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Several serum inflammatory biomarkers have been associated with blood pressure and hypertension prevalence in cross-sectional studies. Few of these associations have been evaluated prospectively. We examined associations for 10 serum inflammatory biomarkers with incident hypertension among 471 postmenopausal women (mean age = 65) in the Buffalo OsteoPerio Study. Concentrations of C-reactive protein, interleukin (IL)-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-α, monocyte chemoattractant protein (MCP)-1, adiponectin, and leptin were measured using multiplexed sandwich immunoassays on fasting serum samples collected at baseline (1997-2001). Incident hypertension (195 cases) was defined as physician-diagnosed hypertension and treatment with medication identified on annual mailed health surveys during follow-up (mean 10 years). Cox regression was used to estimate hazard ratios (HR) and 95% confidence intervals (CI) between log-transformed biomarkers (per 1-SD) and hypertension. When adjusted for age, leptin was significantly associated with hypertension risk (HR = 1.55, 95% CI: 1.04, 2.29), however, the association was attenuated and not significant after adjustment for demographic and lifestyle factors, including BMI. Significant (P < 0.10) interactions were observed for smoking (never, ever) with CRP (HR: never, 1.31; ever, 0.91; P = 0.06) and MCP-1 (HR: never, 0.59; ever, 5.11; P = 0.004); for BMI (

Diabetes mellitus is a group of metabolic disorders with high mortality and morbidity associated with complications such as cardiovascular disease, kidney disease, and stroke. The prevalence of diabetes is 9.4% in US adults, and prevalence increases markedly with age, with 1 in 4 adults aged ≥65 years affected by diabetes. The estimated number of adults with type 2 diabetes globally almost tripled between 2002 and 2017, reflecting increases seen in the USA and elsewhere. This increase raises concerns about the increased morbidity and mortality associated with the complications of diabetes, including periodontal disease and tooth loss. There is a reciprocal adverse relationship between diabetes and periodontal disease, with diabetes as a major risk factor for periodontal disease, and in those patients with diabetes who also have periodontal disease then there are adverse effects on glycemic control and complications such as cardiovascular disease and end stage renal disease. In this review, those studies detailing the adverse effects of periodontal disease and diabetes will be discussed. Also, evidence is accumulating that periodontitis may play a role in increasing the incidence of new cases of type 2 diabetes, and possibly gestational diabetes. Of course, these studies need to be expanded to better understand the effects of periodontitis on diabetes glycemic control, complications, prediabetes, and the incidence of new cases. However, given the tremendous burden of diabetes on society, the dental profession should be proactive in preventing and treating periodontal disease, not only to preserve the dentition, but also to minimize the adverse effects of periodontitis on diabetes and its complications.

Epidemiologic and cancer control studies on the association of periodontal disease and cancer risk mostly suggest a positive association with overall cancer risk and certain specific types of cancer. These findings are generally consistent among cross‐sectional and longitudinal studies. In this paper, we review epidemiologic studies and current knowledge on periodontal disease and cancer, with a focus on those studies conducted in the years following the Joint European Federation of Periodontology/American Academy of Periodontology Workshop on “Periodontitis and Systemic Diseases” in November 2012. This review also explores the role of chronic inflammation as a biologically plausible mechanistic link between periodontal disease and risk of cancer. Furthermore, it highlights studies that have examined the potential importance of certain periodontal pathogens in this association.

The most important development in the epidemiology of periodontitis in the USA during the last decade is the result of improvements in survey methodologies and statistical modeling of periodontitis in adults. Most of these advancements have occurred as the direct outcome of work by the joint initiative known as the Periodontal Disease Surveillance Project by the Centers for Disease Control and Prevention and the American Academy of Periodontology that was established in 2006. This report summarizes some of the key findings of this important initiative and its impact on our knowledge of the epidemiology of periodontitis in US adults. This initiative first suggested new periodontitis case definitions for surveillance in 2007 and revised them slightly in 2012. This classification is now regarded as the global standard for periodontitis surveillance and is used worldwide. First, application of such a standard in reporting finally enables results from different researchers in different countries to be meaningfully compared. Second, this initiative tackled the concern that prior national surveys, which used partial-mouth periodontal examination protocols, grossly underestimated the prevalence of periodontitis of potentially more than 50%. Consequently, because previous national surveys significantly underestimated the true prevalence of periodontitis, it is not possible to extrapolate any trend in periodontitis prevalence in the USA over time. Any difference calculated may not represent any actual change in periodontitis prevalence, but rather is a consequence of using different periodontal examination protocols. Finally, the initiative addressed the gap in the need for state and local data on periodontitis prevalence. Through the direct efforts of the Centers for Disease Control and Prevention and the American Academy of Periodontology initiative, full-mouth periodontal probing at six sites around all nonthird molar teeth was included in the 6 years of National Health and Nutrition Examination Surveys from 2009-2014, yielding complete data for 10 683 dentate community-dwelling US adults aged 30 to 79 years. Applying the 2012 periodontitis case definitions to the 2009-2014 National Health and Nutrition Examination Surveys data, the periodontitis prevalence turned out to be much greater than previously estimated, namely affecting 42.2% of the population with 7.8% of people experiencing severe periodontitis. It was also discovered that only the moderate type of periodontitis is driving the increase in periodontitis prevalence with age, not the mild or the severe types whose prevalence do not increase consistently with age, but remain ~ 10%-15% in all age groups of 40 years and older. The greatest risk for having periodontitis of any type was seen in older people, in males, in minority race/ethnic groups, in poorer and less educated groups, and especially in cigarette smokers. The Centers for Disease Control and Prevention and the American Academy of Periodontology initiative reported, for the first time, the periodontitis prevalence estimated at both local and state levels, in addition to the national level. Also, this initiative developed and validated in field studies a set of eight items for self-reported periodontitis for use in direct survey estimates of periodontitis prevalence in existing state-based surveys. These items were also included in the 2009-2014 National Health and Nutrition Examination Surveys for validation against clinically determined cases of periodontitis. Another novel result of this initiative is that, for the first time, the geographic distribution of practicing periodontists in relation to the geographic distribution of people with severe periodontitis is illustrated. In summary, the precise periodontitis prevalence and distribution among subgroups in the dentate US noninstitutionalized population aged 30-79 years is better understood because of application of valid periodontitis case definitions to full-mouth periodontal examination, in combination with reliable information on demographic and health-related measures. We now can monitor the trend of periodontitis prevalence over time as well as guide public health preventive and intervention initiatives for the betterment of the health of the adult US population.

Background Localized aggressive periodontitis (LAgP) occurs in 2% of African-American adolescents but only 0.15% of white adolescents. First molars and incisors are affected by rapid onset and progression. Methods This nonsystematic critical review evaluated published data for LAgP and chronic periodontitis (CP), focusing on potential differences in epidemiology, microbiology, immunology, genetics, and response to therapy. Results LAgP differs from CP by localization to incisors and first molars, early onset and rapid progression in adolescents and young adults, and a 10-fold higher prevalence in populations of African or Middle Eastern origin, often with strong familial aggregation. The bacterium Aggregatibacter actinomycetemcomitans and hyperresponsive neutrophils are frequently observed. Antibiotic and nonsurgical therapies are highly effective. Conclusions LAgP differs in many ways from the far more common CP that affects older adults. The substantial evidence of dissimilarities summarized in this review strongly supports the classification of LAgP as a distinct form of periodontitis. Practical Implications Classifying LAgP as a distinct subcategory of periodontitis will encourage future research and does not conflict with the newly proposed “staging and grading” system. The silent onset and rapid progression of LAgP make early diagnosis and frequent follow-up with patients essential for effective treatment.

