59 research outputs found

    Inflammatory Muscle Diseases

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    Inflammatory myopathies, also called idiopathic inflammatory myopathy or myositis, are rare conditions characterized by the involvement of various organs in addition to muscle tissue. These changes can lead to severe impairments and adversely impact the quality of life of affected individuals. The diagnosis and treatment of inflammatory myopathies involve the participation of an interdisciplinary team, due to the complexity of the disease and the high variety of possible signs and symptoms. In this chapter we will discuss the epidemiology and characteristics of the main subtypes of inflammatory myopathies, such as polymyositis, dermatomyositis, necrotizing myopathy, overlap myositis, and myositis of inclusion bodies. Next, we will discuss the existence of crosstalk between inflammatory processes in the oral cavity and their consequences on skeletal muscle. As oral inflammation can increase infiltration of macrophages in muscle tissue and this increase is related to the production of proinflammatory cytokines in this tissue, these cytokines can cause muscle weakness. It is important to consider the prevention of chronic inflammatory processes in order to maintain muscle integrity or even prevent the worsening of the clinical condition of patients with inflammatory muscle diseases

    Alveolar bone healing process in spontaneously hypertensive rats (SHR): A radiographic densitometry study

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    Hypertension is one of the most important public health problems worldwide. If undiagnosed or untreated, this pathology represents a systemic risk factor and offers unfavorable conditions for dental treatments, especially those requiring bone healing. Objectives: The purpose of this study was to demonstrate, by analysis of bone mineral density (BMD), that the alveolar bone healing process is altered in spontaneously hypertensive rats (SHRs). Material and Methods: Wistar rats and SHRs were submitted to extraction of the upper right incisor and were euthanized 7, 14, 21, 28 and 42 days after surgery. Right maxillae were collected, radiographed and analyzed using Digora software. BMD was expressed as minimum (min), middle (med) and maximum (max) in the medium (MT) and apical (AT) thirds of the dental alveolus. Results: The results were compared across days and groups. Wistar showed difference in med and max BMD in the MT between 7 and 28 and also between 14 and 28 days. The AT exhibited significant difference in med and min BMD between 7 and 28 days, as well as difference in min BMD between 28 and 42 days. SHRs showed lower med BMD in the MT at 28 days when compared to 21 and 42 days. Differences were observed across groups in med and min BMD at day 28 in the MT and AT; and in max BMD at 14, 21 and 42 days in the MT. Conclusions: These results suggest that the alveolar bone healing process is delayed in SHRs comparing with Wistar rats

    Daily melatonin administration improves osseointegration in pinealectomized rats

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    The hypothesis of this study was that the peri-implant bone healing of the group of pinealectomized rats would differ from the control group. The samples were subjected to immunohistochemical, microtomographic (total porosity and connectivity density), and fluorochrome (mineralized surface) analyses. Objectives: The goal of this study was to investigate the cellular changes and bone remodeling dynamics along the bone/implant interface in pinealectomized rats. Material and Methods: The total of 18 adult male rats (Rattus norvegicus albinus, Wistar) was divided into three groups (n=6): control (CO), pinealectomized without melatonin (PNX) and pinealectomized with melatonin (PNXm). All animals were submitted to the first surgery (pinealectomy), except the CO group. Thirty days after the pinealectomy without melatonin, the second surgery was conducted, in which all animals received an implant in each tibia (36 titanium implants with surface treatment were installed – Implalife® São Paulo, SP, Brazil). By gavage, the rats of the PNX group received the vehicle solution, and the procedure. Results: Immunohistochemical analysis for runt-related transcription factor 2 (RUNX2), alkaline phosphatase (ALP), osteopontin (OP) and osteocalcin (OC) showed that the bone repair process in the PNXm group was similar to that of the CO group, whereas the PNX group showed a delay. The microtomographic parameters of total porosity [Po(tot)] and bone surface (BS) showed no statistically significant differences, whereas for the connective density (Conn.Dn) a statistical difference was found between the CO and PNXm groups. Fluorochrome analysis of the active mineralized surface showed statistically significant difference between the CO and PNX and between the CO and PNXm groups. Conclusion: The absence of the pineal gland impaired the bone repair process during osseointegration, however the daily melatonin replacement was able to restore this response

    Effect of fluoride intake on carbohydrate metabolism, glucose tolerance, and insulin signaling

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    Fluoride is known to cause both local and systemic alterations in animals and humans, such as dental fluorosis and disturbances in glucose homeostasis. The effects of fluoride are dose dependent and can produce decreased insulin secretion, inhibition of glycolysis, glycogen depletion, hyperglycemia, and insulin resistance. Because excessive ingestion of fluoride during tooth brushing can lead to deterioration in health, the use of low-fluoride dentifrices is recommended for young children with diabetes.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

    Distribution of serotype-specific genotypes of Aggregatibacter actinomycetemcomitns in Brazilian patients with Down syndrome with different periodontal conditions

