Can a Tooth Infection Cause High Blood Pressure
J Hypertens. Author manuscript; available in PMC 2022 Jul 24.
Published in final edited form as:
PMCID: PMC3403746
NIHMSID: NIHMS390485
PERIODONTAL Leaner AND HYPERTENSION: The Oral Infections and Vascular Disease Epidemiology Study (INVEST)
Moïse Desvarieux
aDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY
bINSERM, UMR-S 707, Paris, F-75012; Universite Pierre et Marie Curie-Paris6, UMR S 707, Paris, F-75012
Ryan T. Demmer
aDepartment of Epidemiology, Mailman School of Public Wellness, Columbia University, New York, NY
David R. Jacobs, Jr
cSegmentation of Epidemiology and Customs Health, School of Public Health, University of Minnesota, Minneapolis, MN
dDepartment of Nutrition, University of Oslo, Oslo, Norway
Tatjana Rundek
eastSection of Neurology, Miller School of Medicine, University of Miami, Miami, FL
Bernadette Boden-Albala
fDepartments of Neurology, Columbia University College of Physicians and Surgeons, New York, NY
gSociomedical Sciences, Mailman School of Public Health, Columbia University, New York, NY
Ralph L. Sacco
eastwardDepartment of Neurology, Miller School of Medicine, University of Miami, Miami, FL
Panos Northward. Papapanou
hDivision of Periodontics, Section of Oral and Diagnostic Sciences, Higher of Dental Medicine, Columbia University, New York, NY
Abstruse
Objective
Chronic infections, including periodontal infections, may predispose to cardiovascular affliction. We investigated the relationship betwixt periodontal microbiota and hypertension. Methods and Results: 653 dentate men and women with no history of stroke or myocardial infarction were enrolled in INVEST. We collected 4533 subgingival plaque samples (average of 7 samples/bailiwick). These were quantitatively assessed for xi periodontal bacteria using Dna-Deoxyribonucleic acid checkerboard hybridization. Cardiovascular risk gene measurements were obtained. Blood force per unit area and hypertension (systolic blood pressure≥140 mmHg, diastolic blood pressure≥90 mmHg or taking antihypertensive medication, or self-reported history) were each regressed on the level of leaner: (1) considered causative of periodontal affliction (etiologic bacterial burden); (2) associated with periodontal affliction (putative bacterial burden); (3) associated with periodontal wellness (wellness associated bacterial burden). All analyses were adjusted for age, race/ethnicity, gender, pedagogy, body mass index, smoking, diabetes, LDL and HDL cholesterol. Etiologic bacterial burden was positively associated with both blood force per unit area and prevalent hypertension. Comparing the highest vs. lowest tertiles of etiologic bacterial burden, SBP was 9 mmHg higher, DBP was v mmHg higher (p for linear trend <0.001 in each example), and the odds ratio for prevalent hypertension was three.05 (95%CI:1.lx,5.82) after multivariable adjustment.
Conclusions
Our information provide bear witness of a straight relationship between the levels of subgingival periodontal bacteria and both systolic and diastolic claret force per unit area likewise as hypertension prevalence.
Keywords: infection, inflammation, hypertension, claret pressure, epidemiology, periodontitis
INTRODUCTION
Numerous studies take reported positive associations between periodontal infections and clinical cardiovascular disease (CVD). Amidst these studies, a pattern has emerged in which findings are markedly stronger for stroke as compared to coronary outcomes.1, 2 1 possible explanation for these trends is that periodontal infections might contribute to clinical CVD through risk factors that are more strongly linked to stroke than to coronary pathophysiology. While both hypertension and abnormal cholesterol profiles are established risk factors for stroke and coronary heart illness (CHD), it is generally accepted that hypertension is a stronger run a risk factor for strokeiii while cholesterol profiles are more strongly linked to CHD.4 Therefore, if periodontal infections contribute to the development of hypertension simply take picayune or no influence on lipid metabolism and cholesterol levels, one would wait periodontal infections to exist more strongly associated with stroke, as compared to CHD. There is currently a need for more research on periodontal infections and hypertension to inform this hypothesis, although it is noteworthy that in regard to associations between periodontal infections and cholesterol, well-nigh studies accept reported weak associations.five–7
A biological relationship between periodontal infections and hypertension is plausible in light of several findings demonstrating associations betwixt periodontal disease and either subclinical atherosclerosisviii–12 or endothelial dysfunction.13, xiv Chronically elevated levels of systemic inflammation could also mediate associations between periodontal infections and hypertension, as both conditions have been linked to inflammation.14–16 At least two studies have reported positive associations between periodontal disease and hypertension.17, xviii However, these reports have relied on surrogate markers of infectious periodontal exposure, namely tooth loss, and there are currently no studies that accept directly examined bacterial species known to be strongly associated with periodontal infections in relation to hypertension.
