Open Access
Open Peer Review

This article has Open Peer Review reports available.

How does Open Peer Review work?

Periodontal disease and atherosclerosis from the viewpoint of the relationship between community periodontal index of treatment needs and brachial-ankle pulse wave velocity

  • Koichi Miyaki1, 2,
  • Katsunori Masaki1,
  • Mariko Naito3,
  • Toru Naito4,
  • Keika Hoshi5,
  • Asako Hara1,
  • Shugo Tohyama1 and
  • Takeo Nakayama6Email author
BMC Public Health20066:131

DOI: 10.1186/1471-2458-6-131

Received: 14 November 2005

Accepted: 14 May 2006

Published: 14 May 2006



It has been suggested that periodontal disease may be an independent risk factor for the development of atherosclerosis. However, the relationship between periodontal disease and atherosclerosis has not been fully elucidated. This study aimed to assess the effects of periodontal disease on atherosclerosis.


The study design was a cross-sectional study. Subjects were 291 healthy male workers in Japan. We used the Community Periodontal Index of Treatment Needs (CPITN) score, average probing depth and gingival bleeding index (rate of bleeding gums) to assess the severity of periodontal disease. We also used the Brachial-Ankle Pulse Wave Velocity (baPWV) as the index for the development of atherosclerosis.


The unadjusted odds ratio (OR) of atherosclerosis in relation to the CPITN score was 1.41 [95% CI: 1.16–1.73]. However, after adjustment for age, systolic blood pressure and smoking, the CPITN score had no relationship with atherosclerosis (adjusted OR: 0.91 [0.68–1.20]).


Our results show no relationship between mild periodontal disease and atherosclerosis after appropriate adjustments.


For many people, periodontal disease causes problems in day-to-day life due to loss of teeth. Recently, it has been argued that periodontal disease may be an independent risk factor for the development of atherosclerosis. The potential mechanisms that could explain a role for periodontal disease in atherosclerosis are general inflammatory mechanisms and specific bacterial interactions. One hypothesis is that the cause of atherosclerosis is direct injury to vascular endothelial cells by an infecting organism; another is that inflammatory cytokines contribute to atherosclerosis [1, 2]. It has been reported that the infected or inflamed area in periodontitis is associated with macrophage activation via increased serum lipopolysaccharide concentrations [3]. It has also been reported that subjects with advanced periodontal disease had endothelial dysfunction and evidence of systemic inflammation, possibly placing them at an increased risk for cardiovascular disease [4]. The relationship between periodontal disease and diseases of the blood vessels, such as peripheral vascular disease and coronary heart disease (CHD), has been discussed in several reports [59]. For example, a meta-analysis of nine cohort studies (eight prospective and one retrospective) comparing individuals with and without periodontal disease showed that the relative risk (RR) of cardiovascular events was 1.19 [1.08–1.32]. When the outcome was restricted to stroke only, the RR was 2.85 [1.78–4.56] [9].

More than 70% of all people have gum problems [10]. Among Japanese, the prevalence of advanced periodontal disease is 32% in people in their 40 s and 47% in people in their 50 s [11]. Advanced periodontal disease is defined by a Community Periodontal Index score (CPITN score) of 3–4. The CPITN score, which is defined by the World Health Organization (WHO) protocol and provides a standardized means of measurement, makes it easy to compare reports. Periodontal disease is one of the most widespread diseases in the world [12], and if it affects atherosclerosis, it must be considered an important aspect of public health. Therefore, it is essential to clarify the relationship between periodontal disease and atherosclerosis.

We defined atherosclerosis by using Pulse wave velocity (PWV), an index of arterial stiffness [13, 14] regarded as a non-invasive marker of vascular damage [1517]. Previous studies have shown that PWV is a marker of the severity of cardiovascular disease [18] and a predictor of future cardiovascular events [1921]; moreover, it can be applied as a screening tool for cardiovascular risk in a general population [16, 22]. Recently, a simple device for measuring brachial-ankle PWV (baPWV) has been developed and made available [23, 24].

In this study, we assessed the effect of periodontal disease on atherosclerosis from the viewpoint of the relationship between CPITN score and Brachial-Ankle Pulse Wave Velocity (baPWV), by which we non-invasively assessed the progress of atherosclerosis.


