Annals of periodontology最新文献

{"title":"Participants in the Periodontal-Systemic Connection: A State-of-the-Science Symposium","authors":"","doi":"10.1902/annals.2001.6.1.224","DOIUrl":"https://doi.org/10.1902/annals.2001.6.1.224","url":null,"abstract":"","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"224"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138022093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poster Session Abstracts: Diabetes Section","authors":"","doi":"10.1902/annals.2001.6.1.150","DOIUrl":"https://doi.org/10.1902/annals.2001.6.1.150","url":null,"abstract":"","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"150-152"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138024059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Relationship Between Infections and Adverse Pregnancy Outcomes: An Overview","authors":"Ronald S. Gibbs Dr.","doi":"10.1902/annals.2001.6.1.153","DOIUrl":"10.1902/annals.2001.6.1.153","url":null,"abstract":"<p>Preterm birth with its subsequent morbidity and mortality is the leading perinatal problem in the United States. Infants born before the thirty-seventh week of gestation account for approximately 6% to 9% of all births, but 70% of all perinatal deaths and half of all long-term neurologic morbidity. Current approaches focus on symptomatic treatment. Despite widespread use of drugs to arrest preterm labor (tocolytics), there has been no decrease in low birth weight or preterm infants in the last 20 years. It is likely that therapy directed at preventing or treating underlying causes would be more successful. Evidence from many sources links preterm birth to symptomatic infections, for example, of the urinary or respiratory tracts. In the last decade, great interest has been generated to support the hypothesis that subclinical infection is an important cause of preterm labor. Evidence to support this may be categorized as follows: histological chorioamnionitis is increased in preterm births; clinical infection is increased after preterm birth; there is significant association of some lower genital tract organisms and infections with preterm birth or preterm premature rupture of the membranes; there are positive cultures of amniotic fluid or membranes from some patients with preterm labor and preterm birth; there are markers of infections in preterm birth; bacteria or their products induce preterm birth in animal models; and some antibiotic trials have shown a lower rate of preterm birth or have deferred preterm birth. In the last 5 years, additional exciting information has suggested that not only is subclinical infection responsible for preterm birth but also many serious neonatal sequelae including periventricular leukomalacia, cerebral palsy, respiratory distress, and even bronchopulmonary dysplasia and necrotizing enterocolitis. In sum, a large body of clinical and laboratory information suggests that subclinical infection is a major cause of preterm birth, especially those occurring before 30 weeks. This concept holds promise that new approaches can be developed to prevent prematurity. <i>Ann Periodontol 2001;6:153-163.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"153-163"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.153","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68175278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Relationship Between Skeletal and Oral Bone Mineral Density: An Overview","authors":"Charles H. Chesnut III Dr.","doi":"10.1902/annals.2001.6.1.193","DOIUrl":"10.1902/annals.2001.6.1.193","url":null,"abstract":"<p>Is oral osteopenia (bone loss of the jaws) a component of systemic osteopenia/osteoporosis (systemic bone loss, with or without fracture) or only an accompanying manifestation of periodontal disease? Put other ways: 1) is systemic osteopenia a risk factor for periodontitis; 2) is systemic osteopenia a risk factor for oral osteopenia independent of periodontal disease; or 3) is periodontal disease the primary (exclusive) risk factor for oral osteopenia? Despite 2 decades of scientific inquiry into these questions, the answers remain elusive. <i>Ann Periodontol 2001;6: 193-196.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"193-196"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.193","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68176860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral Bacteria and Respiratory Infection: Effects on Respiratory Pathogen Adhesion and Epithelial Cell Proinflammatory Cytokine Production","authors":"Frank A. Scannapieco Dr.,&nbsp;Bingyan Wang,&nbsp;Harlan J. Shiau","doi":"10.1902/annals.2001.6.1.78","DOIUrl":"10.1902/annals.2001.6.1.78","url":null,"abstract":"<p>Several microbiologic and epidemiologic studies have suggested an association between dental plaque, poor oral health, and respiratory diseases such as nosocomial pneumonia and chronic obstructive pulmonary disease (COPD). A number of hypotheses are suggested to help explain how oral bacteria may participate in the pathogenesis of respiratory infection. Resident bacteria in oral secretions are likely aspirated along with respiratory pathogens and may affect the adhesion of the later organisms to the respiratory epithelium. Preliminary studies performed in our laboratory suggest that oral bacteria may modulate the adhesion of respiratory pathogens to epithelial cell lines. In addition, oral bacterial products or cytokines in oral/pharyngeal aspirates may stimulate cytokine production from respiratory epithelial cells, resulting in recruitment of inflammatory cells. The resulting inflamed epithelium may be more susceptible to respiratory infection. Further preliminary data are presented that some species of oral bacteria may induce the release of proinflammatory cytokines from epithelial cell lines to an extent similar to that seen for respiratory pathogens. <i>Ann Periodontol 2001;6:78-86.