Study of denture-induced fibrous hyperplasia cases diagnosed from 1979 to 2001

Objective: the purpose of this research was to study the cases of inflammatory fibrous hyperplasia (IFH) at the Clinic of Semiology, Department of Bioscience and Oral Diagnosis, Sao Jose dos Campos Dental School, State University of São Paulo, Brazil. Methods and materials: A total of 141 clinical file cards indicating a final diagnosis of IFH, from the archives of the Department of Bioscience and Oral Diagnosis and dated from 1979 to 2001, were included in the study. of these files, 50 indicated a diagnosis of denture-induced fibrous hyperplasia. Sex, age, race, duration, and clinical features that confirm their classification in the non-neoplastic proliferating process were analyzed statistically. Results: of the 50 analyzed cases of denture-induced lesion, 22% occurred in men and 78% in women. Patients in the age group of 41 to 50 years presented the highest frequency of the lesion. Conclusions: Inflammatory fibrous hyperplasia occurs more frequently in women (71.63%), and denture-induced lesions appear mainly in patients over 40 years of age (70% of cases). Patients with denture-induced hyperplasia reported pain associated with the lesion (70%).

Anti-inflammatory effects of low-level laser therapy (LLLT) with two different red wavelengths (660 nm and 684 nm) in carrageenan-induced rat paw edema

It has been suggested that low-level laser therapy (LLLT) can modulate inflammatory processes. The aim of this experiment was to investigate what effects red laser irradiation with two different wavelengths (660 nm and 684 nm) on carrageenan-induced rat paw edema and histology. Thirty two male Wistar rats were randomly divided into four groups. One group received a sterile saline injection, while inflammation was induced by a sub-plantar injection of carrageenan (1 mg/paw) in the three other groups. After 1 h, LLLT was administered to the paw in two of the carrageenan-injected groups. Continuous wave 660 nm and 684 nm red lasers respectively with mean optical outputs of 30 mW and doses of 7.5 J/cm(2) were used. The 660 nm and 684 nm laser groups developed significantly (P < 0.01) less edema (0.58 ml [SE +/- 0.17] ml and 0.76 ml [SE +/- 0.10] respectively) than the control group (1.67 ml [SE +/- 0.191) at 4 h after injections. Similarly, both laser groups showed a significantly lower number of inflammatory cells in the muscular and conjunctive sub-plantar tissues than the control group.We conclude that both 660 nm and 684 nm red wavelengths of LLLT are effective in reducing edema formation and inflammatory cell migration when a dose of 7.5 J/cm(2) is used. (c) 2007 Elsevier B.V. All rights reserved.

PARTICIPATION OF MACROPHAGES IN CHLORAMPHENICOL-POTENTIATED CARRAGEENAN-INDUCED PERITONITIS IN RATS

1. We investigated the possible potentiating effect of chloramphenicol succinate (30 mg/kg, every 12 h for 4 days, ip) on the response of polymorphonuclear neutrophils to carrageenin (150 mug, ip) or dextran (100 mug, ip) in the peritoneal cavity of male Wistar rats (180-230 g; N = 12 in each group).2. Chloramphenicol potentiated the cell migration induced by carrageenin (35%) but not that induced by dextran. Previous macrophage depletion in the peritoneal cavity by washing with sterile saline abolished the cell response, whereas a previous thioglycollate-induced increase in macrophage numbers enhanced the potentiating effect (60%).3. These results suggest that the potentiating effect on polymorphonuclear neutrophil migration induced by chloramphenicol may be related to chemotactic factors released by macrophages.

Smoking status and tumor necrosis factor-alpha mediated systemic inflammation in COPD patients

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

Endogenous corticosteroids and insulin in acute inflammation

Carrageenin-induced inflammatory responses in the hindpaws of rats were quantitated by measuring: (1) alterations in volumes of the paws; and (2) alterations in concentration of dye, previously injected intravenously, which was recovered in perfusates from the paws. The inflammatory response in one paw was attenuated by previously inducing an inflammatory response in the contralateral paw. The effect was abolished by pretreatment with insulin. Indexes of adrenal activity were increased after the induction of the inflammatory response and they were not attenuated by pretreatment with insulin. Adrenal hyperactivity was characterized by increased serum corticosterone concentration, decreased adrenal ascorbic acid content, and reduced number of circulating eosinophils. It is concluded that inflammatory stimuli which lead to alterations in microvessels depend on a facilitatory effect of insulin. This effect is antagonized by glucocorticoids released in enhanced concentrations after the application of noxious stimuli. Therefore, endogenous insulin and glucocorticoids act as modulators of inflammatory responses.