The Oral Infections and Vascular Illness Epidemiology Study (INVEST) was specifically designed to study the hypothesis that periodontal infections predispose to accelerated progression of carotid atherosclerosis and incidence of stroke, myocardial infarction and CVD expiry. In this report, nosotros investigated whether periodontal bacteria previously shown to be strongly associated with clinical periodontal diseasexix were also associated with prevalent hypertension and elevated continuous blood pressure measurements. The study assessed the subgingival levels of eleven bacterial species, including, i) four species believed to be causal (or strong correlates of currently unidentified causal species) of periodontitis; ii) five species regarded as putative periodontal pathogens and known to be prevalent in states of gingivitis and periodontitis; and iii) two species that take been oft reported to exist prevalent in states of periodontal health. The latter ii groups served as inherent controls, to assess the specificity of the relationship between prevalent hypertension and those bacterial species deemed etiologic of periodontal disease. Therefore, nosotros hypothesized a priori that prevalent hypertension would be positively associated with increased etiologic bacterial burden and either unrelated, or inversely related to the putative and health associated bacterial burdens in a style like to our previous findings for subclinical atherosclerosis.ten Our study also paid item attention to the assessment of social and cardiovascular chance factors identified every bit potential confounders in other studies, every bit previously described.ten
METHODS
Every bit previously described,10 INVEST is a randomly sampled prospective population-based accomplice report investigating the relationship betwixt oral infections, carotid atherosclerosis and stroke. 1056 subjects were selected by random digit dialing from Northern Manhattan, including Hispanics, Blacks, and Whites. Participants alive together in this area and have similar admission to medical intendance. The selection process was derived from the Northern Manhattan Study (NOMAS) in which patients are also enrolled.20 Participants were ≥55 years old and had no baseline history of stroke, myocardial infarction, or chronic inflammatory atmospheric condition such every bit systemic lupus erythematosus, Lyme's disease, gonococcal arthritis or bacterial endocarditis. 841 participants were dentate. Blood pressure measurements and subgingival plaque samples were available for 731 subjects. Some other 78 patients were excluded from multivariate analyses because of missing body mass alphabetize (n=vii), smoking data (n=xv), LDL (n=60), HDL (n=57) or diabetes (northward=two) information (some patients lacked several variables). Therefore 653 patients were included in the final analyses, representing 78% of the dentate patients. The Institutional Review Boards canonical the report and all subjects provided informed consent.
Oral Examination
Subjects received a complete oral exam by trained, calibrated dental examiners. Assessment of periodontal status was done at half dozen sites per tooth (mesiobuccal, midbuccal distobuccal, mesiolingual, midlingual and distolingual) for all teeth present. Probing depth (mm) and location of the gingival margin in relation to the cementoenamel junction was measured using a UNC-15 manual probe (HuFriedy, Chicago, IL).
Subgingival Plaque Collection and Bacterial Quantification
Up to eight subgingival plaque samples (hateful 7; median 8) were collected from pre-adamant tooth sites in each subject area. 5369 bacterial plaque samples were nerveless contained of periodontal disease status, from the two well-nigh posterior teeth in each quadrant as available (mesiopalatal sites in the maxilla and mesiobuccal sites in the mandible). Due to the aforementioned missing covariate data, iv,533 samples are included in the nowadays analysis. Sterile Gracey curettes were inserted into the pocket until its base was reached and subgingival plaque was nerveless past a single scaling stroke. The nerveless plaque mass from each site was transferred into an individual Eppendorf tube containing 200 μl of sterile T-E buffer (10mM Tris HCl, one.0mm EDTA, pH vii.6). The tubes were immediately transferred into the laboratory and the plaque pellet was re-suspended, vigorously vortexed, and 200 μl of a 0.5M NaOH solution were added. The samples were kept at +4 °C until immobilization onto nylon membranes (see below), inside a few days from sample drove.
