Depuis la fin des années 1980, de nombreuses études épidémiologiques ont montré une association positive et indépendante entre les maladies cardiovasculaires et les maladies parodontales. Les maladies parodontales, responsables de bactériémies transitoires et répétées, ont la capacité d’initier ou d’aggraver les lésions d’athérosclérose. Deux mécanismes pathogéniques majeurs sont aujourd’hui avancés. L’un est indirect par augmentation des médiateurs de l’inflammation induite par les parodontites et l’autre est direct lié au microbiote oral. Cette hypothèse majeure repose sur deux mécanismes non exclusifs, la translocation des bactéries parodontales au sein des plaques d’athérosclérose par la circulation générale et sur la modification du microbiote intestinal. L’objectif de la thèse était d'explorer l'association entre l’exposition systémique aux bactéries parodontales et leur présence au sein des plaques d’athérosclérose sur les complications cardio- et neuro-vasculaires chez l’homme. Les résultats obtenus montrent que les bactéries parodontales sont associées à un phénotype vulnérable des plaques d’athérosclérose coronariennes et carotidiennes. Les lésions d’athérosclérose compliquées par des hémorragies intraplaques sont le siège d’une activation plus intense des neutrophiles. Les effets délétères des leucocytes sur les tissus vasculaires sont potentiellement augmentés et entretenus par les bactéries majorant la vulnérabilité à la rupture des plaques d’athérosclérose. La confirmation clinique de la relation biologique entre le microbiote parodontal et les complications cardio- et neuro-vasculaires de l’athérosclérose est une perspective importante de cette thèse. / Since the late 1980s, many epidemiological studies have shown a positive and independent association between cardiovascular disease and periodontal disease. Periodontal disease inducing transient bacteraemia, can initiate or worsen atherosclerotic lesions. Two major pathophysiologic mechanisms are supported by evidence. One is by indirect increase in inflammatory systemic periodontitis-induced mediators and the other is directly related to the oral microbiota. This major hypothesis is based on two non-exclusive mechanisms, the translocation of periodontal bacteria in atherosclerotic plaques by the general circulation and the impact on the gut microbiota.The aim of the thesis was to explore the association between systemic exposure to periodontal bacteria and their presence in atherosclerotic plaques on the cardiovascular and neurovascular complications in human.The results obtained show that periodontal bacteria are associated to a vulnerable phenotype of coronary and carotid atherosclerotic plaques. Atherosclerotic lesions complicated by intraplaque haemorrhage are the trigger of a super activation of neutrophils. The deleterious effects of leukocytes to the vascular tissues are potentially increased and maintained by the bacteria which increase the atherosclerotic plaques vulnerability to rupture.The clinical confirmation of the biological relationship between periodontal microbiota and cardio- and neurovascular complications of atherosclerosis is an important perspective of this thesis.

Mechanical stress has been shown to play a role in bone remodelling during orthodontic tooth movement. Receptor activator of nuclear factor kβ - ligand (RANKL), osteoprotegerin (OPG), monocyte colony stimulating factor (M-CSF) and interleukin 1-β (IL-1β) play key roles in the regulation of bone remodelling, but the role of these cytokines in orthodontic tooth movement is poorly understood. Aim: The aim of this experiment was to examine the response of periodontal ligament (PDL) fibroblasts in monolayer culture to intermittent tensile stress as regards RANKL, OPG, M-CSF and IL-1β production. Methods: Human PDL fibroblasts were dissected from premolars extracted for orthodontic purposes. Explants were seeded out in 1cm wells and grown to confluence in Dulbecco�s modification of Eagle�s medium, containing 10% foetal calf serum and antibiotics, at 37�C in a humidified atmosphere of 5% CO₂/95% air. Upon reaching confluence, the cells were passaged into sequentially larger flasks. Fibroblasts were passaged 6 times. After reaching confluence in T175 flasks, the cells were detached and plated at a cell density of 10⁵/dish in 35mm Bioflex� Plates coated with type 1 collagen. The cells were placed under a continuous uni-axial strain of 12% for 6s of every 90s by a Flexercell FX 4000C[TM] for 0, 12, 24 and 48 hours. Cells were then detached and stored in RNAlater. Quantitative RT-PCR was used to determine the mRNA of the cytokines of interest. Results: Tensile force led to the down regulation of mRNA expression for OPG and IL-1β at 12 and 24 hours respectively, while M-CSF was up-regulated at 6 hours. RANKL was not detected at a significant level for quantification. Conclusion: This osteoclastic-type response indicates the complexity of mechanotransduction in an in vitro setting. Acknowledgments: This research was supported by the New Zealand Dental Research Foundation, the New Zealand Lottery Grants Board and the New Zealand Association of Orthodontists.

Thesis (M.D.S.)--University of Hong Kong, 1989. / Includes bibliographical references (p. 116-125) Also available in print.

Thesis (M.S.)--School of Dentistry. University of Missouri--Kansas City, 2005. / "A thesis in dental hygiene education." Advisor: Karen B. Williams. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed March 12, 2007. Includes bibliographical references (leaves 57-65). Online version of the print edition.

<p>Periodontitis is a bacterially induced chronic inflammatory disease that destroys the supporting tissues of teeth. Clinical observations and experimental evidence indicates that there is a genetic influence of risk factors for periodontitis. A specific pattern of IL-1 polymorphisms (known as the composite IL-1 genotype) has been found to influence the severity of chronic periodontitis. The objective of this study was to evaluate the association between the IL-1 gene polymorphisms and the severity of periodontal disease in a selected Xhosa ppopulation of South africa.</p>

El objetivo del presente estudio fue determinar la prevalencia, extensión y severidad de la recesión gingival en una población de pacientes del Hospital Central de la Fuerza Aérea del Perú. Para este propósito se evaluó periodontalmente a 133 pacientes. Se midieron en todas las piezas presentes la distancia margen gingival – unión cemento esmalte en las caras vestibular y lingual, y se consideró como recesión gingival en aquellos dientes en que esta fuera mayor o igual a 1 mm. Los dientes que presentaron recesión gingival también fueron clasificados de acuerdo a la clasificación propuesta por Miller. Los resultados mostraron una prevalencia de 72,9% de pacientes afectados por algún grado de recesión gingival y se encontró un promedio de 5.79 + 0.555 dientes afectados por persona. De acuerdo a su longitud coronoapical, las recesiones gingivales fueron clasificadas como de severidad leve en un 64,0%, moderadas en 28,3% y avanzadas en 7,7%. De acuerdo a la clasificación de Miller se encontró que un 64,7% fueron clasificadas como Clase I, un 9,4% como Clase II, 17,5% como Clase III y 8,4% como Clase IV. La mayor prevalencia, extensión y severidad de la recesión gingival en los sujetos adultos nos sugiere un efecto acumulativo de la lesión asociado a períodos largos de exposición a los agentes etiológicos. Es de importancia identificar y remover estos agentes tan pronto como sea posible para reducir e incluso evitar un empeoramiento de esta condición clínica.

N/A (only background that is 10+ pgs)

Thesis (doctoral)--Lunds Universitet, Malmö, 1984. / Extra t.p. with thesis statement inserted. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M.D. Sc)--University of Queensland, 2002. / Includes bibliographical references.

Thesis (Ph. D.)--University of Queensland, 2003. / Includes bibliographical references.