Oral Health in Women During Preconception and Pregnancy: Implications for Birth Outcomes and Infant Oral Health

The mouth is an obvious portal of entry to the body, and oral health reflects and influences general health and well being. Maternal oral health has significant implications for birth outcomes and infant oral health. Maternal periodontal disease, that is, a chronic infection of the gingiva and supporting tooth structures, has been associated with preterm birth, development of preeclampsia, and delivery of a small-for-gestational age infant. Maternal oral flora is transmitted to the newborn infant, and increased cariogenic flora in the mother predisposes the infant to the development of caries. It is intriguing to consider preconception, pregnancy, or intrapartum treatment of oral health conditions as a mechanism to improve women's oral and general health, pregnancy outcomes, and their children's dental health. However, given the relationship between oral health and general health, oral health care should be a goal in its own right for all individuals. Regardless of the potential for improved oral health to improve pregnancy outcomes, public policies that support comprehensive dental services for vulnerable women of childbearing age should be expanded so that their own oral and general health is safeguarded and their children's risk of caries is reduced. Oral health promotion should include education of women and their health care providers ways to prevent oral disease from occurring, and referral for dental services when disease is present

Biological foundation for periodontitis as a potential risk factor for atherosclerosis

Links between periodontal diseases and systemic diseases have been well documented by epidemiological studies. Recently, research has shifted to elucidating the biologic mechanism for a causal relationship. One focus of interest is atherosclerosis, the underlying event of cardiovascular diseases due to its serious health impact. However, it is still not clear whether periodontopathic pathogens are truly etiologic agents or ubiquitous bystanders. This article reviews the current understanding about the molecular biological interactions between periodontal disease and atherosclerosis and the biological plausibility of periodontitis as a potential risk factor for cardiovascular disease. Materials and methods:  The current literature regarding periodontal diseases and atherosclerosis and coronary vascular disease was searched using the Medline and PubMed databases. Results:  In vitro experiments and animal models are appropriate tools to investigate the biological interactions between periodontal disease and atherosclerosis at the cell molecular level. The concepts linking both pathologies refer to inflammatory response, immune responses, and hemostasis. In particular, Porphyromonas gingivalis appears to have unique, versatile pathogenic properties. Whether or not these findings from isolated cells or animal models are applicable in humans with genetic and environmental variations is yet to be determined. Likewise, the benefit from periodontal therapy on the development of atherosclerosis is unclear. Approaches targeting inflammatory and immune responses of periodontitis and atherosclerosis simultaneously are very intriguing. Conclusion:  An emerging concept suggests that a pathogenic burden from different sources might overcome an individual threshold culminating in clinical sequela. P. gingivalis contributes directly and indirectly to atherosclerosis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66109/1/j.1600-0765.2004.00771.x.pd

The effects of periodontal therapy on vascular endothelial function: A pilot trial

Background Chronic periodontal infection is associated with an increased risk of coronary heart disease. Although the mechanism responsible for the relationship between periodontal disease and cardiovascular events is not fully understood, it is hypothesized that the chronic inflammatory burden of periodontal disease may lead to impaired functioning of the vascular endothelium. Methods Twenty-two otherwise healthy adults with moderate to severe periodontitis who underwent complete mouth disinfection were evaluated to determine if periodontal therapy would result in improved endothelial function and a decrease in serum inflammatory markers. Subjects had measurements of periodontal disease severity, flow-mediated (endothelium-dependent), and nitroglycerin-mediated (endothelium-independent) dilation of the brachial artery, serum C-reactive protein (CRP) and interleukin 6 (IL-6), and serum total and high-density lipoprotein cholesterol levels on 2 baseline visits separated by 1 month and, again, 1 month after treatment. Results There were no significant changes in clinical periodontal measures, flow-mediated dilation, nitroglycerin-mediated dilation, CRP, IL-6, total cholesterol, or high-density lipoprotein cholesterol between the repeated baseline measurements. Periodontal treatment, however, resulted in significant improvements in periodontal pocketing, flow-mediated dilation, and serum IL-6, as well as a trend toward reduction in serum CRP; there were no significant changes in nitroglycerin-mediated dilation or in cholesterol levels. Conclusions These results represent proof of concept that improvement in endothelial function, as measured by flow-mediated dilation of the brachial artery, may be possible through near-elimination of chronic oral infection and suggest that the conduct of a larger controlled trial is justified

Association of Systemic Oxidative Stress with Suppressed Serum IgG to Commensal Oral Biofilm and Modulation by Periodontal Infection

