138 resultados para Plasminogen-activator


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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Aim: To demonstrate the magnitude and direction of skeletal changes in the maxilla and mandible during and after the use of bionator, as well as their rotations. Methods: Partial superimposition on the maxilla and mandible on the metallic implants and total superimposition on the cranial base were performed at three periods, T1 before bionator therapy, T2 after bionator therapy, and T3 5.68 years after T2. Results: There was total clockwise maxillary rotation and counterclockwise mandibular rotation, in the North American technique, throughout the study period, as well as extensive remodeling on the condylar region, especially in vertical direction and on the gonial region in horizontal direction. Conclusions: The total maxillary rotation seemed to be significantly affected by therapy than the mandible. There was a clear change in the direction of condylar remodeling compared to the period of bionator therapy and posterior bionator therapy. Considering the entire study period, it was observed that intra-matrix rotation of the maxilla and mandible masked their total rotation, causing minimum changes in the matrix rotation.

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The study aimed to assess the degree of dental crowding correction on the lower anterior region of patients treated with T4k functional appliance using Little’s irregularity index. Twenty caucasian patients of both gender (10 female and 10 male) were selected. They featured malocclusion Class I and II in mixed dentition, with chronological age between 5.7 and 11 years. The treatment lasted from 1 year and 11 months up to 3 years and 11 months. Lower anterior crowding was measured using Little’s irregularity index. Measurements were obtained on study models achieved before and after functional orthopedic therapy, using a digital caliper in millimeters and placed parallel to the occlusal plane. Overjet and overbite measurements were also performed using a caliper. Results demonstrated that the therapy provided significant decrease in overjet (average = 1.55 mm) and also in the irregularity index (average = 1.23 mm). There was a nonsignificant raise in overbite. There was no relation between the studied variables and the treatment period or even with the patient’s age in the beginning of the therapy. The treatment with T4k resulted on reduction and improvement of dental crowding.

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The aim of this study was to evaluate the vertical and horizontal dentoskeletal changes induced by the Klammt Open Elastic Activator in the treatment of the Class II Division 1 malocclusion. The sample of 34 children was divided into two groups of 17 subjects each (ten girls, seven boys), matched by age and gender and with an initial mean age of 8.5 years. The data was analyzed using a Student's t-test for intragroup and intergroup comparison. The results showed that the appliance promoted dentoalveolar restriction of the maxilar growth within normal anteroposterior and vertical growth of the maxillary apical base; increment in the vertical displacement the mandibular symphysis associated with normal horizontal growth of the mandible; palatal tipping of the upper incisors; restriction of the anterior migration of the upper molars; greater eruption pattern and normal anterior displacement of the lower incisors and molars. It was concluded that Klammt appliance induce changes that are predominantly horizontal dentoalveolar in upper arch and vertical dentoalveolar in lower arch and vertical skeletal changes in the mandible.

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The deficiency of data in the literature took us to evaluate the Bionator of Balters appliance in the alterations of the dimensions and the relationship of the dental archs in children with malocclusion Class II, division 1 of Angle. The experimental group was constituted by 36 pairs cast Caucasians patients, aged between 7 years and 10 months - 11 years and 8 months, being 10 females and 8 males. The Levene´s test showed statistical evidences of likeness among the groups. Statistical analysis was preceded and showed significant alterations (p < 0,005) in the variable indicatives of maxillary first molars' distance, overjet, upper arch total length, upper arch anterior length, right molar relationship, left molar relationship, right canine relationship and left canine relationship. On the other hand, there wasn't significant alteration related to the lower arch and maxillary intercanines distance. The Balters' Bionator appliance had a favorable effect in the improvement of the correction of the malocclusion in Class II (foremost in molars and canines relationship) and transversal increase of the upper arch, mainly in the posterior area of arch.

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The Jasper Jumper appliance was developed as a fixed orthopedic device that is connected to the upper and lower leveling arches to promote the Class II correction by restricting the maxillary growth (headgear effect), mandibular growth inducement (activator effect) and dentoalveolar changes.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone resorption. However, the biological mechanisms by which DM1 modulates PD are not fully understood. The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. PD was induced by means of ligature in nondiabetic and in streptozotocyn-induced DM1 rats. Morphological and morphometric analyses, stereology and osteoclast counting were performed. RANKL and OPG mRNA levels, protein content, and location were determined. PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. DM1 alone showed alveolar bone destruction and an increased number of osteoclasts at the periapical and furcal regions. DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. This work demonstrates that the effects of PD and DM1 enhance bone destruction, confirms the importance of the RANKL signaling pathway in bone destruction in DM1 in animal models and suggests the existence of alternative mechanisms potentiating bone degradation in PD.