Eleven bacterial species (Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Fusobacterium nucleatum, Prevotella intermedia, Campylobacter rectus, Parvimonas micra, Eikenella corrodens, Veillonella parvula, Actinomyces naeslundii) were assessed using checkerboard Deoxyribonucleic acid-DNA hybridization as previously described.10, 21
Claret Pressure level and Hypertension Assessment
Claret pressure was measured after 5 minutes serenity sitting using a calibrated standard aneroid sphygmomanometer (Omron). Two blood pressure measurementswereseparated by fifteen minutes.
Hypertension was divers equally a systolic blood pressure recording ≥140 mm Hg or a diastolic claret pressure level recording ≥xc mm Hg (basedon the average of the 2 aforementioned claret pressure measurements) or thepatient'due south self-report of a history of antihypertensiveuse.
C-Reactive Protein and White Blood Cell Measurements
C-reactive protein (CRP) measurements were performed at the Academy of Vermont.22 The assay range is 0.175–1100 mg/50. CRP was available on 538 (82%) of the analyzed patients. White blood cells (WBC) were measured with automatic cell counters via standard techniques (Coulter STK-R and Coulter STK-S, Coulter Electronics, and Sysmex SE-9500, TOA Medical Electronics).23 WBC counts were bachelor on 611 (93%) of analyzed patients.
Run a risk Cistron Assessment
Physical and neurological examinations were conducted past written report physicians. Trained physicians and inquiry assistants administered standardized questionnaires and obtained in-person anthropomorphic measurements and fasting (overnight) blood specimens using standardized protocol. Data on sociodemographic characteristics, cardiovascular hazard factors, and other medical atmospheric condition were obtained through interview using standardized questions adapted from the Centers for Disease Control and Prevention Behavioral Take chances Factor Surveillance System.nine Race/ethnicity was based on self-identification.20 All assessments were conducted in English or Spanish. Height and weight were determined using calibrated scales. Blood samples were sent for complete blood count on enrollment. Fasting glucose and lipid panels were measured as described previously.24 LDL-C was computed using the Friedewald equation.24 Diabetes mellitus was defined by a history of diagnosed diabetes or the use of insulin or hypoglycemic medication, or a fasting glucose ≥126 mg/dL (7.0mmol/L). Smoking was assessed both categorically (currently smoking, former smoking or never smoking) and continuously as total pack years of cigarette smoking equally previously described.ix
STATISTICAL Assay
All analyses were performed using SAS for windows version 9. The laboratory reported the quantity of bacteria per subgingival plaque sample relative to known standards. For each species, bacterial values were natural log transformed, averaged within mouth, and standardized by dividing these values by the log transformed population standard divergence; we treated one standard deviation on the natural log scale every bit equivalent across microbes.
Standardized values for the 11 species were summed to define cumulative burden. Subsets of the cumulative burden were further divers as etiologic brunt (EB), putative burden (Atomic number 82), and health associated burden (HAB).10 We utilized (i) the consensus of the 1996 World Workshop in Periodontics identifying iii bacterial species every bit causally related to periodontal disease (P. gingivalis, T. forsythia and A. actinomycetemcomitans),25 and (2) Socransky's Red Complex26 further identifying T. denticola every bit a species that closely co-varies with P. gingivalis, and T. forsythia in pathological periodontal pockets, to create an etiologic burden score, comprising the four species (A. actinomycetemcomitans, P. gingivalis, T. forsythia and T. denticola). The 5 bacterial species deemed putatively associated with periodontal disease (C. rectus, Eastward. corrodens, F. nucleatum, Chiliad. micros and P. intermedia) were grouped as PB.25 HAB included two 'health-associated' bacterial species, A. naeslundii and 5. parvula.nineteen, 26
In order to compare results from the same bacterial definitions to clinical measures of periodontal affliction, nosotros also considered two boosted exposure definitions based on probing depth (PD) and/or zipper loss (AL) as follows. First, using the joint CDC/American Academy of Periodontology guidelines27, periodontitis was classified as follows: ane) severe periodontitis; due north=248 participants with at least two teeth having interproximal AL≥6 mm and at to the lowest degree 1 tooth having interproximal PD≥five mm; 2) moderate periodontitis; n= 352 participants with at to the lowest degree two teeth having interproximal AL≥4 mm or at to the lowest degree two teeth having interproximal PD≥5 mm; 3) no periodontitis: n=53 participants not coming together the same criteria. In a second approach, participants were categorized into tertiles based on the percent of sites/mouth with ≥ 3 mm PD (%PD≥3). The former definition focused on accepted definitions of clinical periodontitis while the latter was intended to represent a broader spectrum of periodontal disease and was based on previous data from INVEST demonstrating that %PD≥three better represents the underlying periodontal microbiota28.