A lung computed tomographic assessment of positive end-expiratory pressure-induced lung overdistension

The aim of this study was to assess positive end-expiratory pressure (PEEP)-induced lung overdistension and alveolar recruitment in six patients with acute lung injury (ALI) using a computed tomographic (CT) scan method. Lung overdistension was first determined in six healthy volunteers in whom CT sections were obtained at FRC and at TLC with a positive airway pressure of 30 cm H2O. In patients, lung volumes were quantified by the analysis of the frequency distribution of CT numbers on the entire lung at zero end-expiratory pressure (ZEEP) and PEEP. In healthy volunteers at FRC, the distribution of the density histograms was monophasic with a peak at -791 ± 12 Hounsfield units (HU). The lowest CT number observed was -912 HU. At TLC, lung volume increased by 79 ± 35% and the peak CT number decreased to -886 ± 26 HU. More than 70% of the increase in lung volume was located below -900 HU, suggesting that this value can be considered as the threshold separating normal aeration from overdistension. In patients with ALI, at ZEEP the distribution of density histograms was either monophasic (n = 3) or biphasic (n = 3). The mean CT number was -319 ± 34 HU. At PEEP 13 ± 3 cm H2O, lung volume increased by 47 ± 19% whereas mean CT number decreased to -538 ± 171 HU. PEEP induced a mean alveolar recruitment of 320 ± 160 ml and a mean lung overdistension of 238 ± 320 ml. In conclusion, overdistended lung parenchyma of healthy volunteers is characterized by a CT number below -900 HU. This threshold can be used in patients with ALI for differentiating PEEP-induced alveolar recruitment from lung overdistension.

A novel biological activity for galectin-1: Inhibition of leukocyte-endothelial cell interactions in experimental inflammation

Galectin-1 (Gal-1), the prototype of a family of β -galactoside-binding proteins, has been shown to attenuate experimental acute and chronic inflammation. In view of the fact that endothelial cells (ECs), but not human polymorphonuclear leukocytes (PMNs), expressed Gal-1 we tested here the hypothesis that the protein could modulate leukocyte-EC interaction in inflammatory settings. In vitro, human recombinant (hr) Gal-1 inhibited PMN chemotaxis and trans-endothelial migration. These actions were specific as they were absent if Gal-1 was boiled or blocked by neutralizing antiserum. In vivo, hrGal-1 (optimum effect at 0.3 μg equivalent to 20 pmol) inhibited interleukin-1β-induced PMN recruitment into the mouse peritoneal cavity. Intravital microscopy analysis showed that leukocyte flux, but not their rolling velocity, was decreased by an anti-inflammatory dose of hrGal-1. Binding of biotinylated Gal-1 to resting and post-adherent human PMNs occurred at concentrations inhibitory in the chemotaxis and transmigration assays. In addition, the pattern of Gal-1 binding was differentially modulated by PMN or EC activation. In conclusion, these data suggest the existence of a previously unrecognized function of Gal-1, that is inhibition of leukocyte rolling and extravasation in experimental inflammation. It is possible that endogenous Gal-1 may be part of a novel anti-inflammatory loop in which the endothelium is the source of the protein and the migrating PMNs the target for its anti-inflammatory action.

