American Journal of Cardiology
Volume 102, Issue 11 , Pages 1509-1513, 1 December 2008

Usefulness of Self-Reported Periodontal Disease to Identify Individuals With Elevated Inflammatory Markers at Risk of Cardiovascular Disease

  • Heidi Mochari, MPH, RD

      Affiliations

    • Columbia University Medical Center/New York Presbyterian Hospital, New York, New York
    • ,
  • John T. Grbic, DMD, MMedSc

      Affiliations

    • Columbia University, College of Dental Medicine, New York, New York
    • ,
  • Lori Mosca, MD, MPH, PhD

      Affiliations

    • Columbia University, College of Physicians and Surgeons/New York Presbyterian Hospital, New York, New York
    • Corresponding Author InformationCorresponding author: Tel: 212-305-4866; fax: 212-342-5238

Received 23 May 2008; received in revised form 15 July 2008; accepted 15 July 2008. published online 17 September 2008.

Article Outline

Periodontal disease has been associated with cardiovascular disease (CVD), and inflammation may represent a common pathophysiology. Oral health screening in the context of CVD risk assessment represents a potential opportunity to identify individuals at risk for CVD. The purposes of this study were to determine if self-reported oral health status is independently associated with inflammatory markers and if oral health assessment as part of CVD risk screening can identify at-risk individuals without traditional CVD risk factors. A baseline analysis was conducted among participants in the National Heart, Lung, and Blood Institute's Family Intervention Trial for Heart Health (FIT Heart; n = 421, mean age 48 ± 13.5 years, 36% nonwhite) without CVD or diabetes who underwent standardized assessment of oral health, lifestyle, CVD risk factors, and the inflammatory markers high-sensitivity C-reactive protein and lipoprotein-associated phospholipase A2. Statistical associations between oral health, risk factors, and inflammatory markers were assessed, and logistic regression was used to adjust for effects of lifestyle and potential confounders. Periodontal disease was independently associated with being in the top quartile of lipoprotein-associated phospholipase A2 compared with the lower 3 quartiles (odds ratio 1.9, 95% confidence interval 1.1 to 3.2) after adjustment for lifestyle and risk factors. Histories of periodontal disease were reported by 24% of nonoverweight, nonhypertensive, nonhypercholesterolemic participants, and of these participants, 37% had elevated high-sensitivity C-reactive protein (≥3 mg/L) or lipoprotein-associated phospholipase A2 (≥215 ng/ml) levels. In conclusion, self-reported periodontal disease is independently associated with inflammation and common in individuals without traditional CVD risk factors.

 

Periodontal disease is highly prevalent, affecting approximately 34% of adults aged >30 years (about 36 million individuals),1 and has been correlated with the presence of cardiovascular disease (CVD).2 Whether this association is causal is not yet determined, but research suggests that there may be common underlying pathophysiology. Chronic infection has been linked to vascular inflammation, and infection and inflammation have been associated with periodontal disease and incident CVD events.2, 3 However, not all previous research has controlled for diet and/or lifestyle factors that may be associated with CVD and periodontal disease.3 The purposes of this study were (1) to examine whether self-reported oral health status is independently associated with novel inflammatory markers for CVD risk, including high-sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2), and (2) to assess whether self-reported oral health status identifies individuals with histories of periodontal disease who do not have traditional CVD risk factors in a diverse population of participants eligible for the primary prevention of CVD.

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Methods 

This was a cross-sectional baseline substudy of consecutively enrolled participants in the National Heart, Lung, and Blood Institute's Family Intervention Trial for Heart Health (FIT Heart; n = 421, mean age 48 ± 13.5 years, 36% racial or ethnic minorities), designed to test the effectiveness of a screening and educational intervention for family members of patients hospitalized with CVD. Participants were eligible if they were family members or cohabitants of patients hospitalized with CVD, were aged 20 to 79 years, did not have CVD or diabetes, and spoke either English or Spanish. Demographic information was obtained by standardized questionnaire. All participants provided written informed consent to be a part of the study. The study was approved by the Columbia University Medical Center Institutional Review Board.