Using linear regression models, systolic blood pressure level, diastolic blood pressure and hypertension prevalence were separately regressed as dependent variables beyond tertiles of the aforementioned bacterial burden scores (EB, Pb and HAB). All adjusted models included the post-obit covariates: age, torso-mass alphabetize, sexual practice, race/ethnicity (Hispanic, Black, White), education (defined dichotomously as completed high school yeah or no), smoking (defined as never, former or current), physical activity level (low, low-cal, moderate or heavy) diabetes, LDL-cholesterol, HDL-cholesterol. We also considered models adjusting for WBC and CRP in add-on to the aforementioned CVD risk factors to assess the evidence that inflammation might mediate the clan betwixt bacterial burden and either hypertension or blood pressure. Similarly, logistic regression models were utilized to obtain odds ratios for prevalent hypertension beyond tertiles of bacterial burden scores. A fix of identical analyses were conducted modeling either periodontitis (healthy, moderate, severe) or %PD≥iii (tertiles) every bit the periodontal exposure.
All analyses were conducted among gender subgroups to examine whether the associations differed by gender. Nosotros as well performed a subgroup analysis amongst 405 participants without a self-report history of hypertension and who were therefore not taking hypertension medications.
RESULTS
Full general Characteristics
Sixty percent of the 653 participants were females, and males were younger (67±eight vs. 70±9 years) (p<0.001). The written report population was predominantly tri-indigenous with 56% Hispanics, 23% Black non-Hispanic and 18% White non-Hispanic (the remaining iii% reported 'other'). Ninety-five percentage of Hispanics were foreign built-in with most from the Dominican Democracy.9 Table 1 presents additional characteristics of the written report participants beyond tertiles of etiologic bacterial burden.
Tabular array 1
Characteristics beyond Etiologic Bacterial Burden Tertiles, Adapted for Age and Gender (% or mean±SE)
| Variable | Tertile I N=217 | Tertile II N=218 | Tertile III N=218 |
|---|---|---|---|
| Socio-Demographic Variables | |||
| Age* | 70±0.six | 70±0.6 | 67±0.six |
| Female | 63% | 56% | 62% |
| Completed high school | 52% | 57% | 51% |
| Hispanic | 54% | 54% | 52% |
| Blackness | 22% | 21% | 26% |
| White | 21% | 23% | eighteen% |
| Other | 2% | 3% | 2% |
| Life-way and Behavioral Variables | |||
| Never smokers | 52% | 51% | 51% |
| Quondam smokers | 32% | 40% | 35% |
| Current smokers | 15% | xi% | 13% |
| Pack years | 111.half-dozen | 12±i.six | 13±one.6 |
| No physical activity* | 35% | 40% | 50% |
| Light physical activeness* | 53% | 45% | 41% |
| Moderate/Heavy concrete action | 13% | 12% | 12% |
| Brushing at least one/twenty-four hours | 97% | 97% | 99% |
| Flossing at least 1/day* | 52% | 44% | 39% |
| Medical Variables | |||
| Diabetes† | xix% | 15% | 21% |
| Serum total cholesterol (mmol/fifty) | 5.15±0.06 | 5.19±seventy.06 | 5.18±0.06 |
| HDL-cholesterol (mmol/l) | 1.35±0.03 | i.33±0.03 | one.28±0.03 |
| LDL-cholesterol (mmol/l) | 3.xv±0.06 | 3.20±0.06 | 3.27±0.06 |
| Torso Mass Alphabetize (Kg/Mii) | 28.3±0.4 | 29.0±0.iv | 28.0±0.4 |
| WBC* | 5.58±0.13 | 6.08±0.xiii | 6.01±0.thirteen |
| hs-CRP | 4.07±0.59 | 4.31±0.58 | 4.15±0.59 |
Mean(±SD) systolic and diastolic blood pressures were 139±xix and 79±12 mmHg respectively and 62% (north=406) of participants were hypertensive, 39% of whom were undiagnosed. Amongst participants who reported blood pressure medication the prevalence of drug class was as follows: 39% ACE inhibitors, 37% calcium-aqueduct blockers, 32% diuretics, 27% used beta-blockers and 20% other. Afterward historic period and body mass alphabetize adjustment, systolic claret pressure was equivalent in males and females, while males had slightly elevated diastolic blood pressure level (80 vs. 78 mmHg p=0.01). There were no gender differences in the prevalence of hypertension.