Background The extent to which the composition and diversity of the oral microbiome varies with age is not clearly understood. Methods The 16S rRNA gene of subgingival plaque in 1219 women, aged 53–81 years, was sequenced and its taxonomy annotated against the Human Oral Microbiome Database (v.14.5). Composition of the subgingival microbiome was described in terms of centered log(2)-ratio (CLR) transformed OTU values, relative abundance, and prevalence. Correlations between microbiota abundance and age were evelauted using Pearson Product Moment correlations. P-values were corrected for multiple testing using the Bonferroni method. Results Of the 267 species identified overall, Veillonella dispar was the most abundant bacteria when described by CLR OTU (mean 8.3) or relative abundance (mean 8.9%); whereas Streptococcus oralis, Veillonella dispar and Veillonella parvula were most prevalent (100%, all) when described as being present at any amount. Linear correlations between age and several CLR OTUs (Pearson r = − 0.18 to 0.18), of which 82 (31%) achieved statistical significance (P P P Conclusions We identified associations between several bacterial species and age across the age range of postmenopausal women studied. Understanding the functions of these bacteria could identify intervention targets to enhance oral health in later life.

Understanding of the oral microbiome in relation to periodontal disease in older adults is limited. The composition and diversity of the subgingival microflora and their oligotypes in health and levels of periodontal disease were investigated in this study on older postmenopausal women. The 16S rRNA gene was sequenced using the Illumina MiSeq platform in 1,206 women aged 53 to 81 y. Presence and severity of periodontal disease were defined by Centers for Disease Control and Prevention/American Academy of Periodontology criteria. Composition of the microbiome was determined by 16S rRNA amplicon sequencing and the abundance of taxa described by the centered log2-ratio (CLR) transformed operational taxonomic unit (OTU) values. Differences according to periodontal disease status were determined by analysis of variance with Bonferroni correction. Bacteria oligotypes associated with periodontal disease and health were determined by minimum entropy decomposition and their functions estimated in silico using PICRUSt. Prevalence of none/mild, moderate, and severe periodontal disease was 25.1%, 58.3%, and 16.6%, respectively. Alpha diversity of the microbiome differed significantly across the 3 periodontal disease categories. β-Diversity differed between no/mild and severe periodontal disease, although considerable overlap was noted. Of the 267 bacterial species identified at ≥0.02% abundance, 56 (20.9%) differed significantly in abundance according to periodontal disease status. Significant linear correlations for pocket depth and clinical attachment level with bacterial amounts were observed for several taxa. Of the taxa differing in abundance according to periodontal disease status, 53% had multiple oligotypes appearing to differ between none/mild and severe periodontal disease. Among older women, taxonomic differences in subgingival microbiome composition and diversity were observed in relation to clinical periodontal disease measures. Potential differences in bacterial subspecies (oligotypes) and their function were also identified in periodontal disease compared with health.

OBJECTIVES: A possible role of the oral microbiome, specifically oral nitrate reducing flora, in blood pressure (BP) homeostasis, if proven etiologic in nature, could lead to novel mechanism-based therapy to improve hypertension prevention and control. This cross-sectional study characterized and compared the oral microbiome between four study groups based on BP status among 446 postmenopausal women aged 53-82 years. METHODS: Three study groups were not taking hypertension medication and were separated based on BP, as follows: normal BP (systolic 140 or diastolic > 90; N=42). The forth group consisted of anyone taking hypertension medications, regardless of BP (N=119). Subgingival microbiome composition was determined using 16S rRNA sequencing with the Illumina MiSeq platform. Kruskal-Wallis tests were used to compare species-level relative abundance of bacterial operational taxonomic units across the four groups. RESULTS: Sixty-five bacterial species demonstrated significant differences in relative abundance in women with elevated BP or using hypertension medication as compared to those with normal BP. After correction for multiple testing, two species, Prevotella oral (species 317) and Streptococcus oralis, remained significant and were lower in abundance among women taking antihypertension medications compared to those with normal BP (corrected P

Background Periodontitis is more common and severe in people with diabetes than the general population. We have reported in the Joslin Medalist Study that people with type 1 diabetes of ≥50 years (Medalists) may have endogenous protective factors against diabetic nephropathy and retinopathy. Methods In this cross-sectional study, the prevalence of periodontitis according to the Centers for Disease Control/American Academy of Periodontology classification in a subset (n = 170, mean age = 64.6 ± 6.9 years) of the Medalist cohort, and its associations to various criteria of periodontitis and diabetic complications were assessed. Results The prevalence of severe periodontitis in Medalists was only 13.5% which was lower than reported levels in diabetic patients of similar ages. Periodontal parameters, including bleeding on probing, plaque index, gingival index, and demographic traits, including male sex, chronological age, and age at diagnosis were significantly associated with severity of periodontitis, which did not associate with diabetes duration, hemoglobin A1c (HbA1c), body mass index, and lipid profiles. Random serum C-peptide levels inversely associated with severity of periodontitis (P = 0.03), lower probing depth (P = 0.0002), and clinical attachment loss (P = 0.03). Prevalence of cardiovascular diseases (CVD) and systemic inflammatory markers, plasma interleukin-6 (IL-6), and serum immunoglobulin G titer against Porphyromonas gingivalis positively associated with severity of periodontitis (P = 0.002 and 0.02, respectively). Antibody titer to P. gingivalis correlated positively and significantly with CVD, serum IL-6, and high-sensitivity C-reactive protein. Conclusions Some Medalists could be protected from severe periodontitis even with hyperglycemia. Endogenous protective factors for periodontitis could possibly be related to residual insulin production and lower levels of chronic inflammation.

Atherosclerosis is central to the pathology of cardiovascular diseases, a group of diseases in which arteries become occluded with atheromas that may rupture, leading to different cardiovascular events, such as myocardial infarction or ischemic stroke. There is a large body of epidemiologic and animal model evidence associating periodontitis with atherosclerotic disease, and many potential mechanisms linking these diseases have been elucidated. This chapter will update knowledge on these mechanisms, which generally fall into 2 categories: microbial invasion and infection of atheromas; and inflammatory and immunologic. With respect to the invasion and infection of atheromas, it is well established that organisms from the subgingival biofilm can enter the circulation and lodge in most distant tissues. Bacteremias resulting from oral interventions, and even oral hygiene activities, are well documented. More recently, indirect routes of entry of oral organisms (via phagocytes or dendritic cells) have been described for many oral organisms, into many tissues. Such organisms include the periodontal pathogens Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Tannerella forsythia, and Fusobacterium nucleatum. Intracellular survival of these organisms with dissemination to distant sites (The Trojan Horse approach) has been described. Their relative contribution to atheroma formation and progression has been studied mainly in experimental research, with results demonstrating that these organisms can invade endothelial cells and phagocytic cells within the atheroma, leading to pathogenic changes and progression of the atheroma lesion. The second category of mechanisms potentially linking periodontitis to atherosclerosis includes the dumping of inflammatory mediators originating from periodontal lesions into the systemic circulation. These inflammatory mediators, such as C-reactive protein, matrix metalloproteinases, fibrinogen, and other hemostatic factors, would further accelerate atheroma formation and progression, mainly through oxidative stress and inflammatory dysfunction. Moreover, direct effects on lipid oxidation have also been described. In summary, the evidence supports the concept that periodontitis enhances the levels of systemic mediators of inflammation that are risk factors for atherosclerotic diseases.