Study subjects and design

This was a cross-sectional study. The setting was a Japanese chemical company. After receiving approval from the ethical committee of Keio University School of Medicine, we obtained informed consent from 291 male employees of the chemical company who were selected for participation in the cross-sectional study. In September 2004, we gave the participants questionnaires about their daily life and dental habits. Oral and medical examinations were performed in October 2004, at which time the questionnaires were also collected.

Periodontal measurements

We used the CPITN score, average probing depth and gingival bleeding index (rate of bleeding gums) to determine the severity of periodontal disease. Dental examinations were conducted by two dentists who, according to the WHO protocol, used flat dental mirrors and periodontal probes [25]. Teeth numbers 2, 3, 8, 14, 15, 18, 19, 24, 30 and 31 were studied, and six segments of each tooth were evaluated. Probing depth was measured at two locations per index tooth. Each sextant was designed as either healthy (Score 0), bleeding but no dental calculus detected (Score 1), calculus detected but no pockets (Score 2), a probing depth of more than 4 mm (Score 3) or a probing depth of more than 6 mm (Score 4), according to the highest score recorded at the index teeth. The highest score was recorded as the CPITN score of the participant. The assignment of the two dentists to subjects was carried out at random. Interexaminer agreement between the dentists was tested at baseline and calculated using the Kappa statistics. The same dentists carried out the dental examinations during the entire study period.

Medical measurements

We used baPWV as the index for atherosclerosis. Nurses measured the baPWV and blood pressure of each subject twice using a baPWV/ABI device (Nippon Colin, Aichi, Japan) while the subject was at rest in a supine position. This device, approved by the US Food and Drug Administration as VP-2000/1000, can monitor bilateral brachial and ankle pressure wave forms simultaneously using the volume plethysmographic method, with two optional tonometry sensors for carotid and femoral arterial wave measurements. The nurses practiced baPWV measurements beforehand and made arrangements for standardization.

Age and smoking status were self-reported, and medical history was acquired by interview. We applied pack-years (smoking period [years] × number of packs [/day]) as the cumulative smoking index. Height, weight, systolic and diastolic blood pressures (SBP and DBP), fasting blood glucose level, serum lipid levels [total cholesterol, triglyceride and high-density lipoprotein (HDL) cholesterol] and HbA1c were measured in all subjects.

Statistical analyses

The distributions of triglyceride, HDL cholesterol and HbA1c were skewed and regarded as log-normal. Therefore, these data were logarithmically transformed, and the Student's t-test was applied. For age, as the distribution was skewed and not log-normal, the Wilcoxon's rank sum test was applied. The other variables were regarded as normally distributed, and the Student's t-test was applied.

We divided the subjects based on CPITN score, average probing depth and gingival bleeding index. Subjects with CPITN scores of 0, 1, 3 and 4 were defined as healthy, having periodontal disease, having advanced periodontal disease and having severe periodontal disease, respectively. Similarly, for average probing depth and gingival bleeding index, we placed the subjects in four groups. The boundary values for average probing depth were 2 mm, 3 mm and 4 mm, and those for gingival bleeding index were 25%, 50% and 75%.

We defined atherosclerosis as baPWV 1400 (cm/sec), which is an independent variable for risk stratification by the Framingham score and for the discrimination of patients with atherosclerotic cardiovascular disease. It is the commonly used cut-off value in clinical practice [16].

Odds ratios (ORs) and 95% CIs were calculated using logistic regression analysis. All statistical analyses were performed using SPSS for Windows version 12.0 (Statistical Product and Service Solutions, IL, USA), and statistical significance was accepted at p < 0.05.


Mean age and body mass index were 46.6 ± 11.5 years and 23.4 ± 3.66 kg/m2 (mean ± SD), respectively, which are typical values in healthy male Japanese workers. The maximum and minimum ages were 21 and 63. The biochemical values of blood did not reveal any significantly abnormal characteristics. The distribution of the CPITN score was typical in Japanese people and in people from other countries [10, 12, 2628]. The case-control ratio was 0.99 (case: N = 145, control: N = 146). Between the case and control groups, significant differences were found in age, blood pressure, pack-years, periodontal measurements and other variables (Table 1). The periodontal conditions of the case group were worse than those of the control group. For example, in the case group, the prevalence of severe periodontal disease was about one-ninth, but in the control group, it was about one-fourth (Table 1). [Note: I don't quite understand what "one-ninth" and "one-fourth" mean in the above sentence.] The agreement between examiners was fairly high (Kappa statistics = 0.767, p value = 0.029).
Table 1