Oral health status data were collected using the following standardized questions: (1) “Have you ever been informed that you have periodontal (gum) disease?” (2) “Have you ever received treatment for periodontal disease?” (3) “Do you have removable partial or complete dentures?” and (4) “When was the last time you had your teeth cleaned?” Self-reported measures of periodontal disease such as these have been shown to be predictive of clinical attachment loss and periodontitis.4, 5

Dietary assessments were completed using the full-length Block 98 Food Frequency Questionnaire.6, 7, 8 High saturated fat intake was defined as ≥10% of calories from saturated fat per day. High dietary cholesterol intake was defined as ≥300 mg/day. Suboptimal fruit and vegetable intake was defined as <5 combined servings of fruits and vegetables per day. Higher alcohol intake was defined as being at or above the 75th percentile for daily percentage of calories from alcohol.

Physical activity level was assessed using standardized questions adapted from the Centers for Disease Control and Prevention Behavioral Risk Factor Surveillance System Questionnaire.9 Suboptimal exercise level was defined as exercise <3 days per week for 30 minutes per session. Current smoking status was defined by self-report as smoker or nonsmoker and confirmed using carbon monoxide breath testing.

Waist circumference and body mass index (BMI) were assessed by trained examiners using National Heart, Lung, and Blood Institute clinical guidelines.10 Above optimal waist circumference was defined as >102 cm (>40 in) in men and >88 cm (>35 in) in women. Overweight or obese status was defined as BMI ≥25.0 kg/m2.

Systolic and diastolic blood pressure was assessed by an automated blood pressure monitor at the Columbia University Clinical and Translational Science Award Center using standard protocol.11 Hypertension was defined as systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg.12

All participants underwent fasting blood draws at their baseline study visits. Serum and plasma aliquots were prepared from fasting blood samples immediately after blood draws. Determination lipids were performed on blood analyzed (Roche Diagnostics GmbH, Mannheim, Germany) at the Columbia University Clinical and Translational Science Award Center. Low-density lipoprotein (LDL) cholesterol was calculated using the Friedewald equation. HsCRP and Lp-PLA2, inflammatory markers that are indicators of CVD risk, were systematically measured in all participants using blood collected at baseline visits. HsCRP was assessed using a Kamiya hsCRP kit (Kamiya Biomedical Corporation, Seattle, Washington) on serum samples. High hsCRP levels were defined as ≥3 versus <3 mg/L. HsCRP values ≥10 mg/L were excluded from analysis on the basis of previous work suggesting that they reflect acute or nonvascular inflammation.13 Lp-PLA2 mass was measured using the PLAC test (diaDexus, Inc., South San Francisco, California) on plasma samples. Elevated Lp-PLA2 levels were defined as being at or above the 75th percentile.

Metabolic syndrome was evaluated using the National Cholesterol Education Program Adult Treatment Panel III definition of the presence of ≥3 of the following risk factors: (1) abdominal obesity, (2) triglycerides ≥150 mg/dl, (3) high-density lipoprotein cholesterol level <40 mg/dl in men and <50 mg/dl in women, (4) blood pressure ≥130/85 mm Hg, and (5) fasting glucose ≥110 mg/dl.14

All data were collected using standardized forms, double entered into a Microsoft Access database (Microsoft Corporation, Redmond, Washington), and exported to SAS version 9.1 (SAS Institute Inc., Cary, North Carolina) for statistical analysis. Continuous and categorical variables were characterized using means and frequency statistics, respectively. Spearman's coefficients were used to assess the correlations between hsCRP and Lp-PLA2 and between each of these inflammatory markers and age. Associations between oral health and inflammatory markers, oral health and lifestyle and risk factors for CVD, and lifestyle and risk factors for CVD and inflammatory markers were assessed using chi-square statistics. Multiple logistic regression models were used to assess the associations between oral health exposure variables and inflammation markers, controlling for age, gender, race or ethnicity, smoking, and potential confounders.