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"78-86"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.78","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68178785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment of Periodontal Disease and Control of Diabetes: An Assessment of the Evidence and Need for Future Research","authors":"Sara G. Grossi Dr.","doi":"10.1902/annals.2001.6.1.138","DOIUrl":"10.1902/annals.2001.6.1.138","url":null,"abstract":"<p>Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. Genetics, age, and, nutrition are important signals for this increased response and as reported more recently, infections and inflammation. Persistent elevation of IL-1β, IL-6, and TNF-α in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. In addition, TNF-α, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. Collectively, the evidence supports a role for cytokine elevation in the pathophysiology and metabolic abnormalities associated with diabetes. Periodontitis is an infection that is twice as prevalent in diabetic individuals compared to non-diabetics. <i>Porphyromonas gingivalis</i>, one of the microorganisms responsible for this infection, is able to invade endothelial cells and is a potent signal for monocyte and macrophage activation. Thus, once established in the diabetic host, this chronic infection complicates diabetes control and increases the occurrence and severity of microvascular and macrovascular complications. Unlike treatment of acute infections, modalities of treatment for chronic infections are a matter of debate. Evidence indicates that mechanical removal of subgingival infection does not result in complete elimination of periodontal infection and consequently there is no effect on diabetes control measured as reduction in glycated hemoglobin. On the other hand, studies incorporating systemic antibiotics as adjuncts to mechanical debridement result in a reduction of <i>P. gingivalis</i> to nondetectable levels and a concomitant reduction in glycated hemoglobin, independent of the hypoglycemic effects of diabetes drugs or insulin. The evidence supports the notion that treatment of chronic periodontal infection is essential in the diabetic patient. Assessment of infection status in diabetic patients is fundamental for appropriate treatment decisions. <i>Ann Periodontol 2001;6:138-145.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"138-145"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.138","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68175002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role for Periodontal Bacteria in Cardiovascular Diseases","authors":"Howard K. Kuramitsu Dr.,&nbsp;Mingshan Qi,&nbsp;In-chol Kang,&nbsp;Wen Chen","doi":"10.1902/annals.2001.6.1.41","DOIUrl":"10.1902/annals.2001.6.1.41","url":null,"abstract":"<p><b>Background:</b> Several epidemiological studies as well as a recent animal model approach have suggested a role for periodontal diseases in the development of cardiovascular disease (CVD). This relationship could be mediated by inflammatory responses induced by periodontal pathogens as well as direct interaction of these organisms with cardiac tissue.</p><p><b>Methods:</b> In order to explore these possibilities, the effects of the periodontal pathogen <i>Porphyromonas gingivalis</i> on cellular events proposed to play a role in CVD were investigated.</p><p><b>Results:</b> <i>P. gingivalis</i>, as well as its outer membrane vesicles (OMV), was able to induce foam cell formation (an important characteristic of CVD) in the murine macrophage cell line J774 A.1. This property appears to be mediated by the lipopolysaccharide (LPS) fraction of the cells. Several other oral bacteria were also able to induce foam cell formation. Furthermore, since the rupture of the fibrous cap of plaque appears to be an important factor in acute coronary syndrome, it was demonstrated that <i>P. gingivalis</i> 381 degraded fibrous caps isolated from autopsy samples. In addition, it was observed that strain 381 strongly induced matrix metalloproteinase (MMP)-9 protease activity, implicated in plaque rupture, from the J774 A.1 macrophages. Finally, strain 381 was able to enhance monocyte chemoattractant protein-1 (MCP-1) and NADH oxidase expression from endothelial cells.</p><p><b>Conclusions:</b> Therefore, <i>P. gingivalis</i> exhibits several properties which could play a role in CVD as mediators of LDL oxidation, foam cell formation, and rupture of atherosclerotic plaque. <i>Ann Periodontol 2001;6:41-47.