Annals of periodontology最新文献

{"title":"Maternal periodontitis and prematurity. Part II: Maternal infection and fetal exposure.","authors":"Robert P. N. Madianos, S. Lieff, A. Murtha, K. Boggess, R. Auten, J. Beck, S. Offenbacher","doi":"10.1097/01.OGX.0000074320.16796.CE","DOIUrl":"https://doi.org/10.1097/01.OGX.0000074320.16796.CE","url":null,"abstract":"Clinical data from the first 812 deliveries from a cohort study of pregnant mothers entitled Oral Conditions and Pregnancy (OCAP) demonstrate that both antepartum maternal periodontal disease and incidence/progression of periodontal disease are associated with preterm birth and growth restriction after adjusting for traditional obstetric risk factors. In the current study we present measures of maternal periodontal infection using whole chromosomal DNA probes to identify 15 periodontal organisms within maternal periodontal plaque sampled at delivery. In addition, maternal postpartum IgG antibody and fetal exposure, as indexed by fetal cord blood IgM level to these 15 maternal oral pathogens, was measured by whole bacterial immunoblots. The potential role of maternal infection with specific organisms within 2 bacterial complexes most often associated with periodontitis, conventionally termed \"Orange\" (Campylobacter rectus, Fusobacterium nucleatum, Peptostreptococcus micros, Prevotella nigrescens, and Prevotella intermedia) and \"Red\" (Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola) complexes, respectively, to prematurity was investigated by relating the presence of oral infection, maternal IgG, and fetal cord IgM, comparing full-term to preterm (gestational age < 37 weeks). The prevalence of 8 periodontal pathogens was similar among term and preterm mothers at postpartum. There was a 2.9-fold higher prevalence of IgM seropositivity for one or more organisms of the Orange or Red complex among preterm babies, as compared to term babies (19.9% versus 6.9%, respectively, P = 0.0015, chi square). Specifically, the prevalence of positive fetal IgM to C. rectus was significantly higher for preterm as compared to full-term neonates (20.0% versus 6.3%, P = 0.0002, as well as P. intermedia (8.8% versus 1.1%, P = 0.0003). A lack of maternal IgG antibody to organisms of the Red complex was associated with an increased rate of prematurity with an odds ratio (OR) = 2.2; confidence interval (CI) 1.48 to 3.79), consistent with the concept that maternal antibody protects the fetus from exposure and resultant prematurity. The highest rate of prematurity (66.7%) was observed among those mothers without a protective Red complex IgG response coupled with a fetal IgM response to Orange complex microbes (combined OR 10.3; P < 0.0001). These data support the concept that maternal periodontal infection in the absence of a protective maternal antibody response is associated with systemic dissemination of oral organisms that translocate to the fetus resulting in prematurity. The high prevalence of elevated fetal IgM to C. rectus among premature infants raises the possibility that this specific maternal oral pathogen may serve as a primary fetal infectious agent eliciting prematurity.","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1 1","pages":"175-82"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/01.OGX.0000074320.16796.CE","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61584852","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":"Coagulation and Thrombosis in Cardiovascular Disease: Plausible Contributions of Infectious Agents","authors":"Mark C. Herzberg Dr.","doi":"10.1902/annals.2001.6.1.16","DOIUrl":"10.1902/annals.2001.6.1.16","url":null,"abstract":"<p>An occlusive thrombus in the coronary arteries is the critical pathological event that immediately precedes most cases of myocardial infarction. Often the thrombus originates with a bleed from a fissured atheroma. Atheroma formation, therefore, creates risk of thrombosis; asymptomatic episodes of thrombosis and healing contribute to the pathogenesis of atherosclerosis and the development of atherosclerotic plaques. Based largely on in vitro and animal model evidence, infectious agents and their products can activate the coagulation cascade enzymatically or by up-regulating tissue factor. By initiating a procoagulant response, infectious agents can indirectly trigger a prothrombotic response. Alternatively, some microbes can directly trigger platelet aggregation in vitro and in animal models, suggesting direct prothrombotic potential in human cardiovascular disease. Activation of coagulation and thrombosis characterizes the pathological response to infectious agents in human disseminated intravascular coagulation and infective endocarditis. Given the underlying biological plausibility, the cumulative lifetime burden of chronic pathogens may be expected to create risk of atherosclerosis and thrombosis, and, indirectly, signs of cardiovascular disease. <i>Ann Periodontol 2001;6:16-19.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"16-19"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.16","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68174798","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":"Insulin Resistance and Periodontal Disease: An Epidemiologic Overview of Research Needs and Future Directions","authors":"Richard P. Donahue Dr.,&nbsp;Tiejian Wu","doi":"10.1902/annals.2001.6.1.119","DOIUrl":"10.1902/annals.2001.6.1.119","url":null,"abstract":"<p>Poor periodontal health is known to be associated with Type 2 diabetes mellitus (DM). This relationship and underlying mechanisms are discussed elsewhere in this issue. Less is known concerning the link between the metabolic precursors to DM, including insulin resistance (IR), and its possible association with periodontitis. Indeed, there has been relatively little research to date in human populations concerning periodontal disease, IR, and the subsequent risk of chronic diseases, including DM. This paper will present an epidemiologist's view of how IR may link periodontal disease with DM and suggest several avenues of investigation to help clarify some of the outstanding issues. <i>Ann Periodontol 2001;6:119-124.