Characteristics of study participants


Atherosclerosis (+)** (N = 45)

Atherosclerosis (-)** (N = 146)

p Value



± SD


± SD








Weight [kg]






BMI [kg/m2]






Systolic blood pressure [mmHg]






Diastolic blood pressure [mmHg]






Total cholesterol [mg/dl]






Triglyceride [mg/dl]






HDLcholesterol [mg/dl]






Fasting plasma glucose concentrations [mg/dl]






HbA1c [%]












baPWV [cm/sec]






CPITN score






Average probing depth [mm]






Gingival bleeding index [%]






Prevalence of periodontal disease***[%]






Prevalence of advanced periodontal disease***[%]






Prevalence of severe periodontal disease***[%]






Number of teeth






† BMI: body mass index, HDL: high-density lipoprotein, HbA1c: hemoglobin A1c, baPWV: brachial-ankle pulse wave velocity, CPITN: Community Periodontal Index of Treatment Needs

* p value < 0.05

**Atherosclerosis is defined as baPWV 1400 (cm/sec)

*** Periodontal disease, advanced periodontal disease and severe periodontal disease are defined by CPITN scores of 1, 3 and 4, respectively.

The results of logistic regression are shown in Tables 2 and 3. The unadjusted ORs of atherosclerosis relating to the CPITN score, average probing depth and gingival bleeding index were 1.41 [1.16–1.73], 1.77 [1.35–2.32] and 2.03 [1.04–3.95], respectively (Table 2). However, after adjustment for age, no significant risk levels were found in CPITN score, average probing depth and gingival bleeding index (Ors = 0.98 [0.77–1.25], 1.09 [0.80–1.47] and 1.01 [0.46–2.19], respectively). In addition, after adjustment for age, SBP and pack-years were less than 1.0 (0.91 [0.68–1.20], 0.99 [0.70–1.38] and 0.71 [0.28–1.79], respectively). Age, SBP and pack-years were the major confounding factors for baPWV.
Table 2

Odds ratios of atherosclerosis and their 95% CI-related indices of periodontal disease (CPITN score, average probing depth and gingival bleeding index) before and after adjustment for the confounding factor of baPWV



Adjusted for age

Adjusted for age and SBP

Adjusted for age, SBP and pack-years

CPITN† score

1.41* [1.16–1.73]

0.98 [0.77–1.25]

0.86 [0.65–1.13]

0.91 [0.68–1.20]

Average probing depth

1.77* [1.35–2.32]

1.09 [0.80–1.47]

0.92 [0.66–1.28]

0.99 [0.70–1.38]

Gingival bleeding index

2.03* [1.04–3.95]

1.01 [0.46–2.19]

0.61 [0.25–1.50]

0.71 [0.28–1.79]

SBP: systolic blood pressure, CPITN: Community Periodontal Index of Treatment Needs, baPMV: brachial-ankle pulse wave velocity

* p value < 0.05

Atherosclerosis is defined as baPWV 1400 (cm/sec).

Table 3

Odds ratios of atherosclerosis and their 95% CI when categorized by indices of periodontal disease (CPITN score, average probing depth and gingival bleeding index) before and after adjustment for age, systolic blood pressure and pack-years



Adjusted for age, SBP, pack-years

Periodontal disease (CPITN score 1)

1.51 [0.71–3.19]

0.50 [0.18–1.42]

Advanced periodontal disease (CPITN score 3)

2.58* [1.56–4.26]

0.58 [0.26–1.29]

Severe periodontal disease (CPITN score = 4)

2.46* [1.30–4.64]

1.13 [0.50–2.53]

Average probing depth 2 mm

2.06 [0.81–5.28]

0.42 [0.12–1.53]

Average probing depth 3 mm

2.62* [1.61–4.28]

1.02 [0.52–1.99]

Average probing depth 4 mm

3.19 * [1.66–6.13]

1.34 [0.59–3.04]

Gingival bleeding index 25%

1.34 [0.82–2.09]

0.64 [0.33–1.26]

Gingival bleeding index 50%

1.59 [0.99–2.55]

0.81 [0.43–1.53]

Gingival bleeding index 75%

1.73* [1.04–3.09]

1.14 [0.56–2.29]

† SBP: systolic blood pressure, CPITN: Community Periodontal Index of Treatment Needs

* p value < 0.05

Atherosclerosis is defined as baPWV 1400 (cm/sec).