Severe periodontitis is defined by extensive loss of the tooth attachment apparatus. It is the sixth most common human disease and is estimated to affect 11.2% of the global adult population, hence representing a significant healthcare, social, and economic burden. Since the 1990s, multiple epidemiologic, experimental, and interventional studies have evidenced how periodontitis may also impact systemic health and it has been independently associated with the majority of chronic noncommunicable diseases. The evidence supporting these associations, mainly focusing on diabetes, pregnancy complications, and cardiovascular disease, was thoroughly reviewed in 2012 by an international consensus workshop. In the last 5 years, however, important advances have been made, not only in our understanding of the etiopathogenesis of periodontitis, or concerning the mounting evidence regarding the independent associations between periodontitis, diabetes, and cardiovascular disease, but also with many other systemic diseases including metabolic disease and obesity, rheumatoid arthritis, certain cancers, respiratory diseases, and cognitive disorders including Alzheimer's disease. This review describes these scientific advances by gathering together the existing evidence on the importance and relevance of the associations between periodontitis and many systemic diseases.

Diabetes affects one in 10 adults and periodontal disease affects four in 10 adults in the USA, and they are linked. Individuals with diabetes are more likely to suffer from periodontal disease and periodontal disease affects glycemic control and complications of diabetes. The role of diabetes as a risk factor for periodontal disease and other oral conditions will be discussed in this review. The fact that type 2 diabetes, especially uncontrolled, is a risk factor for periodontal disease has long been recognized. However, the role of type 1 diabetes and gestational diabetes in periodontal risk has recently been described. Also, diabetes as a risk factor for tooth loss has more recently been described and the deleterious effects of tooth loss, especially edentulism, in comparing the diets of patients with diabetes is now fully appreciated. From longitudinal studies it is clear that diabetes often precedes periodontitis and, hence, may contribute to the causal pathway of periodontitis. Other oral manifestations of diabetes include increased risk of oral and nonoral (vaginal) fungal infections. In patients with diabetes there is often reduced salivary flow associated with diabetes medications and neuropathy affecting the salivary glands. This may lead to increased caries. Burning mouth, resulting from diabetes neuropathy, and taste impairment may also be seen. It has long been known that there is delayed wound healing in patients with diabetes, especially if uncontrolled. Hence, it is critical to achieve good glycemic control before carrying out surgical procedures or dental implant placement in patients with diabetes.

It has become increasingly clear that we live in a symbiotic relationship with microbes within us. We are just beginning to unravel the nature and strength of this relationship and its impact on both physiology and by extension, pathology. While microorganisms have long been known to have carcinogenic potential, their role may have been underestimated. The knowledge of the role of the microbiome in carcinogenesis is rapidly evolving. This evolution has reached a tipping point with current omics technologies used for cataloguing the microbiome. The lung is an organ constantly exposed to the environment. It is now clear that the lung has a distinct microbiome and that this may influence the development of lung cancer. In addition, evidence suggests that this microbiome originates from the oral microbiome. This review summarizes current knowledge about the role of microbiome, especially the oral and lung microbiome in human lung cancer. The goal of the manuscript is to provide a summary of this rapidly evolving field while providing a context of the general role of the microbiome in carcinogenesis. In addition, a primer of the current technology used in evaluating the microbiome is provided to familiarize the practicing clinician with the experimental methods used to generate the information that will likely impact the field of lung cancer.

Motivation Sequence analysis is arguably a foundation of modern biology. Classic approaches to sequence analysis are based on sequence alignment, which is limited when dealing with large-scale sequence data. A dozen of alignment-free approaches have been developed to provide computationally efficient alternatives to alignment-based approaches. However, existing methods define sequence similarity based on various heuristics and can only provide rough approximations to alignment distances. Results In this article, we developed a new approach, referred to as SENSE (SiamEse Neural network for Sequence Embedding), for efficient and accurate alignment-free sequence comparison. The basic idea is to use a deep neural network to learn an explicit embedding function based on a small training dataset to project sequences into an embedding space so that the mean square error between alignment distances and pairwise distances defined in the embedding space is minimized. To the best of our knowledge, this is the first attempt to use deep learning for alignment-free sequence analysis. A large-scale experiment was performed that demonstrated that our method significantly outperformed the state-of-the-art alignment-free methods in terms of both efficiency and accuracy. Availability and implementation Open-source software for the proposed method is developed and freely available at https://www.acsu.buffalo.edu/∼yijunsun/lab/SENSE.html. Supplementary information Supplementary data are available at Bioinformatics online.

Several lines of evidence suggest that gut bacterial microbiota is altered in patients with chronic kidney disease (CKD), though the mechanism of which this dysbiosis takes place is not well understood. Recent studies delineated changes in gut microbiota in both CKD patients and experimental animal models using microarray chips. We present 16S ribosomal RNA gene sequencing of both stool pellets and small bowel contents of C57BL/6J mice that underwent a remnant kidney model and establish that changes in microbiota take place in the early gastrointestinal tract. Increased intestinal urea concentration has been hypothesized as a leading contributor to dysbiotic changes in CKD. We show that urea transporters (UT)-A and UT-B mRNA are both expressed throughout the whole gastrointestinal tract. The noted increase in intestinal urea concentration appears to be independent of UTs’ expression. Urea supplementation in drinking water resulted in alteration in bacterial gut microbiota that is quite different than that seen in CKD. This indicates that increased intestinal urea concentration might not fully explain the CKD- associated dysbiosis.

BACKGROUND Hypertension and periodontal disease are common conditions among postmenopausal women. Periodontal disease has been found associated with hypertension in previous studies, but data in postmenopausal women is limited. METHODS We assessed the cross-sectional associations of clinically measured periodontal disease with prevalent hypertension and measured systolic blood pressure (SBP) among 1341 postmenopausal women enrolled in the Buffalo Osteoporosis and Periodontal Disease (OsteoPerio) study, an ancillary study of the Women's Health Initiative-Observational Study. RESULTS Clinical attachment level (CAL) and number of teeth missing were positively associated with SBP among those not taking antihypertensive medication in crude and multivariable adjusted linear regression models (both P

Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non-periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non-dental plaque biofilm-induced gingival diseases and dental plaque-induced gingivitis. Non-dental plaque biofilm-induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque-induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque-induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non-periodontitis patient or in a currently stable "periodontitis patient" i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced). A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1), and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient-centered approach to care, and therefore, creates differences in the way in which a "case" of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations. ispartof: JOURNAL OF PERIODONTOLOGY vol:89 pages:S74-S84 ispartof: location:IL, Chicago status: published

Background: Periodontal pathogens have been isolated from precancerous and cancerous lesions and also shown to promote a procarcinogenic microenvironment. Few studies have examined periodontal disease as a risk factor for total cancer, and none have focused on older women. We examined whether periodontal disease is associated with incident cancer among postmenopausal women in the Women's Health Initiative Observational Study. Methods: Our prospective cohort study comprised 65,869 women, ages 54 to 86 years. Periodontal disease information was obtained via self-report questionnaires administered between 1999 and 2003, whereas ascertainment of cancer outcomes occurred through September 2013, with a maximum follow-up period of 15 years. Physician-adjudicated incident total cancers were the main outcomes and site-specific cancers were secondary outcomes. HRs and 95% confidence intervals (CI) were calculated using Cox proportional hazards regression. All analyses were conducted two-sided. Results: During a mean follow-up of 8.32 years, 7,149 cancers were identified. Periodontal disease history was associated with increased total cancer risk (multivariable-adjusted HR, 1.14; 95% CI, 1.08–1.20); findings were similar in analyses limited to 34,097 never-smokers (HR, 1.12; 95% CI, 1.04–1.22). Associations were observed for breast (HR, 1.13; 95% CI, 1.03–1.23), lung (HR, 1.31; 95% CI, 1.14–1.51), esophagus (HR, 3.28; 95% CI, 1.64–6.53), gallbladder (HR, 1.73; 95% CI, 1.01–2.95), and melanoma skin (HR, 1.23; 95% CI, 1.02–1.48) cancers. Stomach cancer was borderline (HR, 1.58; 95% CI, 0.94–2.67). Conclusions: Periodontal disease increases risk of total cancer among older women, irrespective of smoking, and certain anatomic sites appear to be vulnerable. Impact: Our findings support the need for further understanding of the effect of periodontal disease on cancer outcomes. Cancer Epidemiol Biomarkers Prev; 26(8); 1255–65. ©2017 AACR.