After adjusting for age, gender and BMI, average systolic blood pressure level was highest among Blacks (144 mmHg), followed by Hispanics (139 mmHg) and Whites (135 mmHg) (p for any difference=0.001). Diastolic blood pressure was equal among Blacks and Hispanics (80 mmHg) simply lower among Whites (77 mmHg) (p for any departure=0.05). 72% of Blacks were hypertensive, equally compared to 63% and 51% for Hispanics and Whites respectively (p=0.0004).
The mean±SD of %PD≥3 was 43%±27%. Mean±SD values of etiologic, putative and health associated brunt were 31±4, 57±3 and 26±2 (units are sum of standard deviations of ln(bacterial counts over species groupings), respectively and there were no gender differences in these distributions. An assay of the periodontal microbial profiles showed an unequal distribution with a predominance of A. naeslundii (34%) followed by P. intermedia (xx%), those 2 bacteria accounting for 54% of the subgingival microbiota assessed. The 4 etiologic bacteria accounted for 23% of the microbiota assessed in absolute numbers. In the standardized values presented in a higher place, each contributing species represented ~9% of the cumulative burden and the four species comprising the etiologic brunt deemed for 35% of the cumulative burden.10
Cumulative Periodontal Bacterial Burden
Afterward aligning for conventional risk factors, hateful systolic blood force per unit area increased beyond tertiles of cumulative bacterial brunt from 136 mmHg to 138 mmHg to 143 mmHg (p for trend =0.0004). Diastolic blood pressure level also increased as follows: 77 mmHg, 79 mmHg and 81 mmHg (p for trend <0.0001). The prevalence of hypertension increased from 57% to 62% to 68% across tertiles (p for tendency =0.02). These trends remained essentially unchanged in analyses of the subsample (n=453) with additional adjustments for both white blood cell count and CRP.
Etiologic, Putative and Health Associated Bacterial Burden
Subsequently aligning for health-associated and putative bacterial burden in improver to conventional adventure factors, both mean systolic and diastolic blood pressure increased across tertiles of etiologic bacterial brunt (Figures 1 & two, Table 2). These trends strengthened afterward further adjustment for white claret cell count and C-reactive protein. There was no clan betwixt claret pressure and either health-associated or putative bacterial burden (Figures one & 2). There was evidence for an inverse association between putative burden and hypertension amid the reduced sample (model four, Tabular array two).
Mean Systolic Blood Pressure across Tertiles of Bacterial Burden: adapted for etiologic, putative and health-associated bacterial burdens, historic period, trunk mass index, smoking, race/ethnicity, gender, diabetes, educational activity, LDL-C, HDL-C (n=653). P for linear trend: causal<0.001, putative=0.54 and protective=0.10
Hateful Diastolic Blood Pressure across Tertiles of Bacterial Burden: adjusted for etiologic, putative and health-associated bacterial burdens, age, body mass alphabetize, smoking, race/ethnicity, gender, diabetes, instruction, LDL-C, HDL-C (due north=653). P for linear trend: causal<0.001, putative=0.84 and protective=0.37
Tabular array 2
Prevalence and Odds Ratios of Hypertension beyond Increasing Tertiles of Bacterial Burden
| Model | Tertile I N=217 | Tertile II Northward=218 | Tertile III N=218 | P for linear tendency | |||
|---|---|---|---|---|---|---|---|
| | |||||||
| Prevalence | OR (95%CI) | Prevalence | OR (95%CI) | Prevalence | OR (95%CI) | ||
| Etiologic Burden | |||||||
| | |||||||
| i. | 56% | 1.0 | 64% | one.40(0.95,2.05) | 67% | 1.61(ane.09,2.37) | 0.02 |