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"41-47"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.41","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68177630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Inflammatory and Immunological Mediators in Periodontitis and Cardiovascular Disease","authors":"Ernesto De Nardin Dr.","doi":"10.1902/annals.2001.6.1.30","DOIUrl":"10.1902/annals.2001.6.1.30","url":null,"abstract":"<p>Epidemiological studies have implicated periodontitis (PD) as a risk factor for development of cardiovascular disease (CVD). Persistent infections such as periodontitis induce inflammatory and immune responses which may contribute to coronary atherogenesis, and, in conjunction with other risk factors, may lead to coronary heart disease (CHD). In this review, mechanisms are described that may help explain the association between periodontal infections and CHD. Periodontal diseases are bacterial infections associated with bacteremia, inflammation, and a strong immune response, all of which may represent significant risk factors for the development of atherogenesis, CHD, and myocardial infarction (MI). Several mechanisms may participate in this association, including those induced by oral organisms, and those associated with host response factors. This review will focus on host factors. Oral pathogens and inflammatory mediators (such as interleukin [IL]-1 and tumor necrosis factor [TNF]-α) from periodontal lesions intermittently reach the bloodstream inducing systemic inflammatory reactants such as acute-phase proteins, and immune effectors including systemic antibodies to periodontal bacteria. This review will describe the potential role of various inflammatory as well as immunologic factors that may play a role in periodontitis as a possible risk factor for CHD. <i>Ann Periodontol 2001;6:30-40.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"30-40"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.30","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68177990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poster Session Abstracts: Osteoporosis and Adverse Pregnancy Outcomes Sections","authors":"","doi":"10.1902/annals.2001.6.1.218","DOIUrl":"https://doi.org/10.1902/annals.2001.6.1.218","url":null,"abstract":"","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"218-220"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.218","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138025452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Association Between Periodontal Diseases and Cardiovascular Diseases: A State-of-the-Science Review","authors":"James D. Beck Dr.,&nbsp;Steven Offenbacher","doi":"10.1902/annals.2001.6.1.9","DOIUrl":"10.1902/annals.2001.6.1.9","url":null,"abstract":"<p>Early case-control and cross-sectional studies demonstrating associations between chronic periodontitis and cardiovascular disease (CVD) were quickly followed by secondary analyses of data available from existing longitudinal studies, which indicated that individuals with periodontitis, as determined by clinical measures, were at greater risk for CVD events. Many of these studies contained large numbers of subjects and were adjusted for traditional risk factors. Within the last 18 months, one case-control study and one longitudinal study have reported finding positive associations that were not statistically significant. The earlier studies stimulated a number of studies focused on identifying potential biological mechanisms that might underlie this association. While still early in that process, such studies have implicated a systemic role for oral microorganisms and for the quality and quantity of the host inflammatory response as key biologic processes that may underlie the association of CVD with the clinical manifestation of periodontitis. It is a positive development when changes in our knowledge regarding biologic mechanisms result in reevaluation of past studies, and this reevaluation leads to new studies that incorporate the design elements demanded by this new knowledge. In that spirit, we conclude that all longitudinal studies reported to date can be characterized as follows: none were initially designed to actually test the association of interest; almost all were restricted to clinical measures of periodontitis to index the exposure and lacked measures of infectious burden and host response; and they used a variety of cardiovascular clinical events to index the outcome and did not include subclinical measures of atherosclerosis. In addition, the longitudinal studies that failed to show a significant association between periodontitis and CVD used the least sensitive and crudest clinical measures of periodontal disease. Based upon the current state-of-the-science, all previous studies should be viewed as lacking sufficiently sensitive and comprehensive measures of periodontal disease as a systemic exposure. Since the potential health care impact of this relationship might be extensive, it is time to enter the next phase of research by conducting molecular epidemiology studies that are appropriately designed to test our current understanding of the molecular and cellular mechanisms involved. <i>Ann Periodontol 2001;6:9-15.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"9-15"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68178923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}