No description available.

Diss. (sammanfattning) Umeå : Univ., 2004. / Härtill 4 uppsatser.

Thesis (M.S.)--University of Southern California, 1999. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Washington, 1996. / Vita. Includes bibliographical references (leaves [141]-172).

Thesis (M.S.)--University of Southern California, 1999. / Includes bibliographical references.

CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior / Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico / Porphyromonas gingivalis e Aggregatibacter actinomycetemcomitans sÃo periodontopatÃgenos associados à periodontite agressiva. A fÃmbria, uma estrutura relacionada à adesÃo e à invasÃo de cÃlulas, à um dos principais fatores de virulÃncia de P. gingivalis. Baseado na sequÃncia de nucleotÃdeos, seis genÃtipos(fimA) que codificam a fÃmbria principal dessas bactÃrias foram identificados, sendo o fimA II mais comumente relacionado à destruiÃÃo periodontal. O objetivo deste trabalho foi avaliar, por meio de reaÃÃo em cadeia da polimerase em amostras de placa subgengival dos sÃtios com maior profundidade de sondagem de pacientes com periodontite agressiva, a prevalÃncia de P. gingivalis, do genÃtipo fimA II de P. gingivalis e de A. actinomycetemcomitans, assim como relacionar a presenÃa desses patÃgenos ou genÃtipo à idade e aos parÃmetros clÃnicos periodontais (Ãndice de placa, Ãndice de sangramento gengival, profundidade de sondagem e nÃvel de inserÃÃo) encontrados nesses pacientes. Foram selecionados 45 pacientes com periodontite agressiva generalizada, com idade entre 15 e 40 anos. Nessa populaÃÃo, 64,4% apresentaram P. gingivalis e 28,8% apresentaram A. actinomycetemcomitans em sua microbiota subgengival. Dos pacientes positivos para P. gingivalis, 82,6% apresentaram o genÃtipo fimA II. Ao se relacionar a presenÃa ou ausÃncia das bactÃrias ou genÃtipo aos dados clÃnicos e idade, foi observada diferenÃa estatisticamente significante entre o nÃvel clÃnico de inserÃÃo do sÃtio coletado de pacientes com presenÃa de P. gingivalis e seu genÃtipo fimA II quando comparados aos pacientes negativos para essa bactÃria e genÃtipo, sendo a perda de inserÃÃo significativamente maior em pacientes que apresentaram P. gingivalis e em paciente com seu genÃtipo fimA II. AlÃm disso, foi encontrada mÃdia de idade significativamente mais elevada em pacientes positivos para P. gingivalis que em pacientes negativos para essa bactÃria. Concluiu-se, assim, que P. gingivalis e seu genÃtipo fimA tipo II estÃo presentes em alta prevalÃncia em pacientes com periodontite agressiva, que A. actinomycetemcomitans està presente em menor proporÃÃo de indivÃduos na populaÃÃo estudada e que P. gingivalis parece ser mais comumente encontrada em bolsas mais profundas e em indivÃduos mais velhos. / Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans are periodontal pathogens associated with aggressive periodontitis. The fimbriae, a structure related to adhesion and invasion of cells, is one of the major virulence factors of P. gingivalis. Based on the nucleotide sequence, six genotypes(fimA) encoding the major fimbriae of these bacteria were identified, and the fimA II is the most commonly associated with periodontal destruction. The objective of this study was to evaluate, by polymerase chain reaction in subgingival plaque samples from sites with highest probing depth in patients with aggressive periodontitis, the prevalence of P. gingivalis, P. gingivalis genotype fimA II and A. actinomycetemcomitans, and relate the presence of these pathogens or genotype to age and clinical periodontal parameters (plaque index, gingival bleeding index, probing depth and clinical attachment level) in these patients. We selected 45 patients with generalized aggressive periodontitis, aged from 15 to 40 years. 64.4% of these patients harbored P. gingivalis and 28.8% harbored A. actinomycetemcomitans in their subgingival microbiota. In patients positive for P. gingivalis, 82.6 % presented the genotype fimA II. In relation to the presence or absence of bacteria or gene to clinical data and age, a statistically significant difference between clinical attachment level was observed in the selected sites of patients with the presence of P. gingivalis and its genotype fimA II when compared to patients negative for these bacteria and genotype, with periodontal loss significantly higher in patients harboring P. gingivalis and in patients harboring genotype fimA II. In addition, the average age in patients positives for P. gingivalis was significantly higher than in negative ones. It is therefore concluded that P. gingivalis and its genotype fimA II are present in high prevalence in patients with aggressive periodontitis, A. actinomycetemcomitans is present in a smaller proportion of individuals in the studied population and P. gingivalis seems to be more commonly found in deeper sites and older individuals.