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"119-124"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.119","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68175095","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":"Receptor for Advanced Glycation End Products, Inflammation, and Accelerated Periodontal Disease in Diabetes: Mechanisms and Insights Into Therapeutic Modalities","authors":"Evanthia Lalla,&nbsp;Ira B. Lamster,&nbsp;David M. Stern,&nbsp;Ann Marie Schmidt Dr.","doi":"10.1902/annals.2001.6.1.113","DOIUrl":"10.1902/annals.2001.6.1.113","url":null,"abstract":"<p>In hyperglycemic states found in diabetics, a nonenzymatic glycation and oxidation of proteins and lipids occurs. As a result, advanced glycation end products (AGEs), particularly N^∊-(carboxymethyl) lysine, accumulate in the plasma and tissues of diabetic subjects. This accumulation has been linked to the development of pathogenic complications of diabetes. Many of the effects of AGEs are receptor-dependent and involve a multi-ligand member of the immunoglobulin superfamily of cell surface molecules. The best characterized of these is the receptor for advanced glycation end products (RAGE), which is expressed by multiple cell types including endothelium and mononuclear phagocytes. Based on data from a variety of sources, including studies of RAGE-deficient mice, it appears that RAGE plays a central role in oral infection, exaggerated inflammatory host responses, and destruction of alveolar bone in diabetes. It is possible that antagonists of RAGE might have a valuable adjunctive therapeutic role for the management of periodontal disease found in diabetics. <i>Ann Periodontol 2001;6:113-118.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"113-118"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.113","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68175202","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 Periodontal-Systemic Connection: Implications for Treatment of Patients With Osteoporosis and Periodontal Disease","authors":"Elizabeth A. Krall Dr.","doi":"10.1902/annals.2001.6.1.209","DOIUrl":"10.1902/annals.2001.6.1.209","url":null,"abstract":"<p>Osteoporosis and osteopenia may influence periodontal disease and tooth loss. Medications such as hormone replacement therapy and nutritional supplements that are used to prevent or treat osteoporosis have been evaluated for beneficial effects on oral health in a small number of human studies. Hormone replacement therapy (HRT), which slows the rate of bone loss at skeletal sites such as the hip and spine, also appears to reduce the rate of alveolar bone loss in postmenopausal women. HRT use is consistently associated with greater tooth retention and a reduced likelihood of edentulism in studies of elderly women. The number of studies on the effects of calcium or vitamin D intake on oral outcomes is limited, but suggest that higher intake levels are associated with reduced prevalence of clinical attachment loss and lower risk of tooth loss. Data from a prospective study of oral health in men show a similar association between higher calcium intake and reduced alveolar bone loss. The number of teeth with progression of alveolar bone loss over a 7-year period was significantly lower among men whose calcium intake was at least 1,000 mg per day, compared to men with a calcium intake below this level. Future studies should confirm these findings and evaluate the oral effects of new medications for osteoporosis. If confirmed, the implications for dental professionals may include an expanded array of medications for the treatment of periodontal disease and a greater emphasis on nutrition education for patients. <i>Ann Periodontol 2001;6:209-213</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"209-213"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.209","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68177771","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":"Osteoporosis and Periodontitis: Discussion, Conclusions, and Recommendations","authors":"Michael S. Reddy Dr.","doi":"10.1902/annals.2001.6.1.214","DOIUrl":"10.1902/annals.2001.6.1.214","url":null,"abstract":"","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"214-217"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.214","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68177902","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":"Periodontal Disease and Diabetes Mellitus: Discussion, Conclusions, and Recommendations","authors":"Ira B. Lamster,&nbsp;Evanthia Lalla","doi":"10.1902/annals.2001.6.1.146","DOIUrl":"10.1902/annals.2001.6.1.146","url":null,"abstract":"","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"146-149"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.146","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68175266","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":"Epidemiologic Associations Between Periodontal Disease and Chronic Obstructive Pulmonary Disease","authors":"Raul I. Garcia Dr.,&nbsp;Martha E. Nunn,&nbsp;Pantel S. Vokonas","doi":"10.1902/annals.2001.6.1.71","DOIUrl":"10.1902/annals.2001.6.1.71","url":null,"abstract":"<p>The nature of the relationship of periodontal disease to a number of