| 2. | 51% | 1.0 | 63% | one.66(ane.05,ii.threescore) | 72% | ii.51(one.39,4.53) | 0.002 |
| 3. | 50% | one.0 | 63% | one.83(i.eleven,3.02) | 74% | 3.xiii(i.62,6.03) | <0.001 |
| 4. | 46% | 1.0 | 64% | 2.48(1.33,4.62) | 74% | 3.93(ane.76,8.76) | <0.001 |
| Putative Brunt | |||||||
| | |||||||
| 1. | threescore% | 1.0 | 64% | 1.xviii(0.80,one.74) | 62% | one.07(0.73,one.57) | 0.74 |
| two. | 69% | i.0 | 64% | 0.82(0.52,ane.29) | 54% | 0.52(0.29,0.94) | 0.03 |
| 3. | 67% | 1.0 | 64% | 0.87(0.53,1.43) | 55% | 0.54(0.28,1.03) | 0.07 |
| 4. | 72% | one.0 | 61% | 0.58(0.32,i.07) | 53% | 0.38(0.17,0.85) | 0.02 |
| Health Associated Burden | |||||||
| | |||||||
| 1. | 59% | one.0 | 63% | i.15(0.78,1.seventy) | 64% | 1.22(0.83,one.80) | 0.31 |
| ii. | 64% | 1.0 | 61% | 1.01(0.67,1.52) | 61% | 1.15(0.75,1.75) | 0.50 |
| 3. | 65% | 1.0 | sixty% | 0.83(0.53,1.29) | 61% | 0.86(0.54,i.36) | 0.48 |
| 4. | 61% | one.0 | 60% | 0.98(0.56,1.69) | 63% | 1.12(0.63,i.99) | 0.65 |
The odds of hypertension were iii.05 (95%CI: ane.lx,5.82) times greater amongst participants in the third vs. first tertile of etiologic burden; after farther adjustment for WBC and CRP, the odds ratio increased to 3.93 (95%CI: one.76, 8.76) (Tabular array two).
These results were unchanged in analyses adjusting for brushing, flossing, fourth dimension of last dental visit and family unit history of stroke (data not shown). In add-on, the findings were consistent when restricting the analysis to never smokers (northward=335). Specifically, amongst the never smokers, when comparing first and third tertiles of etiologic burden the prevalence of hypertension increased from 49% to 72% (p<0.01), while systolic and diastolic blood pressure increased by 6 mmHg (p=0.03) and iv mmHg (p=0.08) respectively.
Analyses focused on systolic and diastolic blood force per unit area among participants without a self-study history of claret pressure level medication use (northward=405) were similar: systolic and diastolic blood pressure level increased past 7 mmHg (p=0.02) and 4 mmHg (p=0.05), respectively. Similarly, results were unchanged among participants without a history of beta-blocker use (equally the indication for beta-blocker use is not always hypertension).
Clinical Periodontal Status
After multivariable adjustment, hypertension prevalence, hateful systolic blood pressure or mean diastolic claret pressures across tertiles of %PD≥3 were 57%, 59% and 70% (p for trend=0.004), 136, 138, 143 mmHg (p for trend<0.0001) and 77, 77, 82 mmHg (p for trend<0.0001), respectively. The prevalence of hypertension amongst participants defined as "healthy" or having either moderate or severe periodontitis was 72%, 58% and 66% (p for linear trend=0.64), respectively. Mean systolic and diastolic blood pressures across these same periodontitis categories were 141, 138, 141 mmHg (p=0.26) and 76, 78, 81 mmHg (p=0.001), respectively.
Sexual activity Specific Findings
Positive associations between etiologic burden and either hypertension or blood force per unit area were observed in both men and women after multiple hazard factor adjustment. However, the increase in both hypertension prevalence and mean diastolic blood pressure between the first and tertiary tertiles of etiologic brunt appeared to be over twice as large for males when compared to females. Similarly, the increment in systolic blood pressure amidst men was nearly three times larger when compared to women (Effigy three), although the statistical interaction of blood pressure level predicted from etiologic brunt with gender did non achieve statistical significance. The sex-specific results were nearly identical when defining periodontal status clinically (%PD≥3; information not shown).