Through the use of optimal surveillance measures and standard case definitions, it is now possible to more accurately determine population-average risk profiles for severe (SP) and non-severe periodontitis (NSP) in adults (aged 30 years and older) in the United States.Data from the 2009 to 2012 National Health and Nutrition Examination Survey were used, which, for the first time, used the "gold standard" full-mouth periodontitis surveillance protocol to classify severity of periodontitis following suggested Centers for Disease Control/American Academy of Periodontology case definitions. Probabilities of periodontitis by: 1) sociodemographics, 2) behavioral factors, and 3) comorbid conditions were assessed using prevalence ratios (PRs) estimated by predicted marginal probability from multivariable generalized logistic regression models. Analyses were further stratified by sex for each classification of periodontitis.Likelihood of total periodontitis (TP) increased with age for overall and NSP relative to non-periodontitis. Compared with non-Hispanic whites, TP was more likely in Hispanics (adjusted [a]PR = 1.38; 95% confidence interval 95% CI: 1.26 to 1.52) and non-Hispanic blacks (aPR = 1.35; 95% CI: 1.22 to 1.50), whereas SP was most likely in non-Hispanic blacks (aPR = 1.82; 95% CI: 1.44 to 2.31). There was at least a 50% greater likelihood of TP in current smokers compared with non-smokers. In males, likelihood of TP in adults aged 65 years and older was greater (aPR = 2.07; 95% CI: 1.76 to 2.43) than adults aged 30 to 44 years. This probability was even greater in women (aPR = 3.15; 95% CI: 2.63 to 3.77). Likelihood of TP was higher in current smokers relative to non-smokers regardless of sex and periodontitis classification. TP was more likely in men with uncontrolled diabetes mellitus (DM) compared with adults without DM.Assessment of risk profiles for periodontitis in adults in the United States based on gold standard periodontal measures show important differences by severity of disease and sex. Cigarette smoking, specifically current smoking, remains an important modifiable risk for all levels of periodontitis severity. Higher likelihood of TP in older adults and in males with uncontrolled DM is noteworthy. These findings could improve identification of target populations for effective public health interventions to improve periodontal health of adults in the United States.

Extraoral translocation of oral bacteria may contribute to associations between periodontal disease and cancer. The associations among the presence of three orange-complex periodontal pathogens (Fusobacterium nucleatum, Prevotella intermedia, and Campylobacter rectus), two red-complex periodontal pathogens (Porphyromonas gingivalis and Tannerella forsythia), and cancer risk were investigated.A total of 1,252 postmenopausal females enrolled in the Buffalo Osteoporosis and Periodontal Disease Study were followed prospectively. Baseline subgingival plaque samples were assessed for the presence of periodontal pathogens using indirect immunofluorescence. Incident cancer cases were adjudicated by staff physicians via review of medical records. Cox proportional hazards regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations of periodontal pathogens with total cancer and site-specific cancer risk in unadjusted and multivariable-adjusted models.Neither the presence of individual pathogens nor the presence of any red-complex pathogens was associated with total cancer or site-specific cancers. Borderline associations were seen among the presence of any orange-complex pathogens (F. nucleatum, P. intermedia, and C. rectus), total cancer risk (HR = 1.35, 95% CI = 1.00 to 1.84), and lung cancer risk (HR = 3.02, 95% CI = 0.98 to 9.29).No associations were found between the presence of individual subgingival pathogens and cancer risk. However, there were suggestions of borderline positive associations of the presence of any orange-complex pathogens with total cancer and lung cancer risk. The study is limited by the small number of cancer cases and the assessment of only five oral bacteria. Additional research is needed to understand the possible role of periodontal disease in carcinogenesis.

The aim of this study was to examine the effect of adjunct local minocycline administration on the microbiological parameters of subgingival plaque samples in the residual periodontal pockets. Ten chronic periodontitis patients under a supportive periodontal therapy regimen were recruited. After subgingival debridement, either 2% minocycline gel, Periocline&trade, (Test Group) or a placebo (Control Group) was administered to the selected sites once a week for three weeks. Subgingival plaque was collected at baseline, and at four weeks and eight weeks. The microbiological composition was analyzed by 16S ribosomal RNA sequencing. In the Test Group, &alpha, diversity (evenness) decreased compared to the baseline (p = 0.005) and was lower compared to the control group at four weeks (p = 0.003). The microbial community composition between the two groups was significantly different at four weeks (p = 0.029). These changes were attributable to a decrease in the bacteria associated with periodontitis and an increase in the bacteria associated with periodontal health. Additionally, the improvement in bleeding on probing continued at eight weeks, however, there were little microbial effects of 2% minocycline gel observed at eight weeks. The control group demonstrated no change throughout the eight-week experimental period. Thus, local minocycline administration can change the subgingival microbial community of residual periodontal pockets.

BACKGROUND: Multiple cross-sectional epidemiologic studies have suggested an association between periodontal disease and tooth loss and hypertension, but the temporality of these associations remains unclear. The objective of our study was to evaluate the association of baseline self-reported periodontal disease and edentulism with incident hypertension. METHODS: Study participants were 36,692 postmenopausal women in the Women’s Health Initiative-Observational Study who were followed annually from initial periodontal assessment (1998–2003) through 2015 (mean follow-up 8.3 years) for newly diagnosed treated hypertension. Cox proportional hazards regression with adjustment for potential confounders was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: Edentulism was significantly associated with incident hypertension in crude (HR (95% CI) = 1.38 (1.28–1.49)) and adjusted (HR (95% CI) = 1.21 (1.11–1.30)) models. This association was stronger among those

PurposeThe Buffalo Osteoporosis and Periodontal Disease (OsteoPerio) study is a prospective cohort study focused on the relationship between the microbiome and oral and systemic health outcomes in postmenopausal women. The cohort was established to examine how the oral microbiome is affected by (and how it affects) periodontal disease presence, severity and progression and to characterise the relationship between the microbiome, lifestyle habits and systemic disease outcomes.ParticipantsParticipants (n=1342) were postmenopausal women who were participating in the Women’s Health Initiative observational study at the Buffalo, New York clinical centre. There were 1026 participants at the 5-year follow-up visit and 518 at the 15-year visit.Findings to dateData collected include questionnaires, anthropometric measures, serum blood and saliva samples. At each clinic visit, participants completed a comprehensive oral examination to measure oral health and the oral microbiome. Preliminary findings have contributed to our understanding of risk factors for periodontal disease and the relationship between the oral microbiome and periodontal disease.Future plansThe novel microbiome data collected on a large sample of participants at three time points will be used to answer a variety of research questions focused on temporal changes in the microbiome and the relationship between the oral microbiome and oral and systemic disease outcomes. Little is currently known about the relationship between the oral microbiome and health outcomes in older adults; data from the OsteoPerio cohort will fill this gap. Microbiome samples are currently being analysed using next-generation sequencing technology with an anticipated completion date of late 2018.