Periodontitis is an inflammatory disease caused by bacterial infection that can lead to loss of supporting tissues around the teeth. Studies show that different ethnic populations demonstrate major differences in prevalence of the disease and in which form the disease occur. The presence of the bacteria Aggregatibacter actinomycetemcomitans (A.a) is associated with the aggressive form of the disease, diagnosed primarily in young people.  The present study aims to describe the prevalence of A.a in children aged 7-9 years living in Sweden with different ethnic backgrounds and to evaluate two different ways of extracting bacterial DNA. The hypothesis was that prevalence of A.a would correlate with the origin of the subjects, thus anticipating a higher prevalence in subjects of African origin than those of other ethnicity.  Stimulated saliva samples from 85 children were studied. Two methods were used to extract DNA, manually and automatically. qPCR was used to investigate if the samples contained A.a.  The essential results showed that the highest prevalence of A.a was found in samples belonging to children with African origin. The manual method extracted DNA in a higher amount and from more samples compared to the automatic method. Sweden is nowadays multicultural and the clinical issues change with the population. Other clinical questions needs to be answered and previous truths need to be reassessed, for example periodontal problems in younger individuals. In this study, the manual method of extracting DNA proved to be more sensitive than the automatic, though more studies need to be conducted to draw any conclusions.

No description available.

Aggregatibacter actinomycetemcomitans is strongly associated with aggressive periodontitis and one of several virulence factors is a leukotoxin (LtxA). The toxin has a consequential impact on human leukocytes which leads to an interference with the host ́s defences due to a chain reaction involving activation and release of a pro-inflammatory cytokine; interleukin-1β (IL-1β). As an early phase in this reaction chain the toxin stimulates a massive release of adenosine triphosphate (ATP) from human leukocytes. We hypothesize that leukotoxin-induced pro- inflammatory cell death is initiated by ATP release through pannexin channels in the human monocyte cell membrane. The aim of this study was to investigate if blocking of pannexin channels with carbenoxolone (Cbx) results in a reduction of ATP release. A human monocyte cell line (THP-1 cells) was exposed to purified LtxA, Cbx and oxidized ATP. Colorimetric ATP kit was used to evaluate levels of ATP release and thereafter the samples were read in a spectrophotometer. This study confirms that LtxA induces an ATP release from THP-1 cells. Our conclusion is that blocking of pannexin channels does not result in a statistically significant reduction in ATP release, which indicates that ATP is released by one or several other undetected pathways.