The results showed that mild periodontal disease tended to have a weaker relationship with atherosclerosis than did severe periodontal disease (Table 3). The adjusted OR for men with a CPITN score of 0–3 compared with men with a CPITN score of 4 was 1.13 [0.50–2.53]. Similarly, the OR for a CPITN score of 0–2 versus a CPITN score of = 3–4 was 0.58 [0.26–1.29]. The OR for men with a CPITN score of 0 versus a CPITN score of 1–4 was 0.50 [0.18–1.42]. This trend was observed not only for CPITN score but also for the average probing depth and gingival bleeding index (average probing depth: 1.34 (0–3 vs. 4), 1.02 (0–2 vs. 3–4), 0.42 (0 vs. 1–4); gingival bleeding index: 1.14, 0.81, 0.64).


Despite the existence of many reports, the relationship between periodontal disease and atherosclerosis has not been fully elucidated. Because the absence of a standard definition and measures for periodontal disease complicate the interpretation of results, as do potential confounding risk factors that are common to both conditions, we have no basis for comparison [29]. In the fairly recent past, a report was published quantifying and comparing the severity of periodontal disease and coronary-artery calcification [30]. However, that report referred only to the coronary artery, and calcification is a poor marker of atherosclerosis. Therefore, an assessment of the progress of periodontal disease and atherosclerosis has been necessary.

We used three indices of periodontal disease: CPITN score, average probing depth and gingival bleeding index. Average probing depth is similar to AL. Although AL accurately indicates gum recession and is the best index of periodontal disease, its measurement is very time-consuming. On the other hand, it takes just 3 minutes per person to measure the average probing depth. Our investigation showed the same trend as the report that used AL (Beck's study) [31]. The CPITN score is the global standard measurement, and the method for determining this score has already been established. Within the past 20 years, the CPITN score has become widely accepted as the method of choice for epidemiological and screening studies for periodontal disease [2628]. The gingival bleeding index indicates inflammation in the mouth, which is the major symptom of periodontal disease. We adopted baPWV as the index for atherosclerosis. BaPWV is influenced mainly by age and systolic blood pressure. In our study, we adjusted for these confounding factors. A benefit of baPWV is that it is non-invasive and easy to measure. Therefore, CPITN score and baPWV can be the standard assessment tools of periodontal disease and atherosclerosis.

In our study, before adjustment, the indices of periodontal disease showed a relationship with atherosclerosis. The ORs of atherosclerosis related to the three indices of periodontal disease were more than 1, and their p values were less than 0.05, which agrees with reports and hypotheses that are currently in existence [19, 2934]. However, after adjustments for age, these relationships were not shown (Tables 2 and 3). The ORs of atherosclerosis relating to CPITN score, average probing depth and gingival bleeding index were 0.98 [0.77–1.25], 1.09 [0.80–1.47] and 1.01 [0.46–2.19], respectively. Therefore, due to the relationship between these three indices and baPWV, we found no association between periodontal disease and atherosclerosis. Hujoel et al. reported that, after adjustment for known cardiovascular risk factors, gingivitis was not associated with CHD (hazard ratio (HR): 1.05, 95% CI: 0.88–1.26) in 2000 [32], and the confirmed elimination of chronic dental infections did not lead to a decreased risk of a CHD event (RR: 1.02, 95% CI: 0.86–1.21) in 2001 [35]. They also reported that the presence of periodontitis and gingivitis did not increase CHD risk among these at-risk individuals (HR: 0.97, 95% CI: 0.72–1.31; HR: 1.09, 95%CI: 0.79–1.50, respectively) in 2002 [36]. In addition, some reports have suggested that periodontal disease is not associated with CHD [3739]. Therefore, periodontal disease is probably not associated with atherosclerosis to any large extent, if at all.