Aging invokes physiological changes, such as immunosenescence and inflammation, that could increase host susceptibility to oral microbiome shifts that enable periodontitis progression in later life. At present, there is a dearth of studies specifically evaluating the oral microbiome and periodontitis in older adults. We used high-throughput untargeted sequencing methods and functional metagenomic analyses to assess and compare the subgingival biofilm of postmenopausal women (mean age 71 years) according to periodontitis status. Subgingival plaque samples were obtained from 15 postmenopausal women with no periodontitis, and from 15 women with severe periodontitis, determined by probing measures. The 16S rRNA gene (V1&ndash, V3 region) was sequenced on the 454 FLX platform. The PICRUSt technique was used to provide information on what the potential functional characteristics of microbiota might be in healthy, compared with diseased, periodontium. The subgingival microbiome associated with periodontitis showed clear differences to that associated with health. Of the 464 species identified, 22.8% had elevated abundance in disease, while only 6.3% had elevated abundance in health. Among the 12 most prevalent organisms in periodontitis, one-half have previously been recognized as periodontal pathogens by other investigators. The subgingival microbiome in periodontitis contained genes that could code for specific activities, including microbial mobility, synthesis of endotoxin, and proteolytic degradation. The healthy microbiome included genes that could code for sustaining microbial life, including encoding for transporters, glycolysis, gluconeogenesis, the Krebs cycle, and protein kinases. In the present study on postmenopausal women, aged 60 and older, the subgingival microbiome differed in composition and potential function between those with and without periodontitis. Studies of functional gene expression, such as transcriptomics, are needed to definitively identify the molecules carrying out functions associated with pathogenic subgingival complexes. This, in turn, could lead to identification of targets for enhanced management of periodontitis and, possibly, other diseases, in later life.

Periodontal disease (PD) is more common and severe in people with diabetes than the general population. The presence of severe PD is correlated with decreased survival, since it can potentially affect glycemic control and severity of complications in people with diabetes. We have reported that Medalists (people with T1DM of 50 years or longer duration) may have endogenous protective factors for the development of diabetic nephropathy (DN) and retinopathy (DR). This study assessed the prevalence of PD in the Medalist cohort and correlated it to the known risk factors of PD and diabetic complications. Severity of PD was defined in a subset (n=170) of Medalists with comparable characteristics of the whole cohort, according to the AAP criteria. The prevalence of severe PD was dramatically decreased in Medalists (13.5%) compared with other studies of people with diabetes of similar age, approximately 33%. Clinical parameters, such as male gender, chronological age, age at diagnosis, and total insulin dose were correlated positively with severity of PD (p=0.04, 0.01, 0.03, and 0.02, respectively), while duration of disease, hemoglobin A1c, BMI, and lipid profiles did not exhibit any correlation. Interestingly, detectible plasma C-peptide levels correlated inversely with severity of PD (p=0.04). Systemic inflammatory markers, such as plasma IL-6, clearly correlated positively with the severity of PD (p=0.01). Serum antibody titer against Porphyromonas gingivalis (Pg), a known pathogen of PD, trended with severity of PD (p=0.08). Amongst the various complications, only the prevalence of CVD correlated positively with severity of PD (p=0.02). These results suggest that Medalists are protected from severe PD even with hyperglycemia. The endogenous protective factors for PD could be similar to those for CVD, possibly related to endogenously produced insulin to neutralize the chronic inflammation caused by residual infection with Pg in the gingival tissues. Disclosure T. Shinjo: None. A. Ishikado: Employee; Self; Sunstar Inc.. Employee; Spouse/Partner; Sunstar Inc.. H. Hasturk: None. L.J. Tinsley: None. D.M. Pober: None. I. Wu: None. T.E. Van Dyke: None. R.J. Genco: None. G.L. King: Research Support; Self; Sanofi-Aventis.

Periodontal diseases are infections, and many forms of the disease are associated with specific pathogenic bacteria which colonize the subgingival area. At least two of these microorganisms, Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, also invade the periodontal tissue and are virulent organisms. Initiation and progression of periodontal infections are clearly modified by local and systemic conditions called risk factors. The local factors include pre-existing disease as evidenced by deep probing depths and plaque retention areas associated with defective restorations. Systemic risk factors recently have been identified by large epidemiologic studies using multifactorial statistical analyses to correct for confounding or associated co-risk factors. Risk factors which we know today as important include diabetes mellitus, especially in individuals in whom metabolic control is poor, and cigarette smoking. These two risk factors markedly affect the initiation and progression of periodontitis, and attempts to manage these factors are now an important component of prevention and treatment of adult periodontitis. Systemic conditions associated with reduced neutrophil numbers or function are also important risk factors in children, juveniles, and young adults. Diseases in which neutrophil dysfunction occurs include the lazy leukocyte syndrome associated with localized juvenile periodontitis, cyclic neutropenia, and congenital neutropenia. Recent studies also point to several potentially important periodontal risk indicators. These include stress and coping behaviors, and osteopenia associated with estrogen deficiency. There are also background determinants associated with periodontal disease including gender (with males having more disease), age (with more disease seen in the elderly), and hereditary factors. The study of risk in periodontal disease is a rapidly emerging field and much is yet to be learned. However, there are at least two significant risk factors-smoking and diabetes-which demand attention in current management of periodontal disease. J Periodontol 1996;67:1041-1049.

This paper was prepared by the Research, Science and Therapy Committee of the American Academy of Periodontology. It is intended to provide information for the dental profession and other interested parties. The purpose of this paper is to provide a general overview of oral reconstructive and corrective procedures used in periodontal therapy. It is not intended to be a comprehensive review of this subject.

Declines in endogenous estrogen levels after menopause can lead to systemic bone loss, including loss of oral bone and alveolar crest height (ACH). However, few studies have assessed both serum 17β-estradiol (E2) and exogenous hormone therapy (HT) use in relation to oral bone loss.This study examines the associations among serum E2, HT use, and ACH in 613 postmenopausal women from the Buffalo OsteoPerio study. Baseline ACH levels and 5-year ACH were assessed for groups according to E2 level (undetectable,5.00 to ≤18.00,18.00 to ≤46.07, and46.07 pg/mL) and among HT use (never, ever) using analysis of variance and analysis of covariance. Logistic regression was used to analyze the association of ACH loss with serum E2 and HT use.In cross-sectional analyses, no association was found of serum E2 with whole-mouth mean or worst-site ACH. However, history of HT use was associated with ACH. Women who had never used HT had more ACH loss assessed as a whole-mouth mean ACH (P = 0.01) and as worst-site ACH loss (P = 0.03). In logistic regression analyses of baseline ACH loss severity, HT never-users had two-fold higher odds of being in the severe ACH loss category compared to ever-users (odds ratio, 2.00; 95% confidence interval, 1.11 to 3.62). No association was observed of 5-year change in ACH with baseline serum E2 or HT use.Although this study did not detect an association with current serum E2 level and ACH, HT use was found to be associated with less ACH loss in postmenopausal women.

Aim The goal of the present longitudinal cohort study was to examine patterns of periodontal disease progression at progressing sites and subjects defined based on linear mixed models (LMM) of clinical attachment loss (CAL). Materials and methods A total of 113 periodontally healthy and 302 periodontitis subjects had their CAL calculated bimonthly for 12 months. LMMs were fitted for each site and the predicted CAL levels used to categorize their progression state. Participants were grouped based on the number of progressing sites into unchanged, transitional and active subjects. Patterns of periodontal disease progression were explored using descriptive statistics. Results Progression occurred primarily at molars (50% of progressing sites) and inter-proximal sites (72%), affected a higher proportion of deep than shallow sites (2.7% versus 0.7%), and pocketing was the main mode of progression (49%). We found a low level of agreement (47%) between the LMM and traditional approaches to determine progression such as change in CAL ≥3 mm. Fourteen per cent of subjects were classified as active and among those 93% had periodontitis. The annual mean rate of progression for the active subjects was 0.35 mm/year. Conclusion Progressing sites and subjects defined based on LMMs presented patterns of disease progression similar to those previously reported in the literature.