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Results 

The baseline characteristics of 421 consecutively enrolled participants in the FIT Heart study in this analysis are listed in Table 1. The mean age was 48 ± 13.5 years. The median hsCRP level was 1.05 mg/L (hsCRP ≥10.0 mg/L excluded [n = 1]). The median Lp-PLA2 level among all participants was 189.3 ng/ml, with 25% of participants having Lp-PLA2 levels ≥215 ng/ml. Age and hsCRP were not correlated (r = −0.01, p = 0.85); nor were age and Lp-PLA2 (r = 0.05, p = 0.28) or Lp-PLA2 and hsCRP (r = 0.04, p = 0.39).

Table 1. Characteristics of participants in cardiovascular disease risk screening (n = 421)
Characteristicn (%)
Men147(35%)
Age ≥65 yrs49(12%)
Nonwhite race151(36%)
High school education or less92(22%)
No health insurance62(15%)
LDL cholesterol ≥3.37 mmol/L (≥130 mg/dl)159(38%)
Blood pressure ≥140/90 mm Hg99(24%)
Waist circumference >102 cm (men), >88 cm (women)161(38%)
BMI ≥25 kg/m2274(66%)
Metabolic syndrome75(18%)
Saturated fat ≥10% of calories/d240(57%)
Dietary cholesterol ≥300 mg/d107(26%)
Fruit and vegetables <5 servings/d254(60%)
Dietary alcohol ≥75th percentile (≥5.2% kcal/d)108(25%)
Exercise <3 d/wk for 30 min290(69%)
Current smokers41(10%)
Framingham risk ≥10%35(8%)
Ever diagnosed with periodontal disease95(24%)
Ever treated for periodontal disease82(20%)
Wears partial or complete removable dentures44(10%)
Last dental cleaning >12 mo ago97(23%)

Approximately 1 in 4 participants (23%) had histories of diagnosed periodontal disease. Partial or complete removable dentures were used by 10% of participants (n = 44), of whom 38% reported histories of diagnosed periodontal disease. Durations of >12 months since their last dental cleanings were reported by 23% of participants (n = 97). Among those with >12 months since their last cleanings, 19% reported diagnosed periodontal disease.

Participants with histories of diagnosed periodontal disease were almost 2 times more likely to have Lp-PLA2 levels in the highest quartile compared with the lower 3 quartiles (odds ratio 1.8, 95% confidence interval 1.1 to 3.0) than those who did not have histories of diagnosed periodontal disease. Those reporting no dental cleanings in >1 year were more likely to have hsCRP levels ≥3 versus <3 mg/L (odds ratio 1.7, 95% confidence interval 1.0 to 2.9) compared with those who reported cleanings within the past year. Neither a history of treatment for periodontal disease nor having partial or complete removable dentures was significantly associated with elevated levels of hsCRP or Lp-PLA2 (Table 2).

