-gamma, TNF-alpha) concentration was measured at every time point. Eleven patients developed atrial fibrillation after the CABG. Five of them developed PAF until 1 day post-CABG and six of them after 1 day post-CABG. Patients who developed PAF before 1 day post-CABG were characterized by a higher level of IL-2 in sera before 24 h and 72 h post-CABG compared with patients without PAF. Moreover, the PAF before 1 day post-CABG group was also characterized by the higher level of IFN-gamma and IL-10 at 24 h after intervention. Analysis of patients who developed PAF after 1 day post-CABG revealed a higher level of IL-10 and IFN-gamma at 24 h post-CABG compared with patients without PAF. In this study, we have shown for the first time a straightforward connection between IL-2 sera levels and the development of PAF shortly after CABG

NK cells in children with acute lymphoblastic leukemia and non-Hodgkin lymphoma after cessation of intensive chemotherapy

Intensive, combination chemotherapy for malignant diseases causes a profound immunosuppression, which persists for the whole treatment period and after its completion. Impairment of the NK cells status may increase the risk of severe, disseminated infections and cancer. The aim of the study was the investigation of recovery of NK cells after cessation of intensive chemotherapy in children with acute lymphoblastic leukemia (ALL) and non-Hodgkin lymphoma (NHL). The number of CD3 - CD16+CD56+ cells in peripheral blood and NK cell cytotoxic activity were assessed in 23 children with ALL and 7 children with NHL at 2 weeks and 12 months after the cessation of intensive chemotherapy and in 15 healthy subjects. Absolute leukocyte, lymphocyte and NK cell counts and the percentage of NK cells in children with ALL were significantly lower than in control subjects both at 2 weeks and 12 months after intensive treatment. Additionally, the absolute numbers of leukocytes and lymphocytes decreased significantly after 12 months of observations in comparison to the initial time-point. In children with non-Hodgkin lymphoma at 2 weeks and 12 months after intensive treatment only absolute lymphocyte counts were significantly lower than values in healthy children. The absolute number, the percentage and cytotoxic activity of NK cells were comparable with values in the control group both at the initial and at the last time-point. The occurrence of infections during the 12 months of observations in patients with ALL were higher than in children with NHL and as many as eight of them were hospitalized because of severe infections. The differences between the ALL and NHL patients may be connected with the milder immunosuppressive effect of chemotherapy in the non-Hodgkin lymphoma since the children recovered from acute lymphoblastic leukemia remain with persistent defect of NK cells. It is then recommended that ALL children should be supervised with respect to an increased susceptibility to infections

Changes in number of NK cells after one year from coronary artery bypass graft

Natural Killer cells (NK cells) are components of nonspecific immune response involved in the defense against viral and bacterial infections. Basing on the CD56 cell surface antigen density human NK cells may be divided into two distinct subpopulations: CD56dim - "cytotoxic subset" and CD56bright - "regulatory subset". Our previous work revealed that coronary heart disease (CHD) patients are characterized by a reduction in absolute values and percentage of the CD3-CD56dim and CD3-CD56+ cells. CHD is inflammation dependent disease. Therefore we decided to estimate NK cells status in CHD patients after one year from coronary artery bypass graft (CABG). This procedure improves the heart and vascular status in patients and also remove inflammatory burden. Blood was collected from eighty five patients from the Clinic of Cardiosurgery of the Medical University of Gdańsk before CABG. Blood from eleven CHD patients was examined ones more after one year from CABG. Seventy seven people, of similar age, with excluded coronary heart disease were enrolled into the study as a control group. Percentage of the CD3-CD56+, CD3-CD56dim and CD3-CD56bright cells were analyzed in all samples by flow cytometry. Before CABG blood of the CHD patients was characterized by a low percentage of the CD3-CD56+ and CD3-CD56dim subsets in comparison to control group. However when number of cells were analyzed within one year after CABG we observed a rise of the CD3-CD56+ and CD3-CD56dim cells percentage. The increase of cell percentage was relevant when data were compared to control group and to the results obtained from CHD group before CABG. It may be concluded that a lower NK cells number in CHD is a consequence of inflammation and further that this number may be treated as marker of inflammation