Sexual practice Specific Systolic Blood Pressure and Hypertension Prevalence beyond Tertiles of Etiologic Bacterial Burden: Adjusted for health associated and protective bacterial burdens, age, trunk-mass index, race/ethnicity, smoking, education, diabetes, HDL-C and LDL-C; P for linear hypertension trend among females=0.09 & males=0.01; p for gender interaction = 0.44 P for linear systolic claret force per unit area trend among females=0.05 & males<0.001; p for gender interaction = 0.xv
DISCUSSION
Our electric current findings from INVEST add together of import information to the nascent literature apropos periodontal infections and hypertension. These data provide the commencement direct evidence of a relationship between periodontal infections and hypertension, past using direct assessments of periodontal bacterial brunt as our exposure every bit opposed to using clinical surrogates of past infection such as tooth loss, attachment loss and pocket depth. Nosotros report a strong positive association between increased subgingival colonization by A. actinomycetemcomitans, P. gingivalis, T. forsythia and T. denticola (etiologic bacterial brunt) and prevalent hypertension. After multivariable adjustment, participants in the highest vs. lowest tertile of etiologic bacterial burden experienced an more than a 3-fold increase in the odds of prevalent hypertension. Accordingly, systolic blood pressure increased by 9 mm/Hg and diastolic claret pressure increased by 5 mm/Hg when comparing the highest and lowest tertiles of etiologic burden. These associations remained positive in gender subgroups, although the findings were stronger among men than women. Results were too consistent when using a low threshold clinical periodontal definition reflecting the pct of sites/mouth with ≥ three mm pocket depth. Even so, consistent with previous reports,29 definitions using a higher threshold clinical periodontal definition yielded aught or weak results. Previous reports have suggested an association betwixt tooth loss and hypertension. Taguchi and colleagues found tooth loss to exist associated with hypertension among n=98 postmenopausal women.18 Data from the large, population-based Written report of Health in Pomerania (Transport) also demonstrated an association between tooth loss and both systolic blood pressure and the prevalence of hypertension.17 However, in contrast to the findings by Taguchi et al., the associations in SHIP were bars to men, while no association was observed among women.
The use of direct bacterial assessments in INVEST minimizes potential biases related to the imprecision of traditional clinical assessments, as at that place are several noninfectious causes of tooth loss. Moreover, while AL and PD clearly take infectious etiologies26, 30, other noninfectious risk factors, such as smoking,31 exist.
Our findings were specific to the etiologic bacterial cluster previously reported to demonstrate strong positive associations with clinical periodontal affliction in our population19 and others.26, 32 Accordingly, both blood pressure level level and hypertension prevalence were unrelated to putative or health associated bacterial burden levels. This specificity reduces the likelihood of confounding by good for you lifestyle as previously discussed.10 It is besides noteworthy that the clinical definition of periodontal disease based on the percent of sites per mouth with iii mm pocket depth yielded results most identical to our etiologic bacterial exposure definition. These findings are consistent with prior methodological studies regarding advisable periodontal definitions in studies of infection-induced systemic risk28, 29. As previously discussed29, the concept of subclinical periodontal disease/infection might be important because in population-based settings such as INVEST, substantial exposure to pathological periodontal microbiology likely occurs in shallow periodontal pockets that do not still exhibit usually accustomed clinical signs of frank periodontal affliction28.
The observation that the association between etiologic burden and hypertension was stronger amid men than women, despite non achieving statistical significance, is consequent with previous reports regarding periodontal infections and cardiovascular illness.ii, 8, 17 While this finding could be due to chance, gender differences in the association between clinical periodontal affliction, molar loss and systemic illness take several potential explanations8, 29 such as: i) differential biological susceptibility to infection induced systemic affliction; two) gender variation in historical infectious exposure; iii) more aggressive periodontal treatment practices in women than in men preventing women from realizing infectious thresholds necessary for systemic effects; iv) gender differences in causes of periodontal disease and tooth loss. Notably, the gender divergence reported presently was observed despite comparable levels of prevalent hypertension, claret pressure and bacterial colonization between genders. This may advise the possibility of a gender differential in biological susceptibility to infectious etiologies of hypertension.
The potential for smoking behaviors to confound periodontal/systemic disease associations is a prominent concern. Notwithstanding, the electric current and sometime smoking experience of INVEST participants did not vary across levels of etiologic burden. Moreover, results from subgroup analyses among never smokers were consistent with findings from the full sample. Therefore the potential for spurious findings related to smoking behaviors are substantially minimized in these data.