systemic health outcomes, including chronic obstructive pulmonary disease (COPD), remains unclear. Various causal mechanisms have been proposed to explain the observed epidemiologic associations between periodontal diseases and respiratory diseases. We have reviewed the epidemiologic and clinical evidence for this association. The methodologic approach we have taken is based on a structured systematic review of the indexed biomedical literature on these subjects. The primary focus of this review was on the analysis of periodontal health status measures and their association with COPD, which includes chronic bronchitis and emphysema. We found that a paucity of published results exist on this specific relationship and those which do exist typically represent secondary analyses of existing data sets. Nevertheless, the epidemiologic evidence identified in this systematic review indicates that worse periodontal health status is associated with an increased risk of COPD, with odds ratios ranging from 1.45 to 4.50 (significant at the 95% confidence interval). However, it is possible that residual confounding by tobacco smoking may account in part for the observations. A causal association between periodontal health status and risk of COPD, although biologically plausible, remains speculative. Randomized controlled trials will be required in order to address the question of causality and to better understand the biological basis of these epidemiologic associations. <i>Ann Periodontol 2001;6:71-77.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"71-77"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.71","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68179102","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: Cardiovascular Section","authors":"","doi":"10.1902/annals.2001.6.1.58","DOIUrl":"https://doi.org/10.1902/annals.2001.6.1.58","url":null,"abstract":"","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"58-65"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.58","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138024197","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":"Maternal Periodontitis and Prematurity. Part II: Maternal Infection and Fetal Exposure","authors":"P.N. Madianos Dr.,&nbsp;S. Lieff,&nbsp;A.P. Murtha,&nbsp;K.A. Boggess,&nbsp;R.L. Auten Jr.,&nbsp;J.D. Beck,&nbsp;S. Offenbacher","doi":"10.1902/annals.2001.6.1.175","DOIUrl":"https://doi.org/10.1902/annals.2001.6.1.175","url":null,"abstract":"<p>Clinical data from the first 812 deliveries from a cohort study of pregnant mothers entitled Oral Conditions and Pregnancy (OCAP) demonstrate that both antepartum maternal periodontal disease and incidence/progression of periodontal disease are associated with preterm birth and growth restriction after adjusting for traditional obstetric risk factors. In the current study we present measures of maternal periodontal infection using whole chromosomal DNA probes to identify 15 periodontal organisms within maternal periodontal plaque sampled at delivery. In addition, maternal postpartum IgG antibody and fetal exposure, as indexed by fetal cord blood IgM level to these 15 maternal oral pathogens, was measured by whole bacterial immunoblots. The potential role of maternal infection with specific organisms within 2 bacterial complexes most often associated with periodontitis, conventionally termed “Orange” <i>(Campylobacter rectus, Fusobacterium nucleatum, Peptostreptococcus micros, Prevotella nigrescens, and Prevotella intermedia)</i> and “Red” <i>(Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola)</i> complexes, respectively, to prematurity was investigated by relating the presence of oral infection, maternal IgG, and fetal cord IgM, comparing full-term to preterm (gestational age &lt;37 weeks). The prevalence of 8 periodontal pathogens was similar among term and preterm mothers at postpartum. There was a 2.9-fold higher prevalence of IgM seropositivity for one or more organisms of the Orange or Red complex among preterm babies, as compared to term babies (19.9% versus 6.9%, respectively, <i>P</i> = 0.0015, chi square). Specifically, the prevalence of positive fetal IgM to <i>C. rectus</i> was significantly higher for preterm as compared to full-term neonates (20.0% versus 6.3%, <i>P</i> = 0.0002, as well as <i>P. intermedia</i>(8.8% versus 1.1%, <i>P</i> = 0.0003). A lack of maternal IgG antibody to organisms of the Red complex was associated with an increased rate of prematurity with an odds ratio (OR) = 2.2; confidence interval (CI) 1.48 to 3.79), consistent with the concept that maternal antibody protects the fetus from exposure and resultant prematurity. The highest rate of prematurity (66.7%) was observed among those mothers without a protective Red complex IgG response coupled with a fetal IgM response to Orange complex microbes (combined OR 10.3; <i>P</i> &lt;0.0001). These data support the concept that maternal periodontal infection in the absence of a protective maternal antibody response is associated with systemic dissemination of oral organisms that translocate to the fetus resulting in prematurity. The high prevalence of elevated fetal IgM to <i>C. rectus</i> among premature infants raises the possibility that this specific maternal oral pathogen may serve as a primary fetal infectious agent eliciting prematurity. <i>Ann Periodontol 2001;6:175-182.</i></p>","PeriodicalId":79473,"journal":{"name":"Annals of periodontology","volume":"6 1","pages":"175-182"},"PeriodicalIF":0.0,"publicationDate":"2001-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1902/annals.2001.6.1.175","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138025453","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}