Effects of crude extracts of Agaricus blazei on DNA damage and on rat liver carcinogenesis induced by diethylnitrosamine

The effects of crude extracts of the mushroom Agaricus blazei Murrill (Agaricaceae) on both DNA damage and placental form glutathione S-transferase (GST-P)-positive liver foci induced by diethylnitrosamine (DEN) were investigated. Six groups of adult male Wistar rats were used. For two weeks, animals of groups 3 to 6 were treated with three aqueous solutions of A. blazei (mean dry weight of solids being 1.2, 5.6, 11.5 and 11.5 mg/ml, respectively). After this period, groups 2 to 5 were given a single ip injection 200 mg/kg DEN and groups 1 and 6 were treated with 0.9% NaCl. All animals were subjected to 70% partial hepatectomy at week five and sacrificed 4, 24 and 48 h or 8 weeks after DEN or 0.9% NaCl treatments (10th week after the beginning of the experiment). The alkaline comet assay and GST-P-positive liver foci development were used to evaluate the influence of the mushroom extracts on liver cell DNA damage and on the initiation of liver carcinogenesis, respectively. Previous treatment with the highest concentration of A. blazei (11.5 mg/ml) significantly reduced DNA damage, indicating a protective effect against DEN-induced liver cytotoxicity/genotoxicity. However, the same dose of mushroom extract significantly increased the number of GST-P-positive liver foci.

Methods of experimental induction of periapical inflammation. Microbiological and radiographic evaluation

Aim: To evaluate the influence of coronal filling and apical perforation on the induction of periapical inflammation. Methodology: Fifty-eight root canals in the teeth of dogs were divided into four groups. Groups I and II: root canals were exposed for 180 days; groups III and IV: root canals were exposed for 7 days and then the access cavity filled for 53 days. The root apices of groups I and III were perforated after the coronal opening, whilst those of groups II and IV remained intact. Standard radiographs were taken before and after the experimental periods. Digital images of the radiographs were created and then analysed by three examiners. After induction of periapical inflammation, the root canal contents were collected using paper points. Microbiologic evaluation of the type of microorganism was carried out by culture in different growth media. The radiographic and microbiologic data were statistically analysed using ANOVA at a 5% significance level. Results: There were a greater total number of microorganisms in groups I and II (P < 0.05). The number of anaerobes was greater than the number of aerobes (P < 0.05). The size of the periapical radiolucencies were not significantly different between the experimental groups. Conclusions: The different methods analysed induced similar areas of periapical radiolucency in dogs with predominantly anaerobic bacteria. However, the time required for induction was less when the method with coronal filling was used. © 2005 International Endodontic Journal.

Cytologic analysis of alterations induced by smoking and by alcohol consumption

Objective: To analyze cytologically the buccal mucosa of smoking and nonsmoking volunteers to determine what cellular changes are induced by cigarettes and alcohol consumption. Study Design: In order to evaluate cellular changes induced by smoking and alcohol consumption, exfoliative cytology was used for the analysis of mucosal smears obtained from the buccal mucosa of 25 smokers and 25 nonsmokers. The number of cigarettes consumed, duration of smoking, presence or absence of alcohol ingestion, ingested alcohol dose and frequency of consumption, and most frequently used type of alcoholic beverage were determined using a questionnaire. Three smears from each individual stained by the Papanicolaou method were analyzed quantitatively and qualitatively under a light microscope by 2 experienced examiners in terms of inflammatory and dysplastic alterations and of the degree of epithelial maturation. Results: Although numerous alterations were observed in smokers they corresponded up to only Papanicolaou class II and were not significantly different from nonsmokers (Mann-Whitney and χ 2 tests, p < 0.05). A higher proportion of inflammatory cells (polymorphonuclear and mononuclear cells) were obtained from smokers as compared to nonsmokers, while the proportion of bacteria was similar in the 2 groups. Conclusion: The findings indicate that even after a short period of cigarette use and alcohol consumption, inflammatory alterations were detectable on exfoliative cytology of the buccal mucosa in a young group, demonstrating the usefulness of cytology for early detection in smokers. © The International Academy of Cytology.