Table 2. Associations between oral health, demographic or lifestyle factors, and inflammatory markers
VariablehsCRP (≥3 vs <3 mg/L)Lp-PLA2 (≥215 vs <215 ng/mL)
Ever diagnosed with periodontal disease1.2(0.68–2.0)1.8(1.1–3.0)
Ever treated for periodontal disease1.2(0.65–2.1)1.5(0.89–2.6)
Wears removable dentures0.98(0.45–2.1)1.1(0.54–2.2)
Last dental cleaning >12 mo ago1.7(1.0–2.9)1.5(0.88–2.4)
Men0.58(0.34–0.98)1.6(1.0–2.5)
Age ≥65 yrs1.2(0.60–2.4)1.1(0.56–2.2)
Nonwhite2.2(1.4–3.5)0.36(0.21–0.61)
High school education or less1.2(0.70–2.2)1.0(0.60–1.7)
No health insurance1.4(0.73–2.6)1.4(0.77–2.5)
LDL cholesterol ≥3.37 mmol/L (≥130 mg/dl)0.87(0.53–1.4)2.0(1.3–3.2)
Blood pressure ≥140/90 mm Hg1.2(0.69–2.1)1.3(0.76–2.1)
Waist circumference >102 cm (men), >88 cm (women)3.7(2.2–6.0)1.2(0.74–1.8)
BMI ≥25 kg/m23.1(1.7–5.5)1.4(0.87–2.3)
Metabolic syndrome2.1(1.2–3.7)1.1(0.64–2.0)
Saturated fat ≥10% of calories/d1.3(0.82–2.2)2.0(1.2–3.2)
Dietary cholesterol ≥300 mg/d1.1(0.62–1.8)1.3(0.82–2.2)
Fruit and vegetables <5 servings/d1.4(0.88–2.4)0.72(0.46–1.1)
Dietary alcohol ≥75th percentile0.66(0.37–1.2)1.1(0.66–1.8)
Exercise <3 d/wk for 30 min1.2(0.74–2.1)0.80(0.50–1.3)
Current smoker0.60(0.24–1.5)0.84(0.39–1.8)
Framingham risk ≥10%0.62(0.23–1.6)1.1(0.48–2.3)

Data are expressed as odds ratio (95% confidence interval).

Men were less likely than women to have elevated hsCRP levels ≥3 versus <3 mg/L and more likely than women to have Lp-PLA2 levels in the highest quartile. Nonwhite participants were more likely to have elevated hsCRP levels compared with whites and less likely to have Lp-PLA2 levels in the highest quartile. Age, education level, and having health insurance were not associated with hsCRP or Lp-PLA2 (Table 2).

In univariate assessment of the association between CVD lifestyle and traditional CVD risk factors, high waist circumference was positively associated with hsCRP levels, as was overweight or obese status. Neither was significantly associated with Lp-PLA2 levels. Saturated fat intake was significantly associated with higher Lp-PLA2 and not with hsCRP. Likewise, higher LDL cholesterol levels were significantly associated with higher Lp-PLA2 levels. Dietary cholesterol, alcohol, fruit and vegetable intake, exercise level, smoking, and blood pressure were not significantly associated with increased inflammatory marker levels in this study (Table 2).

The observed association between self-reported periodontal disease and increased Lp-PLA2 levels remained statistically significant when controlling for age, gender, race, smoking, LDL cholesterol, and dietary saturated fat in a multiple logistic model (odds ratio 1.9, 95% confidence interval 1.1 to 3.2). The association between last dental cleaning >12 months ago and hsCRP level did not retain statistical significance after adjustment for age, gender, race, smoking, waist circumference, and BMI.

We examined the prevalence of self-reported histories of periodontal disease in participants without traditional cardiovascular risk factors and found that diagnosed periodontal disease was present 23% to 29% of the time in the absence of individual and multiple lifestyle and risk factors for CVD traditionally measured during CVD risk assessment (Table 3). More than 1 in 5 nonhypertensive participants (24%) without elevated LDL cholesterol levels or overweight or obesity reported histories of periodontal disease diagnosis. Among those with periodontal disease and without these 3 traditional CVD risk factors, 37% had elevated hsCRP or Lp-PLA2 levels.

Table 3. Prevalence of periodontal disease and inflammatory markers by risk factor status
VariableAt Risk Factor Goal% at Risk Factor Goal With Periodontal Disease% At Risk Factor Goal With Periodontal Disease and Elevated Lp-PLA2 or hsCRP
LDL cholesterol <3.37 mmol/L (<130 mg/dl)259(62%)24%11%
Blood pressure <140/90 mm Hg322(76%)24%11%
Waist circumference ≤102 cm (men), ≤88 cm (women)260(62%)23%9%
BMI <25 kg/m2144(34%)24%10%
Saturated fat <10% of calories/d179(43%)28%11%
Dietary cholesterol <300 mg/d312(74%)24%13%
Fruit and vegetable intake >5 servings/d167(40%)29%15%
Exercise >3 d/wk for 30 min130(31%)23%13%
Nonsmoker378(90%)24%12%
LDL cholesterol <3.37 mmol/L (<130 mg/dl) and blood pressure <140/90 mm Hg and BMI <25 kg/m287(21%)24%9%

