leukotoxin and Acute-Disease

The purpose of this study was to determine to what extent the presence or absence of periodontal pathogens can distinguish between subjects with chronic and aggressive periodontitis.. A systematic review of cross sectional and longitudinal studies providing microbiological data both from patients with chronic periodontitis (ChP) and aggressive periodontitis (AgP) at a subject level. Strict inclusion criteria were applied. The presence or absence of five microorganisms was selected as primary study parameters: Actinobacillus actinomycetemcomitans (AA), Porphyromonas gingivalis (PG), Prevotella intermedia (PI), Bacteroides forsythus (BF), and Campylobacter rectus (CR).. The presence or absence of AA could be evaluated in 11 papers. In seven papers the presence or absence of PG could be analysed. Subject specific data on PI were available from six studies. Two studies could be used regarding the presence or absence of BF, and two regarding CR. Sensitivity and specificity of every microbiological test were individually calculated for each selected study, assuming that the clinical diagnosis of AgP or ChP was the true status the tests attempted to detect. AgP was considered to be the condition of interest and ChP was considered equivalent to 'non-AgP'. Receiver Operator Characteristic (ROC) diagrams were constructed using these data. ROC diagrams indicated the limited discriminatory ability of all of the test parameters to identify subjects with AgP. An additional assessment showed that the highly leukotoxic variant of AA was uniquely associated with patients suffering from aggressive periodontitis. However, in a high proportion of patients diagnosed with AgP the presence of this variant could not be detected.. The presence or absence of AA, PG, PI, BF or CR could not discriminate between subjects with AgP from those with ChP.

Topics: Acute Disease; Aggregatibacter actinomycetemcomitans; Bacteroides; Campylobacter; Chronic Disease; Exotoxins; Humans; Periodontitis; Porphyromonas gingivalis; Prevotella intermedia; ROC Curve; Sensitivity and Specificity

Previous studies suggest differences between geographically and racially distinct populations in the prevalence of periodontopathic bacteria as well as greater periodontal destruction associated with infection by highly leucotoxic Actinobacillus actinomycetemcomitans. The present study examined these hypotheses in Brazilians with aggressive or chronic periodontitis.. Clinical, radiographical, and microbiological assessments were performed on 25 aggressive periodontitis and 178 chronic periodontitis patients including 71 males and 132 females, 15-69 years of age.. The prevalence of Porphyromonas gingivalis was similar to that of other South American populations. The prevalence of A. actinomycetemcomitans and its highly leucotoxic subgroup was higher in Brazilians. Highly leucotoxic A. actinomycetemcomitans was more prevalent in aggressive periodontitis (chi2=27.83) and positively associated with deep pockets (>6 mm, chi2=18.26) and young age (<29 years, chi2=18.68). Greater mean attachment loss was found in subjects with highly leucotoxic A. actinomycetemcomitans than in subjects with minimally leucotoxic (p=0.0029) or subjects not infected (p=0.0001).. These data support the hypothesis of differences between populations in the prevalence of periodontopathic bacteria and of greater attachment loss in sites infected with highly leucotoxic A. actinomycetemcomitans. Detection of highly leucotoxic A. actinomycetemcomitans in children and adolescents may be a useful marker for aggressive periodontitis.

Topics: Acute Disease; Adolescent; Adult; Aged; Aggregatibacter actinomycetemcomitans; Bacteroides; Brazil; Campylobacter rectus; Chronic Disease; Colony Count, Microbial; Cross-Sectional Studies; Dental Plaque; DNA, Bacterial; Exotoxins; Female; Humans; Logistic Models; Male; Middle Aged; Periodontitis; Porphyromonas gingivalis; Prevalence; Prevotella intermedia

We studied whether endothelin-1 (ET-1) and leukotoxin (Lx), which have a different effects on vascular tone in isolated perfused rat lungs, also have different effects on mitochondrial function in edematous lung injury. Lung mitochondria were extracted from isolated perfused rat lungs exposed to each mediator. In lungs exposed to 0.5 nmol of ET-1, lung wet weight increased with a markedly elevated perfusion pressure but with no increase in the release of lactate dehydrogenase (LDH), an index of cell damage, into the perfusate. Neither mitochondrial respiration rate no ATP content in the lung tissue differed from those of untreated lungs. In contrast, in lungs treated with 30 mumol of Lx, lung wet weight markedly increased despite a small elevation of perfusion pressure; release of LDH into the perfusate increased, and the mitochondrial respiration rate in state 3 adn 4 significantly decreased while the ATP content in the lung tissue was less than in untreated lungs. We also examined cellular and mitochondrial damage in hydrostatic lung edema caused by raising an outflow reservoir. Mitochondrial respiration was not suppressed, and perfusate LDH activity was not increased, although lung wet weight increased as much as it did after the treatment described above. These results indicate that lung mitochondrial function is differentially affected by ET-1 and Lx, and they suggest that abnormalities in energy production by lung mitochondria are related to permeability edema.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Endothelin-1; Energy Metabolism; Exotoxins; In Vitro Techniques; Inflammation Mediators; L-Lactate Dehydrogenase; Lung; Male; Mitochondria; Organ Size; Oxygen Consumption; Pulmonary Edema; Rats; Rats, Sprague-Dawley

Pulmonary vascular endothelial cells are an important barrier that helps keep lung tissue intact. These cells are exposed to potentially injurious cells and to harmful mediators that are produced in or released into the blood. The endothelial cells may then be stimulated and injured. Stimulated and injured pulmonary vascular endothelial cells can themselves produce and release injury-promoting mediators. Using isolated perfused rat lungs and cultured human pulmonary endothelial cells, we assessed the effect of neutrophil-derived injurious mediators, leukotoxin, and neutrophil elastase on the pulmonary endothelium. Both mediators caused high-permeability pulmonary edema in the isolated lungs and caused dose-dependent and time-dependent damage in the cell cultures. Injury due to leukotoxin was suppressed in the presence of LNMMA or superoxide dismutase and injury due to neutrophil elastase was suppressed by neutrophil elastase inhibitors. These data indicate that these mediators cause lung injury via different mechanisms and that they may synergistically evoke clinical lung injury.

Topics: Acute Disease; Animals; Capillary Permeability; Cells, Cultured; Endothelium, Vascular; Exotoxins; Humans; In Vitro Techniques; Leukocyte Elastase; Male; Pulmonary Edema; Rats; Rats, Sprague-Dawley; Rats, Wistar