Poor Oral Hygiene, Infections in Kids May Promote Atherosclerosis in Adulthood

May 01, 2019

Children with evidence of oral infections, including cavities and bleeding gums, were significantly likely to be in the top tier for carotid intima-media thickness (IMT) measured more than 25 years later in an analysis based on the prospective Cardiovascular Risk in Young Finns Study cohort.

Signs of oral infection in kids were also significantly associated with conventional cardiovascular (CV) risk factors, like elevated blood pressure and body mass index (BMI).

Still, they remained independently associated with greater carotid IMT, a marker of subclinical atherosclerosis considered a proxy marker for coronary disease, after adjustment for lifetime exposure to an array of standard CV risk markers, write the authors of the analysis, led by Pirkko J. Pussinen, PhD, University of Helsinki.

"The results show for the first time, to our knowledge, that childhood oral infections may be a modifiable risk factor for adult cardiovascular disease," they say in their report published April 26 in JAMA Network Open.

It would be a leap to conclude from the current data that such infections may cause adult CV disease or that their prevention might reduce CV risk. But it would be consistent with abundant observational and epidemiologic evidence for an association between oral hygiene and CV disease risk.

Periodontitis, for example, has been directly associated with risk for myocardial infarction (MI), coronary heart disease in general, and stroke, and it can promote tooth loss, which is itself associated with CV disease in epidemiologic studies, Pussinen observed for theheart.org | Medscape Cardiology.

"But all these studies have been done with adult populations. This is the first study with children. It emphasizes the importance of maintaining good oral health already starting from childhood," he said in an email.

An accompanying editorial proposes several potential explanations for the associations seen in the current analysis. Among them is the possibility that "individuals who have poor oral health as children also have poor oral health as adults," and there is more evidence supporting adult periodontal disease as a promoter of atherogenesis and CV risk.

However, it would be unusually challenging to test the idea in a randomized trial, so the question remains "unresolved," observe editorialists Anwar T. Merchant, DMD, ScD, University of South Carolina, Columbia, and Salim S. Virani, MD, PhD, Baylor College of Medicine, Houston.

They describe several other possible explanations for a link between childhood oral health and carotid IMT as adults, but explain how they seem less likely to have played a role in the current analysis.

For example, it may be because "poor cardiovascular and oral health share common risk factors, such as smoking, poor diet, physical inactivity, or unknown genetic factors predisposing individuals to a hyperinflammatory response." However, Merchant and Virani say, the analysis seems to have adequately controlled for such possible confounders.

The cohort's 755 participants, 51% of whom were female, underwent oral examinations at age 6, 9, or 12 years (mean, 8) and clinical follow-up in 2001 when they were 27, 30, or 33 years of age and/or in 2007 at age 33, 36, or 39, Pussinen and associates report.

Oral examinations included evaluations for bleeding on probing, periodontal-probing pocket depth, dental caries, and dental fillings.

Of the cohort, 5.6% had one of the four markers of oral infection at the baseline evaluation, 17.4% had two, 38.3% had three, 34.1% had all four signs, and 4.5% had no signs. There were no significant differences between boys and girls.

Cardiovascular risk markers (systolic and diastolic pressures, BMI, and blood glucose, triglycerides, and high-density-lipoprotein and low-density-lipoprotein cholesterol) were assessed on five follow-up occasions. High risk for each marker on each of the five occasions was defined as measurement at the 75th percentile or higher; low risk was defined as less than the 75% percentile.

The mean number of high-risk measurements went up significantly with the number of childhood signs of oral infection. For example, at assessments in childhood, it rose from 5.31 for no signs to 7.2 for all four signs (P = .008); in adulthood it rose from 4.9 for no signs to 6.1 for four signs (P = .04); and throughout the entire follow-up it rose from 11.4 for no signs to 14.1 for four signs (P = .01).

Subclinical atherosclerosis as defined by carotid IMT was assessed on two occasions, in 2001 and in 2007, both times in most of the cohort and using the same protocol and reader.

The difference in mean carotid IMT between those who had zero vs four signs of oral infection at baseline was 0.056 mm (P = .004) in 2001 and 0.051 mm (P = .003) in 2007.

In multivariate analysis, periodontal disease at baseline significantly correlated with carotid IMT in adulthood (P = .01), as did dental caries (P = .008) and a presence of both caries and periodontal disease (P = .004).

The relative risk (RR) for increased carotid IMT (that is, third tertile vs tertiles 1 and 2) was 1.87 (95% CI, 1.25 - 2.79) for the presence of any of the four signs of oral infection in childhood when adjusted for CV risk markers. The RR for the presence of all four signs was 1.95 (95% CI, 1.28 - 3.00).

Carotid IMT is a marker for generalized atherosclerosis and is thought to correlate with the development of coronary disease. Pussinen said the cohort, now 45 to 50 years of age, continues to be followed, so "perhaps later we will know more" about how their carotid IMT relates to development of CV disease.

Pussinen reported no conflicts. Disclosures for the other authors are in the report. Merchant and Virani reported no relevant conflicts.

JAMA Netw Open. 2019;2:e192523 and e192489. Full text, Editorial

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