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Resident, non-immune cells express various pattern-recognition receptors and produce inflammatory cytokines in response to microbial antigens, during the innate immune response. Alveolar bone resorption is the hallmark of destructive periodontitis and it is caused by the host response to bacteria and their mediators present on the biofilm. The balance between the expression levels of receptor activator of nuclear factorkappa B ligand (RANKL) and osteoprotegerin (OPG) is pivotal for osteoclast differentiation and activity and has been implicated in the progression of bone loss in periodontitis. To assess the contribution of resident cells to the bone resorption mediated by innate immune signaling, we stimulated fibroblasts and osteoblastic cells with LPS from. Escherichia coli (TLR4 agonist), Porphyromonas gingivalis (TLR2 and -4 agonist), and interleukin-1 beta (as a control for cytokine signaling through Toll/IL-1receptor domain) in time-response experiments. Expression of RANKL and OPG mRNA was studied by RT-PCR, whereas the production of RANKL protein and the activation of p38 MAPK and NF-kB signaling pathways were analyzed by western blot. We used biochemical inhibitors to assess the relative contribution of p38 MAPK and NF-kB signaling to the expression of RANKL and OPG induced by TLR2, -4 and IL1β in these cells. Both p38 MAPK and NFkB pathways were activated by these stimuli in fibroblasts and osteoblasts, but the kinetics of this activation varied in each cell type and with the nature of the stimulation. E. coli LPS was a stronger inducer of RANKL mRNA in fibroblasts, whereas LPS from P. gingivalis downregulated RANKL mRNA in periodontal ligament cells but increased its expression in osteoblasts. IL-1β induced RANKL in both cell types and without a marked effect on OPG expression. p38 MAPK was more relevant than NF-kB for the expression of RANKL and OPG in these cell types.

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The myeloid differentiation factor 88 (MyD88) plays a pivotal role in Toll-like receptor (TLR)- and interleukin-1 receptor (IL-1R)-induced osteoclastogenesis. We examined the role of MyD88 on p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) activation and nucleotide-binding oligomerization domain (Nod) induction by lipopolysaccharide (LPS) and IL-1 beta, and their effect on receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) production in bone marrow stromal cell (BMSC). RANKL, Nod1, Nod2, NF-κB, and p38 protein levels were determined by Western blot. Nod2 was stimulated with muramyl dipeptide (MDP) prior to TLR4 stimulation with LPS. MyD88 deficiency markedly inhibited RANKL expression after LPS stimulation and increased OPG messenger RNA (mRNA) production. Also, MyD88 was necessary for NF-κB and p38 MAPK activation. MDP alone did not induce RANKL and OPG expressions; however, when combined with LPS, their expressions were significantly increased (p < 0.05). Our results support that MyD88 signaling has a pivotal role in osteoclastogenesis thought NF-κB and p38 activation. Nod2 and especially Nod1 levels were influenced by MyD88.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Background: Acupuncture has shown the capability of modulating the immuno-inflammatory response of the host. This study aims to evaluate the effects of electroacupuncture (EA) on ligature-induced periodontitis in rats. Methods: Thirty-two animals were divided into four groups: 1) control; 2) experimental periodontitis (EP); 3) sham-treated (EP/EA-sham); and 4) treated with EA (EP/EA). For the EP groups, a ligature was placed around the right mandibular first molars at day 1. Sessions of EA or EA-sham were assigned every other day. For EA treatment, large intestine meridian points LI4 and LI11 and stomach meridian points ST36 and ST44 were used. EA-sham was performed in off-meridian points. Animals were euthanized at day 11. Histomorphometric and microtomographic analyses were performed. Immunolabeling patterns for the receptor activator of nuclear factor kappa B ligand (RANKL), osteoprotegerin (OPG), and tartrate-resistant acid phosphatase (TRAP) were assessed. Expressions of interleukin (IL)-1 beta, matrix metalloproteinase (MMP)-8, IL-6, and cyclooxygenase (COX)-2 messenger RNAs (mRNAs) were evaluated by quantitative reverse transcription-polymerase chain reaction. Data were analyzed statistically (P < 0.05, analysis of variance). Results: Histomorphometric and microtomographic analyses demonstrated that group EP/EA presented reduced alveolar bone loss when compared to group EP (P < 0.05). Reduced RANKL immunolabeling and fewer TRAP-positive multinucleated cells were observed in the EA-treated group in relation to group EP. No differences were observed in OPG expression among groups. EA treatment decreased the genic expression of IL-1 beta and MMP-8 (P < 0.05), increased the mRNA expression of IL-6 (P < 0.05), and did not modify the genic expression of COX-2 in animals with EP (P > 0.05). Conclusion: It can be concluded that EA reduced periodontal tissue breakdown and the expression of some proinflammatory mediators and a proresorptive factor in EP in rats.