Background Few studies have reported associations between periodontitis and cardiovascular disease ( CVD ) risk in older women, which is the objective of the present investigation. Methods and Results Participants were 57 001 postmenopausal women ages 55 to 89 years (mean 68 years; >85% 60 and older) who were enrolled (1993–1998) in the Women's Health Initiative Observational Study, and were without known CVD when history of periodontitis and edentulism was assessed by questionnaire at study Year‐5 (1998–2003). There were 3589 incident CVD events and 3816 total deaths during a mean follow‐up of 6.7 years. In multivariable analysis, periodontitis was not associated with CVD events, but was associated with higher total mortality (hazard ratio ( HR )=1.12, 95% CI : 1.05–1.21). Edentulism was associated with higher age‐ and smoking‐adjusted risks of CVD ( HR =1.42, 95% CI : 1.27–1.59) and mortality ( HR =1.47, 95% CI : 1.32–1.63). Further adjustment eliminated the association with CVD , but mortality remained significantly increased ( HR =1.17, 95% CI : 1.02–1.33). Stratification on age, race‐ethnicity, smoking, and diabetes mellitus yielded comparable results; however, edentulism was more strongly associated with CVD in women reporting ≥1 dental visit ( HR =1.57) compared with HR 1.03, interaction P =0.004) annually. Conclusions In community‐dwelling older women, edentulism was associated with increased risks of CVD and total mortality, and presence of periodontitis, which is more prevalent than edentulism, was associated with 17% higher mortality rate. These findings suggest that improving periodontal condition of the general population could reduce overall mortality.

The objective of this study is to characterize the association between metabolic syndrome (MetS) and periodontitis in women, for which there is limited evidence.Cross-sectional associations between MetS and periodontitis were examined in 657 postmenopausal women aged 50 to 79 years enrolled in a periodontal disease study ancillary to the Women's Health Initiative Observational Study. Whole-mouth measures of alveolar crest height (ACH), clinical attachment level (CAL), probing depth (PD), gingival bleeding, and supragingival plaque and measures to define MetS using National Cholesterol Education Program criteria were from a clinical examination. Study outcomes were defined as: 1) mean ACH ≥3 mm, two sites ≥5 mm, or tooth loss to periodontitis; 2) ≥2 sites with CAL ≥6 mm and ≥1 site with PD ≥5 mm; 3) gingival bleeding at ≥50% of sites; and 4) supragingival plaque at ≥50% of sites. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).In unadjusted analyses, MetS (prevalence: 25.6%) was significantly associated with supragingival plaque (OR = 1.74; 95% CI: 1.22 to 2.50) and non-significantly associated with periodontitis defined by ACH (OR = 1.23; 95% CI: 0.81 to 1.85) and gingival bleeding (OR = 1.20; 95% CI: 0.81 to 1.77). Adjustment for age, smoking, and other confounders attenuated observed associations, though supragingival plaque remained significant (OR = 1.47; 95% CI: 1.00 to 2.16; P = 0.049). MetS was not associated with periodontitis defined by CAL and PD.A consistent association between MetS and measures of periodontitis was not seen in this cohort of postmenopausal women. An association between MetS and supragingival plaque requires further investigation.

Background: Vitamin D is hypothesized to prevent periodontal disease progression through its immune-modulating properties and its role in maintaining systemic calcium concentrations. The authors investigated associations between plasma 25-hydroxyvitamin D [25(OH)D] (collected 1997 to 2000) and the 5-year change in periodontal disease measures from baseline (1997 to 2000) to follow-up (2002 to 2005) among 655 postmenopausal women in a Women’s Health Initiative Observational Study ancillary study. Exploratory analyses were conducted in 628 women who also had 25(OH)D measures at follow-up.Methods: Four continuous measures of the 5-year change in periodontal disease were assessed using alveolar crest height (ACH), clinical attachment level (CAL), probing depth (PD), and percentage of gingival sites that bled on assessment. Linear regression was used to estimate β-coefficients, standard errors, and P values corresponding to change in periodontal disease (a 1-mm change in ACH, CAL, or PD or a 1-unit change in t...

While some evidence suggests that periodontal disease (PD) might be positively associated with lung cancer, prospective studies in women are limited. Previous findings may reflect residual confounding by smoking. The study aims to determine whether history of PD diagnosis is associated with incident lung cancer in a large cohort of postmenopausal women.Prospective analyses were conducted in a cohort of 77,485 postmenopausal women enrolled in the Women's Health Initiative Observational Study. History of PD (prevalence of 26.1 %) was self-reported, and 754 incident lung cancer cases occurred during an average 6.8 (SD ± 2.6) years of follow-up. Cox proportional hazards regression analysis was used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs).Overall, PD was positively associated with lung cancer risk after adjusting for detailed smoking history including smoking status and pack-years of smoking (HR 1.24, 95 % CI 1.07-1.45). There was a positive additive interaction between PD with pack-years of smoking (p = 0.02), suggesting a potential synergistic effect between PD and smoking intensity on lung cancer. The association between PD and lung cancer was stronger in former smokers. When restricted to never-smokers, PD was not associated with lung cancer (HR 1.02, 95 % CI 0.68-1.53).Periodontal disease was not independently associated with lung cancer in non-smoking postmenopausal women. However, smoking and PD jointly increased lung cancer risk beyond that expected from the sum of the each effect separately. The potential synergism between PD and smoking on lung cancer warrants further examination.

Background In this field trial, the authors assess the feasibility of screening for diabetes and prediabetes in dental practices and in a community health center. Methods Dental patients 45 years and older who were not aware of their diabetic status underwent evaluation for diabetes risk with an American Diabetes Association Diabetes Risk Test and with hemoglobin (Hb) A 1c measurement. Participants with an HbA 1c level of 5.7 percent or greater were referred to their physicians for diagnosis. Results Of the 1,022 patients screened, 416 (40.7 percent) had an HbA 1c blood level of 5.7 percent or greater and were referred for diagnosis. The HbA 1c and the American Diabetes Association Diabetes Risk Test were correlated ( P Conclusions The study results show that screening for prediabetes and diabetes is feasible in a dental office, with acceptance by the dentist and dental office staff members, patients' physicians and patients. Patients from the community health center demonstrated good compliance with referrals to physicians; however, compliance was poor among those in the private dental offices. Practical Implications Screening for diabetes and prediabetes in the dental office may provide an important benefit to patients and encourage interprofessional collaboration to achieve a chronic care model in which health care professionals work together to care for a panel of patients.

The purpose of this study was to evaluate the performance of self-reported measures in predicting periodontitis in a representative US adult population, based on 2009-2010 National Health and Nutrition Examination Survey (NHANES) data. Self-reported gum health and treatment history, loose teeth, bone loss around teeth, tooth not looking right, and use of dental floss and mouthwash were obtained during in-home interviews and validated against full-mouth clinically assessed periodontitis in 3,743 US adults 30 years and older. All self-reported measures (> 95% item response rates) were associated with periodontitis, and bivariate correlations between responses to these questions were weak, indicating low redundancy. In multivariable logistic regression modeling, the combined effects of demographic measures and responses to 5 self-reported questions in predicting periodontitis of mild or greater severity were 85% sensitive and 58% specific and produced an ‘area under the receiver operator characteristic curve’ (AUROCC) of 0.81. Four questions were 95% sensitive and 30% specific, with an AUROCC of 0.82 in predicting prevalence of clinical attachment loss ≥ 3 mm at one or more sites. In conclusion, self-reported measures performed well in predicting periodontitis in US adults. Where preferred clinically based surveillance is unattainable, locally adapted variations of these self-reported measures may be a promising alternative for surveillance of periodontitis.