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    This study evaluated the occurrence of highly or minimally leukotoxic strains of Aggregatibacter actinomycetemcomitans (Aa) from patients with Down syndrome and the distribution of the different serotype-specific genotypes of this microorganism. Sixty-seven patients with Down syndrome were subjected to dental, periodontal and radiographic evaluations. Samples of subgingival biofilm were collected and plated onto TSBV agar and characteristic colonies of A. actinomycetemcomitans were identified by biochemical methods. The occurrence of this bacterium was also evaluated directly in the clinical specimens by PCR. The presence of 530 bp deletion in the promoter region was also determined by PCR in order to evaluate distribution of highly or minimally leukotoxic strains. A. actinomycetemcomitans was detected in 11.1% by culture and 22.2% by PCR from periodontally healthy subjects, 100% of the patients with Down syndrome with aggressive periodontitis, 50% and 75% of patients with chronic periodontitis by culture and PCR respectively. Only two patients with aggressive periodontitis were colonized by highly leukotoxic Aa. Serotype-specific genotypes a and c were the most prevalent. The results suggest the role of peculiar characteristics of Aa and patients with Down syndrome in the development of periodontitis and the influence of peculiar characteristics of the population in this process.Este estudio evaluó la presencia de cepas altamente o mínimamente toxicas de Aggregatibacter actinomycetemcomitans (Aa) de los pacientes con síndrome de Down y la distribución de los serotipos genotipos específicos de este microrganismo por cultivo y PCR. Sesenta y siete pacientes con síndrome de Down fueron sometidos a un tratamiento dental y evaluaciones clínicas. Las muestras de biofilme subgingival fueron recogidas y cultivadas en agar TSBV y colonias características de Aa fueran identificadas mediante métodos bioquímicos. La presencia de esta bacteria se evaluó también directamente en las muestras clínicas por PCR. Los aislados y las muestras clínicas también se probaron con el fin de evaluar la distribución de serotipos de genotipos específicos por PCR, mientras que la presencia de delección de 530 bp en la región promotora del gen ltxC también fue determinado por PCR con el fin de evaluar de distribución de las cepas altamente o mínimamente toxicas. Aa fue aislado en 11,1% y 22,2% por PCR de pacientes periodontalmente sanos; en todos los pacientes con síndrome de Down con periodontitis agresiva, y en 50% y 75% de los pacientes con periodontitis crónica por cultivo y PCR, respectivamente. Sólo dos pacientes con periodontitis agresiva fueron colonizados por cepas altamente tóxicas. Los serotipos y genotipos específicos a y c fueron los más frecuentes. Los resultados sugieren una asociación de las peculiares características de Aa con las características de los pacientes con síndrome de Down en el desarrollo de la periodontitis.Fundação do Amparo à Pesquisa do Estado de São Paulo (FAPESP

    Biological effects of insulin on murine melanoma cells and fish erythrophoroma cells: A comparative study

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    Insulin is the hormone that plays an essential role in metabolism and mitosis of normal and tumor cells, exerting its pleiotropic effects through binding to specific membrane receptors and promoting the phosphorylation of tyrosine residues of the receptor itself and of other components of the signaling pathway. The aim of this study was to investigate the effects of insulin on melanogenesis and cell growth in three different cell lines: the goldfish GEM-81 erythrophoroma cells (undifferentiated and differentiated with 1.5% dimethylsulfoxide-DMSO), and the murine B16F10 and Cloudman S91 melanoma cells. Undifferentiated GEM-81 and B16F10 cells responded to insulin with a small increase of cell proliferation, whereas S91 cells responded with a decrease of growth. In the two mammalian cell lines, and in DMSO-differentiated GEM-81 cells, the hormone strongly inhibited melanogenesis, by decreasing tyrosinase activity. In undifferentiated GEM-81 cells, insulin had no effect on tyrosinase activity. An increase in the tyrosine phosphorylation status of pp 185 (insulin receptor substrate 1 and 2-IRS-1/2) phosphorylation degree was observed in S91 mouse melanoma and in differentiated GEM-81 erythrophoroma cells, suggesting that this specific protein was maintained during transformation process and participates in insulin signaling. Our results imply an ancient and diverse history of the insulin signaling system in vertebrate pigment cells. (C) 2008 Elsevier Inc. All rights reserved

    Periodontal disease reduces water and sodium intake induced by injection of muscimol into the lateral parabrachial nucleus

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    Objective: Gamma-aminobutyric acid A (GABAA) receptor activation with muscimol in the lateral parabrachial nucleus (LPBN) induces water and 0.3 M NaCl intake. The purpose of this study was to investigate whether a local inflammatory event, such as periodontal disease (PD), is able to alter the effects of muscimol on water and 0.3 M NaCl intake in fluid-replete rats and in rats treated with furosemide (FURO) combined with captopril (CAP) injected subcutaneously. Design: Male Wistar rats were divided into two groups: with PD and those without PD (control condition). Fifteen days after PD, both groups had cannulas implanted bilaterally into the LPBN. Results: In fluid-replete rats without PD, injections of muscimol (0.5 nmol/0.2 μl) into the LPBN induced 0.3 M NaCl and water intake and a pressor response. In fluid-replete rats with PD, a decrease was observed in water intake and pressor response but not in 0.3 M NaCl intake. In control rats with FURO + CAP treatment, injections of muscimol into the LPBN increased 0.3 M NaCl and water intake. In PD rats with FURO + CAP treatment, a decrease was observed in 0.3 M NaCl and water intake after muscimol in the LPBN. Alveolar bone loss and interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) plasmatic concentration were higher in PD rats in comparison with controls. Conclusion: These results suggest that PD is able to reduce the pressor response and the dipsogenic and natriorexigenic effects induced by the activation of GABAA receptors in the LPBN, probably due to the elevation of the plasmatic concentration of pro-inflammatory cytokines IL-6 and TNF-α. © 2013 Elsevier Ltd. All rights reserved
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