Neutrophil migration induced by IL-1β depends upon LTB4 released by macrophages and upon TNF-α and IL-1β released by mast cells

In the present study, we investigate whether mast cells and macrophages are involved in the control of IL-1β-induced neutrophil migration, as well as the participation of chemotactic mediators. IL-1β induced a dose-dependent neutrophil migration to the peritoneal cavity of rats which depends on LTB 4, PAF and cytokines, since the animal treatment with inhibitors of these mediators (MK 886, PCA 4248 and dexamethasone respectively) inhibited IL-1β-induced neutrophil migration. The neutrophil migration induced by IL-1β is dependent on mast cells and macrophages, since depletion of mast cells reduced the process whereas the increase of macrophage population enhanced the migration. Moreover, mast cells or macrophages stimulated with IL-1β released a neutrophil chemotactic factor, which mimicked the neutrophil migration induced by IL-1β. The chemotactic activity of the supernatant of IL-1β-stimulated macrophages is due to the presence of LTB4, since MK 886 inhibited its release. Moreover, the chemotactic activity of IL-1β-stimulated mast cells supernatant is due to the presence of IL-1β and TNF-α, since antibodies against these cytokines inhibited its activity. Furthermore, significant amounts of these cytokines were detected in the supernatant. In conclusion, our results suggest that neutrophil migration induced by IL-1β depends upon LTB4 released by macrophages and upon IL-1β and TNFα released by mast cells. © 2007 Springer Science+Business Media, LLC.

Cardiovascular remodeling induced by passive smoking

Coronary heart disease (CHD) is the most common cause of death in many developed countries. The major risk factors for CHD are smoking, high blood pressure, diabetes, high cholesterol levels, and lack of physical activity. Importantly, passive smoke also increases the risk for CHD. The mechanisms involved in the effects of passive smoke in CHD are complex and include endothelial dysfunction, lipoprotein modification, increased inflammation and platelet activation. Recently, several studies have shown that exposure to tobacco smoke can result in cardiac remodeling and compromised cardiac function. Potential mechanisms for these alterations are neurohumoral activation, oxidative stress, and MAPK activation. Although the vascular effects of cigarette smoke exposure are well known, the effects of tobacco smoking on the heart have received less attention. Therefore, this review will focus on the recent findings as to the effects of passive smoking in acute and chronic phases of vascular and cardiac remodeling. © 2009 Bentham Science Publishers Ltd.

Cardiac remodeling induced by smoking: Concepts, relevance, and potential mechanisms

Cardiac or ventricular remodeling is characterized by molecular, cellular, and interstitial alterations that lead to changes in heart size, mass, geometry and function in response to a given insult. Currently, tobacco smoke exposure is recognized as one of these insults. Indeed, tobacco smoke exposure induces the enlargement of the left-sided cardiac chambers, myocardial hypertrophy, and ventricular dysfunction. Potential mechanisms for these alterations include hemodynamic and neurohormonal changes, oxidative stress, inflammation, nitric oxide bioavailability, matrix metalloproteinases and mitogen-activated protein kinase activation. This review will focus on the concepts, relevance, and potential mechanisms of cardiac remodeling induced by tobacco smoke. © 2012 Bentham Science Publishers.

Effect of dietary sodium restriction on body water, blood pressure, and inflammation in hemodialysis patients: a prospective randomized controlled study

Purpose: Accumulating evidence suggests an association between body volume overload and inflammation in chronic kidney diseases. The purpose of this study was to evaluate the effect of dietary sodium reduction in body fluid volume, blood pressure (BP), and inflammatory state in hemodialysis (HD) patients. Methods: In this prospective controlled study, adult patients on HD for at least 90 days and those with C-reactive protein (CRP) levels ≥0.7 mg/dl were randomly allocated into two groups: group A, which included 21 patients treated with 2 g of sodium restriction on their habitual diet; and group B, which included 18 controls. Clinical, inflammatory, biochemical, hematological, and nutritional markers were assessed at baseline and after 8 and 16 weeks. Results: Baseline characteristics were not significantly different between the groups. Group A showed a significant reduction in serum concentrations of CRP, tumor necrosis factor-α, and interleukin-6 during the study period, while BP and extracellular water (ECW) did not change. In group B, there were no changes in serum concentrations of inflammatory markers, BP, and ECW. Conclusions: Dietary sodium restriction is associated with the attenuation of the inflammatory state, without changes in BP and ECW, suggesting inhibition of a salt-induced inflammatory response. © 2013 Springer Science+Business Media Dordrecht.