Vitamin D has anti-inflammatory and antimicrobial properties that, together with its influence on bone health, may confer periodontal benefit.Cross-sectional associations (years 1997-2000) between plasma 25-hydroxyvitamin D concentration [25(OH)D] and periodontal measure were investigated among 920 postmenopausal women. Measures of chronic disease were defined based on: 1) alveolar crestal height (ACH) measures from intraoral radiographs and tooth loss and 2) Centers for Disease Control and Prevention (CDC)/American Academy of Periodontology (AAP) criteria using measures of clinical attachment level and probing depth (PD). Acute oral inflammation was assessed by the percentage of gingival sites that bled upon assessment with a probe. Logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) for periodontal disease among participants with adequate [25(OH)D ≥50 nmol/L] compared with deficient/inadequate [25(OH)D50 nmol/L] vitamin D status adjusted for age, dental visit frequency, and body mass index.No association was observed between vitamin D status and periodontal disease defined by ACH and tooth loss (adjusted OR = 0.96, 95% CI = 0.68 to 1.35). In contrast, women with adequate compared with deficient/inadequate vitamin D status had 33% lower odds (95% CI = 5% to 53%) of periodontal disease according to the CDC/AAP definition and 42% lower odds (95% CI = 21% to 58%) of having ≥50% of gingival sites that bled.Vitamin D status was inversely associated with gingival bleeding, an acute measure of oral health and inflammation, and inversely associated with clinical categories of chronic periodontal disease that incorporated PD, an indicator of oral inflammation. However, vitamin D was not associated with chronic periodontal disease based on measures of ACH in combination with tooth loss.

Understanding of longitudinal characteristics of periodontal disease in older females is limited. This study examined 5-year changes in periodontal disease measures among postmenopausal females.Participants were 1,025 postmenopausal, 53- to 83-year-old females who completed baseline (1997 to 2001) and 5-year follow-up (2002 to 2006) whole-mouth oral examinations in a study ancillary to the Women's Health Initiative. Periodontal disease was characterized using probing depth (PD), clinical attachment level (CAL), alveolar crest height (ACH), and tooth loss. Differences in measures between examinations were used to characterize patterns of change.Baseline prevalence of none/mild, moderate, and severe periodontal disease defined using criteria of the Centers for Disease Control and Prevention was 27%, 58%, and 15%, respectively. Tooth loss attributable to periodontitis occurred in 13% of females. Mean ± SD changes in whole-mouth mean measures showed progression when based on ACH (-0.19 ± 0.49 mm) yet relatively stable disease when based on PD (0.11 ± 0.42 mm) and CAL (0.06 ± 0.58 mm). Mean change in worst-site ACH was greater (P0.001) in females with severe periodontitis and osteoporosis at baseline and with tooth loss during follow-up. Periodontal changes did not differ according to baseline age, hormone therapy use, smoking status, or age at menopause.Five-year changes in periodontal measures among generally healthy postmenopausal females were, on average, small and did not suggest a consistent pattern of disease progression. Females with history of severe periodontitis or osteoporosis may experience accelerated oral bone loss despite stability or small improvement in routine probing measures.

Risk factors play an important role in an individual's response to periodontal infection. Identification of these risk factors helps to target patients for prevention and treatment, with modification of risk factors critical to the control of periodontal disease. Shifts in our understanding of periodontal disease prevalence, and advances in scientific methodology and statistical analysis in the last few decades, have allowed identification of several major systemic risk factors for periodontal disease. The first change in our thinking was the understanding that periodontal disease is not universal, but that severe forms are found only in a portion of the adult population who show abnormal susceptibility. Analysis of risk factors and the ability to statistically adjust and stratify populations to eliminate the effects of confounding factors have allowed identification of independent risk factors. These independent but modifiable, risk factors for periodontal disease include lifestyle factors, such as smoking and alcohol consumption. They also include diseases and unhealthy conditions such as diabetes mellitus, obesity, metabolic syndrome, osteoporosis, and low dietary calcium and vitamin D. These risk factors are modifiable and their management is a major component of the contemporary care of many periodontal patients. Genetic factors also play a role in periodontal disease and allow one to target individuals for prevention and early detection. The role of genetic factors in aggressive periodontitis is clear. However, although genetic factors (i.e., specific genes) are strongly suspected to have an association with chronic adult periodontitis, there is as yet no clear evidence for this in the general population. It is important to pursue efforts to identify genetic factors associated with chronic periodontitis because such factors have potential in identifying patients who have a high susceptibility for development of this disease. Many of the systemic risk factors for periodontal disease, such as smoking, diabetes and obesity, and osteoporosis in postmenopausal women, are relatively common and can be expected to affect most patients with periodontal disease seen in clinics and dental practices. Hence, risk factor identification and management has become a key component of care for periodontal patients.

Background Smoking is associated with tooth loss. However, smoking's relationship to the specific reason for tooth loss in postmenopausal women is unknown. Methods Postmenopausal women (n = 1,106) who joined a Women's Health Initiative ancillary study (The Buffalo OsteoPerio Study) underwent oral examinations for assessment of the number of missing teeth, and they reported the reasons for tooth loss. The authors obtained information about smoking status via a self-administered questionnaire. The authors calculated odds ratios (ORs) and 95 percent confidence intervals (CIs) by means of logistic regression to assess smoking's association with overall tooth loss, as well as with tooth loss due to periodontal disease (PD) and with tooth loss due to caries. Results After adjusting for age, education, income, body mass index, history of diabetes diagnosis, calcium supplement use and dental visit frequency, the authors found that heavy smokers (≥ 26 pack-years) were significantly more likely to report having experienced tooth loss compared with never smokers (OR = 1.82; 95 percent CI, 1.10-3.00). Smoking status, packs smoked per day, years of smoking, pack-years and years since quitting smoking were significantly associated with tooth loss due to PD. For pack-years, the association for heavy smokers compared with that for never smokers was OR=6.83 (95 percent CI, 3.40 –13.72). The study results showed no significant associations between smoking and tooth loss due to caries. Conclusions and Practical Implications Smoking may be a major factor in tooth loss due to PD. However, smoking appears to be a less important factor in tooth loss due to caries. Further study is needed to explore the etiologies by which smoking is associated with different types of tooth loss. Dentists should counsel their patients about the impact of smoking on oral health, including the risk of experiencing tooth loss due to PD.

Vitamin D is hypothesized to reduce risk for tooth loss via its influence on bone health, inflammation, and the immune response. The association between plasma 25-hydroxyvitamin D [25(OH)D] concentrations and prevalence and 5-year incidence of tooth loss in a cohort of postmenopausal females was examined.Participants underwent oral examinations at study baseline (1997 to 2000) and follow-up (2002 to 2005) to determine the number of missing teeth and 5-year incidence of tooth loss, respectively. At both visits, females self-reported reasons for each missing tooth. At baseline, 152 females reported no history of tooth loss, and 628 were categorized as reporting a history of tooth loss as a result of periodontal disease (n = 70) or caries (n = 558) (total n = 780). At follow-up, 96, 376, 48, and 328 females were categorized into the aforementioned categories related to tooth loss (total n = 472). Logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) for tooth loss by category of baseline 25(OH)D (nmol/L) concentrations. Models were adjusted for age, income, smoking status, frequency of dental visits, waist circumference, and recreational physical activity. P value for trend was estimated using continuous concentrations of 25(OH)D.Among females with 25(OH)D ≥50 (adequate vitamin D status) compared to50 nmol/L (deficient/inadequate), the adjusted ORs were 1.24 (95% CI = 0.82 to 1.87), P-trend =0.05 for the history (prevalence) of tooth loss resulting from periodontal disease or caries and 1.07 (95% CI = 0.62 to 1.85), P-trend = 0.11 for the incidence of tooth loss resulting from periodontal disease or caries. No statistically significant association was observed between 25(OH)D and the history or incidence of tooth loss caused by periodontal disease. An increased odds of the history of tooth loss attributable to caries was observed with increasing concentrations of 25(OH)D (P-trend =0.05) but was not confirmed in prospective analyses.In this cohort of postmenopausal females, the data do not support an association between vitamin D status and tooth loss.