Systemic inflammation as assessed via WBC and CRP did not explain the current findings between etiologic bacterial burden and hypertension. WBC and CRP are nonspecific markers of systemic inflammation and while several previous studies have reported positive associations betwixt periodontal affliction and both WBC and CRP, the associations are generally weak.five, 10, sixteen, 33 Therefore, elevations in WBC and CRP in the INVEST cohort are likely to be largely owing to factors other than oral bacterial colonization. Moreover, the relatively high mean CRP levels observed in INVEST (as in the ARIC cohort34) might limit the predictive power of CRP, as previously described.10
Direct assessments of bacterial levels readily reflect the infectious nature of periodontal affliction and are easier to interpret than serological assessments of antibody titers to infective agents that are known to be influenced by multiple factors.35 Assessments of periodontal bacterial profiles by ways of Dna-DNA hybridization are well suited for epidemiological studies with large samples sizes and accept been shown to correlate well with culture-based data.36 In addition, they accept the advantage of not requiring microbial viability, which might be important in the written report of chronic bacterial exposures.
Nosotros assessed only eleven species out of the over 700 species that accept been identified in subgingival biofilms to engagement.37, 38 However, we assessed the leaner idea to be causally linked to periodontal disease. While a more comprehensive microbiological assessment might exist more informative, the big sample sizes common to epidemiologic investigations precludes this approach for practical and financial reasons. Indeed, even a moderate expansion (by electric current population-based research standards39) of bacterial cess to thirty or 40 species would still leave us far short of a truly comprehensive representation of the periodontal flora while at the aforementioned time leaving express belittling options based on a priori hypotheses. We therefore believe to have reached a reasonable compromise with these 11 species. Whether the proposed species are causally related to periodontal illness or are simply strong markers for unmeasured causal species is a separate issue to be resolved by detailed microbiological studies. Nevertheless, additional pathogens might have been informative and could conceivably change the overall human relationship.
Our decision to standardize microbiological collection for all subjects (viii near posterior sites/mouth), irrespective of clinical disease, might take adulterate our results by diluting the degree of exposure to pathogenic leaner. Although more than bourgeois, this standardized approach yields results more reflective of the "average" pathogen exposure in our study population and therefore reduces the potential for overestimation of the association betwixt infection and hypertension.
This study shares with others the limitations of cross-exclusive data. Because both hypertension and periodontal microbiology were measured meantime, the time sequence cannot be established and causal inferences cannot be made. We must expect the prospective results of INVEST and other studies to make firmer conclusions. It is as well possible that the variation in bacterial colonization levels observed in INVEST might reflect other chance factors not properly measured or identified, such as salt intake or dietary pattern in general. However, we extensively adapted for confounders and the relationship strengthened afterwards statistical aligning, which minimizes this possibility.
These data provide the first directly microbiological evidence of a possible contributory role for periodontal infections in hypertension etiology. Participants with a relative excess of oral pathogens strongly related to clinical periodontal affliction in INVESTxix had both elevated blood pressure (systolic and diastolic) levels and increased hypertension odds after adjustment for conventional gamble factors. These findings strengthen the hypothesis that periodontal infections may contribute to clinical CVD, and provide insights regarding a mediating mechanism that might explain why periodontal infections have been reported to be a stronger gamble factor for stroke than for CHD. While these results require confirmation in prospective settings, they could be of public health importance every bit both periodontal infections and hypertension are common and hypertension etiology is not completely understood.
Acknowledgments
ACKNOWLEDGMENTS AND FUNDING SOURCES
This enquiry is supported by NIH grants R01 DE-13094 (Dr. Desvarieux), NS-29993 (Dr. Sacco). Dr. Desvarieux is also supported by a Chair of Excellence honour from the French Agency for Enquiry and the Institut National de la Santé et de la Recherche Médicale (R05115DD). Dr. Demmer is supported by K99 DE-018739. Dr. Rundek is likewise supported by NINDS R01 NS-047655. Dr. Jacobs receives support from the Mayo Chair Endowment, Schoolhouse of Public Health, University of Minnesota. We thank the INVEST staff Mr. George Loo, Drs. Mariana Cukier, Yira Flores, Shantanu Lal and Ms. Janet DeRosa for their devoted patient care; Ms. Miriam Herrera-Abreu, Ms. Romi Celenti and Mr. Jun Yang for the laboratory analysis of the dental plaque samples; and almost importantly the patients. Patients were seen at the Columbia University General Clinical Research Center, NIH grant 1UL1RR024156.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403746/
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