To assess the impact of systemic oxidative stress on humoral immune responses, we examined the relation between levels of serum 8-isoprostane and serum IgG antibodies against 17 microorganisms in the commensal oral biofilm among the ARIC population of community-dwelling adults (n = 4,717). Bivariately, serum 8-isoprostane was associated with age, race/center, education, smoking, serum triglycerides, and the extent of periodontal disease severity. Total IgG antibody directed to the oral biofilm was significantly associated with race/center, hypertension, triglycerides, periodontal disease severity, plaque, and serum 8-isoprostane. In multivariate models, the highest quartile of increased 8-isoprostane displayed marked reductions (44%) in biofilm IgG antibody in contrast to small increases in total IgG antibody level for the highest quartiles of oral bacterial burden or periodontal disease severity (19 and 12%, respectively; p < 0.0001). Increased 8-isoprostane was associated with decreased total IgG antibody (p < 0.0001) in subjects with or without extensive periodontal disease and/or biofilm and with suppression of IgG responses across the entire biofilm composition. Increased systemic oxidative stress is associated with a generalized decrease of serum IgG antibody responses to the oral biofilm. Levels of oral microbial burden, periodontitis severity, and smoking are, by comparison, minor modifiers of serum IgG responses to the commensal oral biofilm. Antioxid. Redox Signal. 11, 2973–2983

Associations between IgG antibody to oral organisms and carotid intima-medial thickness in community-dwelling adults

Aims: The aims of this study are to describe the relationships between IgG antibodies to 17 oral organisms and atherosclerosis as indexed by carotid intima-medial wall thickness (IMT) and to evaluate the role of smoking. Methods and results: Our study is based on a subset of participants in the Atherosclerosis Risk in Communities (ARIC) Study, who received a complete periodontal examination during visit 4 (1996-1998). The Outcome was mean carotid IMT &gt;= 1 mm assessed by B-mode ultrasound. The exposures were serum IgG antibody levels against 17 periodontal organisms using a whole bacterial checkerboard immunoblotting technique. Evaluation of all 17 antibodies indicated that antibody to Campylobacter rectus resulted in the best-fitting model (OR = 2.3, 95% Cl = 1.83-2.84) and individuals with both high C. rectus and Peptostreptococcus micros titers had almost twice the prevalence of IMT &gt;= 1 mm than those with only a high C. rectus antibody (8.3% versus 16.3%). Stratification by smoking indicated that all microbial models significant for smokers were also significant for never smokers except for Porphyromonas gingivalis (p = 0.08). Conclusions: This is the first study to report a relationship between IgG antibody reactive to oral organisms and subclinical atherosclerosis with significant relationships evident in both ever and never smokers. (c) 2005 Elsevier Ireland Ltd. All rights reserved

Periodontal disease and coronary heart disease - A reappraisal of the exposure

Background - Results from studies relating periodontal disease to cardiovascular disease have been mixed. Residual confounding by smoking and use of clinical measures of periodontal disease rather than measures of infection have been 2 major criticisms. The aims of this study were to investigate relationships between prevalent coronary heart disease (CHD) and 2 exposures, ( 1) clinical periodontal disease and ( 2) IgG antibodies to 17 oral organisms, and to evaluate the role of smoking in these relationships. Methods and Results - Our study is based on a subset of participants in the Atherosclerosis Risk in Communities ( ARIC) Study, who received a complete periodontal examination during visit 4 ( 1996 - 1998). The exposures were periodontal status and serum IgG antibody levels against 17 periodontal organisms, and the outcome was prevalent CHD at visit 4. Multivariable analyses indicate that periodontal status is not significantly associated with CHD in either ever smokers or never smokers. Similar analyses evaluating antibodies indicate that high antibodies ( above the median) to Treponema denticola (odds ratio [OR] = 1.7; 95% CI, 1.2 to 2.3), Prevotella intermedia ( OR = 1.5; 95% CI, 1.1 to 2.0), Capnocytophaga ochracea ( OR = 1.5; 95% CI, 1.1 to 2.1), and Veillonella parvula ( OR = 1.7; 95% CI, 1.2 to 2.3) are significantly associated with CHD among ever smokers, whereas Prevotella nigrescens ( OR = 1.7; 95% CI, 1.1 to 2.6), Actinobacillus actinomycetemcomitans ( OR = 1.7; 95% CI, 1.2 to 2.7), and Capnocytophaga ochracea ( OR = 2.0; 95% CI, 1.3 to 3.0) were associated with CHD among never smokers. Conclusions - Clinical signs of periodontal disease were not associated with CHD, whereas systemic antibody response was associated with CHD in ever smokers and never smokers. These findings indicate that the quality and quantity of the host response to oral bacteria may be an exposure more relevant to systemic atherothrombotic coronary events than clinical measures