We examined the presence of a monotonic dose-response association in three ways (Table 3). With adjustment for age, SBP and pack-year, severe periodontal disease was statistically different from non-cases, but moderate periodontal disease was not. The adjusted ORs of atherosclerosis relating to periodontal disease, advanced periodontal disease and severe periodontal disease were 0.50, 0.58 and 1.13, respectively. Dose response was observed not only in periodontal disease but also in the average probing depth and gingival bleeding index. Beck et al. reported a similar trend [33].

There were several limitations to our study. First, the number of subjects was relatively small, and the results of this study need to be assessed in a larger sample size. However, the sample size was small because the strength of the relationship that we observed was weaker than the relationship that we had assumed from the previous studies. Second, our cross-sectional study design lacked information on the time sequence of events and so did not permit identification of the causal relationship. To investigate this relationship, it will be necessary to follow this cohort. Finally, the problem of imperfect measurement of confounders can exist. However, it is not a serious problem because adjustments were made for the major confounders. For example, the adjustment for smoking intensity is very important. Hujoel pointed out that the studies that either did not adjust or adjusted poorly for smoking showed a positive chronic periodontitis (CP)-CHD association, while the results of studies controlling for smoking suggested that CP was either not at all or weakly associated with CHD [37]. In addition, he suggested that the lack of rigorous control for smoking history was a plausible explanation for the studies that reported significant CP-CHD associations. In our study, we evaluated an integrated smoking dose as pack-years. After the appropriate adjustment including smoking intensity, we can conclude that mild periodontal disease is not associated with atherosclerosis, which is in agreement with other studies.


In conclusion, we found no relationship between mild periodontal disease and atherosclerosis after appropriate adjustments from this cross-sectional study.


Authors’ Affiliations

Department of Preventive Medicine and Public Health, School of Medicine, Keio University
Department of Molecular Epidemiology, Medical Research Institute, Tokyo Medical & Dental University
Department of Preventive Medicine/Biostatistics and Medical Decision Making, Nagoya University Graduate School of Medicine
Section of General Dentistry, Department of General Dentistry, Fukuoka Dental College
Japan Council for Quality Health Care
Department of Health Informatics, Kyoto University School of Public Health