Biological mediators have been used to enhance periodontal regeneration. The aim of this prospective randomized controlled study was to evaluate the safety and effectiveness of 3 doses of fibroblast growth factor 2 (FGF-2) when combined with a β-tricalcium phosphate (β-TCP) scaffold carrier placed in vertical infrabony periodontal defects in adult patients. In this double-blinded, dose-verification, externally monitored clinical study, 88 patients who required surgical intervention to treat a qualifying infrabony periodontal defect were randomized to 1 of 4 treatment groups—β-TCP alone (control) and 0.1% recombinant human FGF-2 (rh-FGF-2), 0.3% rh-FGF-2, and 0.4% rh-FGF-2 with β-TCP—following scaling and root planing of the tooth prior to a surgical appointment. Flap surgery was performed with EDTA conditioning of the root prior to device implantation. There were no statistically significant differences in patient demographics and baseline characteristics among the 4 treatment groups. When a composite outcome of gain in clinical attachment of 1.5 mm was used with a linear bone growth of 2.5 mm, a dose response pattern detected a plateau in the 0.3% and 0.4% rh-FGF-2/β-TCP groups with significant improvements over control and 0.1% rh-FGF-2/β-TCP groups. The success rate at 6 mo was 71% in the 2 higher-concentration groups, as compared with 45% in the control and lowest treatment groups. Percentage bone fill in the 2 higher-concentration groups was 75% and 71%, compared with 63% and 61% in the control and lowest treatment group. No increases in specific antibody to rh-FGF-2 were detected, and no serious adverse events related to the products were reported. The results from this multicenter trial demonstrated that the treatment of infrabony vertical periodontal defects can be enhanced with the addition of rh-FGF-2/β-TCP ( ClinicalTrials.gov NCT01728844).

This study estimated the prevalence, severity, and extent of periodontitis in the adult U.S. population, with data from the 2009 and 2010 National Health and Nutrition Examination Survey (NHANES) cycle. Estimates were derived from a sample of 3,742 adults aged 30 years and older, of the civilian non-institutionalized population, having 1 or more natural teeth. Attachment loss (AL) and probing depth (PD) were measured at 6 sites per tooth on all teeth (except the third molars). Over 47% of the sample, representing 64.7 million adults, had periodontitis, distributed as 8.7%, 30.0%, and 8.5% with mild, moderate, and severe periodontitis, respectively. For adults aged 65 years and older, 64% had either moderate or severe periodontitis. Eighty-six and 40.9% had 1 or more teeth with AL ≥ 3 mm and PD ≥ 4 mm, respectively. With respect to extent of disease, 56% and 18% of the adult population had 5% or more periodontal sites with ≥ 3 mm AL and ≥ 4 mm PD, respectively. Periodontitis was highest in men, Mexican Americans, adults with less than a high school education, adults below 100% Federal Poverty Levels (FPL), and current smokers. This survey has provided direct evidence for a high burden of periodontitis in the adult U.S. population.

Background: Current literature examining associations between vitamin D and chronic disease generally use a single assessment of 25-hydroxyvitamin D [25(OH)D], assuming the 25(OH)D concentration of an individual is consistent over time. Methods: We investigated the intraindividual variability between two measures of plasma 25(OH)D concentrations collected approximately five years apart (1997–2000 to 2002–2005) in 672 postmenopausal women participating in the Women's Health Initiative. Plasma 25(OH)D was assessed using the DiaSorin LIAISON® chemiluminescence immunoassay. The within-pair coefficient of variation (CV) was 4.9% using blinded quality control samples. Mean and SDs of 25(OH)D at the two time points were compared using a paired t test. An intraindividual CV and intraclass correlation coefficient (ICC) were used to assess intraindividual variability. A Spearman correlation coefficient (r) assessed the strength of the association between the two measures, and concordance in vitamin D status at two time points was compared. Results: Mean 25(OH)D concentrations (nmol/L) significantly increased over time from 60.0 (SD = 22.2) to 67.8 (SD = 22.2; P < 0.05). The CV was 24.6%, the ICC [95% confidence interval (CI)] was 0.59 (0.54–0.64), and the Spearman r was 0.61 (95% CI = 0.56–0.66). Greater concordance over five years was observed in participants with sufficient compared with deficient or inadequate baseline 25(OH)D concentrations (weighted kappa = 0.39). Reliability measures were moderately influenced by season of blood draw and vitamin D supplement use. Conclusion: There is moderate intraindividual variation in 25(OH)D concentrations over approximately five years. Impact: These data support the use of a one-time measure of blood 25(OH)D in prospective studies with ≤ five years of follow-up. Cancer Epidemiol Biomarkers Prev; 21(6); 916–24. ©2012 AACR.

The availability of automated administrative databases in medical and dental healthcare, combined with modern computing power, allows sophisticated multi-layered analyses of the causes and consequences of care delivered to large populations. These automated databases are now also commonly linked to data extracted from electronic medical records, and are used to measure health system performance, adjust payments, assess providers for quality improvement purposes, and inform policy decisions. Use of health insurance databases can be particularly powerful when linked through common unique identifiers to allow examination of the influences of dental care on medical outcomes and costs, and vice versa. This review describes the growing use of these databases for epidemiological and health services research, their advantages and limitations, and presents a case study in which dental claims data are used to identify persons with periodontitis in order to enable critical assessment of the relationship between periodontal interventions and systemic health outcomes/medical costs.

Andriankaja O, Trevisan M, Falkner K, Dorn J, Hovey K, Sarikonda S, Mendoza T, Genco R. Association between periodontal pathogens and risk of nonfatal myocardial infarction. Community Dent Oral Epidemiol 2011; 39: 177–185. © 2011 John Wiley & Sons A/S Abstract – Background: The direct effect of periodontal pathogens on atherosclerotic plaque development has been suggested as a potential mechanism for the observed association between periodontal disease and coronary heart disease, but few studies have tested this theory. Objectives: (i) To assess the association of periodontal pathogens in periodontal pockets with the risk of myocardial infarction (MI) and (ii) to assess whether an increase in the number of periodontal bacterial species increases the risk of MI. Methods: A total of 313 cases and 747 controls, consisting of Caucasian men and women from Western New York, aged 35 to 69 years, were recruited for this study. The presence of microorganisms was assessed by indirect immunofluorescence microscopy, using species-specific polyclonal and monoclonal serodiagnostic reagents. The presence of six periodontal pathogens, Porphyromonas gingivalis (Pg), Tannerella forsythensis (Tf), Prevotella intermedia (Pi), Campylobacter recta (Cr), Fusobacterium nucleatum (Fn), and Eubacterium saburreum (Es), and their co-occurrence (0–6) was compared with the odds of having myocardial infarction. Results: Univariate analyses revealed a higher percentage of the presence of each bacterium in cases compared to controls. In multivariate analyses, only Tf and Pi were statistically associated with an increase in the odds of having MI [Odds ratio OR = 1.62; 95% CI (1.18–2.22); and 1.40; 95% (1.02–1.92), respectively] after adjusting for age, gender, education, cholesterol, high blood pressure, diabetes, and total pack-years of cigarette smoking. An increase in the number of different periodontal bacteria in pockets was also found to increase the odds of MI [adjusted OR = 1.14; 95% CI (1.03–1.26)]. Participants who had three species or more of periodontal pathogens had about 2-fold increase in odds of having nonfatal MI than those who did not have any type of bacterial species [OR = 2.01 (1.31–3.08)]. Conclusion: The presence of periodontal pathogens, specifically Tf or Pi, and an increase in total burden of periodontal pathogenic species were both associated with increased odds of having MI. However, further studies are needed to better assess any causal relationship, as well as the biological mechanisms underlying this association.