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Discussion 

In a diverse population of individuals eligible for the primary prevention of CVD, a history of periodontal disease was associated with significantly higher levels of Lp-PLA2 compared with those without periodontal disease. When adjusted for potential confounders and lifestyle factors, this association remained statistically significant. To our knowledge, this is the first report of an association between oral health and Lp-PLA2. These data support a possible independent association between oral health and inflammation, suggesting that inflammation may be a factor in the relation between oral health and CVD. We also showed that diagnosed periodontal disease is present in patients without traditional CVD risk factors and that many of these individuals have increased inflammatory markers (hsCRP or Lp-PLA2).

In contrast to some studies, we did not find an association between oral health and hsCRP after adjustment for adiposity. Discordance may be due to control for confounders such as BMI, smoking, and other lifestyle factors. Alternatively, lack of significant association may be related to our primary prevention population with lower mean hsCRP levels compared with means reported in patients with established CVD,15, 16, 17 in whom hsCRP and Lp-PLA2 have been independently correlated with CVD risk.18, 19

We did not show a correlation of hsCRP and Lp-PLA2 with each other, which may reflect disparate inflammatory pathways20 and correlations with varying CVD risk factors. For example, central adiposity and obesity were strongly associated with increased hsCRP levels in our study, and in others,19 but were not found to be associated with higher levels of Lp-PLA2. This is consistent with past research in men and women that also failed to correlate Lp-PLA2 levels with BMI21, 22, 23 and supports the specificity of Lp-PLA2 to vascular rather than systemic inflammatory processes.24 Higher levels of Lp-PLA2 have been identified on inflamed, rupture prone plaques, and the active Lp-PLA2 product lysophosphatidylcholine has been correlated with human endothelial dysfunction in patients with early stages of atherosclerosis.24, 25

Periodontal disease diagnoses were reported by 23% of our screening population, which is lower than the nationally estimated prevalence in adults aged >30 years.1 This could be attributed to 10% of study participants being aged <30 years, with only 4 participants in this age range reporting diagnoses of periodontal disease.

Strengths of this study include our population with well-characterized CVD risk, lifestyle, and other risk factors, allowing us to examine interrelations among these, oral health, and inflammation. Participants were ethnically diverse, eligible for the primary prevention of CVD, and actively seeking CVD risk screening, suggesting that these findings may be generalizable and applicable to other primary prevention populations.

A limitation of this study is that we used self-reported data instead of clinical examination to assess oral health status. Nonetheless, past research has shown good correlation between self-report and clinical evaluation,26 and nondifferential misclassification of disease status would generally bias toward the null, making a spurious association unlikely. We are limited in drawing conclusions about the directionality of relations between oral health and inflammatory markers because of the cross-sectional design; specifically, it is not possible to conclude from these data that oral health is a risk marker for CVD or CVD outcomes or that any therapy based on oral health status will be effective. Our data suggest that “at-risk” individuals who may otherwise not be identified by traditional CVD risk screening might be identified through oral health screening. Further research prospectively examining the relation between oral health status, CVD biomarkers, and incident CVD is needed to determine if there is a causal link between oral health and CVD.

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References 

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 This study was funded by a Research Project Award to Dr. Mosca (R01 HL 075101-01A1) from the National Institutes of Health, Bethesda, Maryland, and supported in part by the Clinical and Translational Science Award Center at Columbia University Medical Center, New York, New York, and a Research Career Award to Dr. Mosca (K24 HL076346-01A1) from the National Institutes of Health.

PII: S0002-9149(08)01272-1

doi:10.1016/j.amjcard.2008.07.047

American Journal of Cardiology
Volume 102, Issue 11 , Pages 1509-1513, 1 December 2008

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