  1. Okuda K, Kato T, Ishihara K: Involvement of periodontopathic biofilm in vascular diseases. Oral Diseases. 2004, 10: 5-12. 10.1046/j.1354-523X.2003.00979.x.View ArticlePubMedGoogle Scholar
  2. Kuramitsu HK: Periodontopathic bacteria and their potential involvement in atherosclerosis. Int J Oral-Med Sci. 2002, 1: 1-9.View ArticleGoogle Scholar
  3. Pussinen PJ, Vilkuna-Rautiainen T, Alfthan G, Palosuo T, Jauhiainen M, Sundvall J, Vesanen M, Mattila K, Asikainen S: Severe periodontitis enhances macrophage activation via increased serum lipopolysaccharide. Arterioscler Thromb Vasc Biol. 2004, 24: 2174-80. 10.1161/01.ATV.0000145979.82184.9f.View ArticlePubMedGoogle Scholar
  4. Amar S, Gokce N, Morgan S, Loukideli M, Van Dyke TE, Vita JA: Periodontal disease is associated with brachial artery endothelial dysfunction and systemic inflammation. Arterioscler Thromb Vasc Biol. 2003, 23: 1245-9. 10.1161/01.ATV.0000078603.90302.4A.View ArticlePubMedGoogle Scholar
  5. Mendez MV, Scott T, LaMorte W, Vokonas P, Menzoian JO, Garcia R: An association between periodontal disease and peripheral vascular disease. Am J Surg. 1998, 176: 153-7. 10.1016/S0002-9610(98)00158-5.View ArticlePubMedGoogle Scholar
  6. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S: Periodontal disease and cardiovascular disease. J Periodontol. 1996, 67 (Suppl): 1123-37.View ArticlePubMedGoogle Scholar
  7. DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM: Dental disease and risk of coronary heart disease and mortality. BMJ. 1993, 306: 688-91.View ArticlePubMedPubMed CentralGoogle Scholar
  8. Arbes SJ, Slade GD, Beck JD: Association between extent of periodontal attachment loss and self-reported history of heart attack : an analysis of NHANES III Deta. Dent Res. 1999, 78: 1777-82.View ArticleGoogle Scholar
  9. Janket SJ, Baird AE, Chuang SK, Jones JA: Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2003, 95: 559-69.View ArticlePubMedGoogle Scholar
  10. Ministry of Health, Labour and Welfare: Findings about gums. Dental investigation in Japan in 1999. J Health Welfare Statist. 2000, 47: 42-9.Google Scholar
  11. Ministry of Health, Labour and Welfare: Dental report in Fujinomiya City. 2000, []Google Scholar
  12. WHO Scientific Group on Epidemiology, Etiology and Prevention of Periodontal Diseases: WHO Technical Report Series, No. 621. 1978, Geneva, World Health Organization, 7-9.
  13. Asmar R, Benetos A, Topouchian J, Laurent P, Pannier B, Brisac AM, Target R, Levy BI: Assessment of arterial distensibility by automatic pulse wave velocity measurement: validation and clinical application studies. Hypertension. 1995, 26: 485-90.View ArticlePubMedGoogle Scholar
  14. Lehmann ED: Clinical value of aortic pulse-wave velocity measurement. Lancet. 1999, 354: 528-9. 10.1016/S0140-6736(99)00179-8.View ArticlePubMedGoogle Scholar
  15. Nakamura U, Iwase M, Nohara S, Kanai H, Ichikawa K, Iida M: Usefulness of brachial-ankle pulse wave velocity measurement: correlation with abdominal aortic calcification. Hypertens Res. 2003, 26: 163-7. 10.1291/hypres.26.163.View ArticlePubMedGoogle Scholar
  16. Yamashina A, Tomiyama H, Arai T, Hirose K, Koji Y, Hirayama Y, Yamamoto Y, Hori S: Brachial-ankle pulse wave velocity as a marker of atherosclerotic vascular damage and cardiovascular risk. Hypertens Res. 2003, 26: 615-22. 10.1291/hypres.26.615.View ArticlePubMedGoogle Scholar
  17. Sawabe M, Takahashi R, Matsushita S, Ozawa T, Arai T, Hamamatsu A, Nakahara K, Chida K, Yamanouchi H, Murayama S, Tanaka N: Aortic pulse wave velocity and the degree of atherosclerosis in the elderly: a pathological study based on 304 autopsy cases. Atherosclerosis. 2005, 179: 345-51. 10.1016/j.atherosclerosis.2004.09.023.View ArticlePubMedGoogle Scholar
  18. Lim HE, Park CG, Shin SH, Ahn JC, Seo HS, Oh DJ: Aortic pulse wave velocity as an independent marker of coronary artery disease. Blood Press. 2004, 13: 369-75. 10.1080/08037050410004800.View ArticlePubMedGoogle Scholar
  19. Blacher J, Guerin AP, Pannier B, Marchais SJ, Safar ME, London GM: Impact of aortic stiffness on survival in end-stage renal disease. Circulation. 1999, 99: 1434-9.View ArticleGoogle Scholar
  20. Laurent S, Boutouyrie P, Asmar R, Gautier I, Laloux B, Guize L, Ducimetiere P, Benetos A: Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension. 2001, 37: 1236-41.View ArticlePubMedGoogle Scholar