A Periodontite Agressiva (PA), que atualmente pertence ao grupo das Periodontites estágios 3 e 4, distingue-se dos demais tipos de doença periodontal por seu início precoce, agregação familiar dos casos e por afetar pacientes sistemicamente saudáveis. Além disso, pode ser subclassificada em duas formas, localizada (PAL) e generalizada (PAG), em função de sua extensão. Muitas vezes, os depósitos de biofilme bacteriano são desproporcionais à quantidade de destruição óssea e perda de inserção que o paciente apresenta, independente da subclassificação. O microrganismo mais relacionado à etiopatogênese da doença é o Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), incluindo os seus principais sorotipos a, b e c, amplamente estudados. Associado a estas condições, A. actinomycetemcomitans apresenta alguns fatores de virulência como uma leucotoxina, principalmente ligada ao sorotipo b - clone JP2 (que é altamente leucotóxico) e proteínas de membrana externa (OMPs), especialmente Omp29. A resposta de imunoglobulina G (IgG) sérica contra este patógeno foi anteriormente associada à ambas as formas de PA, porém, são escassos os estudos que avaliaram longitudinalmente a resposta sérica frente a variáveis como estas. Dessa maneira, o objetivo desse estudo foi avaliar a resposta sérica, de 27 pacientes com PA e 10 pacientes periodontalmente saudáveis, contra Omp29 e sorotipos de A. actinomycetemcomitans, através de um ensaio ELISA, correlacionando com o número de cópias de JP2 (obtidos por qPCR em tempo real) e parâmetros clínicos, a partir de dados anteriormente coletados por nosso grupo. Todos os dados foram obtidos antes do início do tratamento e um ano após seu término. O tratamento consistiu de orientações de higiene bucal, tratamento mecânico e antibioticoterapia. Os dados resultantes do estudo mostraram que em ambas as formas de PA houve uma redução significativa na profundidade clínica de sondagem (PCS)(p<0,001), nível clínico de inserção (NCI)(p<0,001) e na resposta sérica contra Omp29 e sorotipo c de A. actinomycetemcomitans(p>0,005). Após 1 ano, os valores de densidade óptica (D.O.) normalizados para Omp29 e sorotipos de A. actinomycetemcomitans, bem como o número de cópias do clone JP2 tornaram-se similares aos níveis encontrados nos controles. A redução no número de cópias do clone JP2 foi correlacionada com redução da PCS em PAL(r=0.80,p=0.0042) e valores de D.O. normalizados de Omp29 em PAG(r=0.66,p=0.005). O estudo concluiu que o tratamento periodontal foi eficaz em alterar a resposta sérica contra Omp29 e sorotipos de A. actinomycetemcomitans, além de reduzir o número de cópias do clone JP2 e melhorar os parâmetros clínicos. / Aggressive Periodontitis (AP), which currently belongs to the group of Periodontites stages 3 and 4, is distinguished from other types of periodontal disease due to its early onset, familial aggregation of cases and to affect systemically healthy patients. In addition, it can be sub classified into two forms, localized (PAL) and generalized (PAG), depending on its extent. Often, bacterial biofilm deposits are disproportionate to the amount of bone destruction and loss of insertion that the patient presents, regardless of sub classification. The most important microorganism related to the etiopathogenesis of the disease is Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), including its main serotypes a, b and c, widely studied. Associated with these conditions, A. actinomycetemcomitans presents some virulence factors such as leukotoxin, mainly linked to serotype b - clone JP2 (which is highly leukotoxic) and outer membrane proteins (Omp\'s), especially Omp29. Serum immunoglobulin G (IgG) response against this pathogen was previously associated with both forms of BP; however, there are few studies that longitudinally evaluated the serum response to variables such as these. Thus, the objective of this study was to evaluate the serum response of 27 patients with AP and 10 periodontally healthy patients against Omp29 and A. actinomycetemcomitans serotypes by an ELISA, correlating with the number of copies of JP2 (obtained by qPCR in real time) and clinical parameters, from data previously collected by our group. All data were obtained prior to initiation of treatment and one year after its completion. The treatment consisted of oral hygiene guidelines, mechanical treatment and antibiotic therapy. Data from the study showed that in both forms of BP there was a significant reduction in clinical depth of sampling (PCS) (p<0,001),, clinical level of insertion (NCI)(p<0,001) and serum response against Omp29 and serotype c of A. actinomycetemcomitans(p>0,005). After 1 year, normalized optical density (O.D.) values for Omp29 and A. actinomycetemcomitans serotypes, as well as the number of copies of clone JP2 became similar to the levels found in the controls. The reduction in copy number of clone JP2 was correlated with reduction of PCS in PAL(r=0.80,p=0.0042) and O.D. normalized from Omp29 to PAG(r=0.66,p=0.005). The study concluded that periodontal treatment was effective in altering the serum response against Omp29 and A. actinomycetemcomitans serotypes, in addition to reducing the number of copies of clone JP2 and improving clinical parameters.