  21. Shokawa T, Imazu M, Yamamoto H, Toyofuku M, Tasaki N, Okimoto T, Yamane K, Kohno N: Pulse wave velocity predicts cardiovascular mortality: findings from the Hawaii-Los Angeles-Hiroshima study. Circ J. 2005, 69: 259-64. 10.1253/circj.69.259.View ArticlePubMedGoogle Scholar
  22. Yamashina A, Tomiyama H, Takeda K, Tsuda H, Arai T, Hirose K, Koji Y, Hori S, Yamamoto Y: Validity, reproducibility, and clinical significance of noninvasive brachial-ankle pulse wave velocity measurement. Hypertens Res. 2002, 25: 359-64. 10.1291/hypres.25.359.View ArticlePubMedGoogle Scholar
  23. Imanishi R, Seto S, Toda G, Yoshida M, Ohtsuru A, Koide Y, Baba T, Yano K: High brachial-ankle pulse wave velocity is an independent predictor of the presence of coronary artery disease in men. Hypertens Res. 2004, 27: 71-8. 10.1291/hypres.27.71.View ArticlePubMedGoogle Scholar
  24. Sakuragi S, Iwasaki J, Tokunaga N, Hiramatsu S, Ohe T: Aortic stiffness is an independent predictor of left ventricular function in patients with coronary heart disease. Cardiology. 2005, 103: 107-12. 10.1159/000082472.View ArticlePubMedGoogle Scholar
  25. Ramfjord SP: The periodontal disease index (PDI). J Periodontol. 1967, 38 (Suppl): 602-10.View ArticlePubMedGoogle Scholar
  26. Strohmenger L, Cerati M, Brambilla E, Malerba A, Vogel G: Periodontal epidemiology in Italy by CPITN. Int Dental J. 1991, 41: 313-5.Google Scholar
  27. Miyazaki H, Pilot T, Lederq M: Periodontal profiles: an overview of CPITN data in the WHO global oral data bank for age groups 15–19 years, 35–44 years. 1992, Geneva, World Health OrganizationGoogle Scholar
  28. Khamrco TY: Assessment of periodontal diseases using the CPITN index in a rural population in Ninevah, Iraq. East Mediterr Health J. 1999, 5: 549-55.PubMedGoogle Scholar
  29. Scannapieco FA, Bush RB, Paju S: Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, andstroke. A systemic review. Ann Periodontol. 2003, 8: 38-53. 10.1902/annals.2003.8.1.38.View ArticlePubMedGoogle Scholar
  30. Nakib SA, Pankow JS, Beck JD: Periodontitis and coronary artery calcification – the atherosclerosis risk in communities (ARIC) Study. J Periodontol. 2004, 75: 505-10. 10.1902/jop.2004.75.4.505.View ArticlePubMedGoogle Scholar
  31. Beck JD, Elter JR, Heiss G, Couper D, Mauriello SM, Offenbacher S: Relationship of periodontal disease to carotid artery intima-media wall thickness : the atherosclerosis risk in communities (ARIC) Study. Arterioscler Thromb Vasc Biol. 2001, 21: 1816-22.View ArticlePubMedGoogle Scholar
  32. Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA: Periodontal disease and coronary heart disease risk. JAMA. 2000, 284: 1406-10. 10.1001/jama.284.11.1406.View ArticlePubMedGoogle Scholar
  33. Beck JD, Pankow J, Tyroler HA, Offenbacher S: Dental infections and atherosclerosis. Am Heart J. 1999, 138: S528-33. 10.1016/S0002-8703(99)70293-0.View ArticlePubMedGoogle Scholar
  34. Mattila KJ, Pussinen PJ, Paju S: Dental infections and cardiovascular diseases: a review. J Periodontol. 2005, 76 (11 Suppl): 2085-8. 10.1902/jop.2005.76.11-S.2085.View ArticlePubMedGoogle Scholar
  35. Hujoel PP, Drangsholt M, Spiekerman C, Deroen TA: Examining the link between coronary heart disease and the elimination of chronic dental infections. J Am Dent Assoc. 2001, 132 (7): 883-9.View ArticlePubMedGoogle Scholar
  36. Hujoel PP, Drangsholt M, Spiekerman C, Deroen TA: Pre-existing cardiovascular disease and periodontitis: a follow-up study. J Dent Res. 2002, 81 (3): 186-91.View ArticlePubMedGoogle Scholar
  37. Hujoel PP: Does chronic periodontitis cause coronary heart disease? A review of the literature. J Am Dent Assoc. 2002, 133 (Suppl): 31S-36S.View ArticlePubMedGoogle Scholar
  38. Howell TH, Ridker PM, Ajani UA, Hennekens CH, Christen WG: Periodontal disease and risk of subsequent cardiovascular disease in U.S. male physicians. J Am Coll Cardiol. 2001, 37: 445-50. 10.1016/S0735-1097(00)01130-X.View ArticlePubMedGoogle Scholar
  39. Joshipura KJ, Rimm EB, Douglass CW, Trichopoulos D, Ascherio A, Willett WC: Poor oral health and coronary heart disease. J Dent Res. 1996, 75 (9): 1631-6.View ArticlePubMedGoogle Scholar
  40. Pre-publication history

    1. The pre-publication history for this paper can be accessed here:


© Miyaki et al; licensee BioMed Central Ltd. 2006

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.