Periodontitis, epicardial adipose tissue and coronary events: the Swedish Cardiopulmonary Bioimage Study

In the relationship between periodontitis and coronary heart disease (CHD), the mechanistic role of subclinical atherosclerosis remains incompletely understood. This study examines whether subclinical atherosclerosis mediates the periodontitis-incident CHD association; how a specific periodontitis phenotype modifies subclinical coronary atherosclerosis; and whether periodontitis is associated with epicardial adipose tissue (EAT) attenuation as a marker of inflammation.

Data from the Swedish CArdioPulmonary bioImage Study (SCAPIS) were linked to national registers for dental data and CHD incidence. Coronary atherosclerosis was quantified using coronary artery calcium scores (CACS) and segment involvement scores (SIS). EAT characteristics were derived from non-contrast cardiac computed tomography. Associations between severe periodontitis and incident CHD events were examined using multivariable regression models, and mediation by CACS and SIS was explored.

Among 29 056 SCAPIS participants, severe periodontitis was present in 6% (n = 1809) and was associated with severe CACS [≥301, odds ratio (OR) 1.69, 95% confidence interval (CI) 1.39-2.06] and severe SIS (>4 segments, OR 1.40, 95% CI 1.17-1.67), with the strongest associations among individuals without concomitant dental caries. Moreover, periodontitis was associated with lower EAT attenuation (β = -0.27 HU, 95% CI -0.48 to -0.05) and a 42% higher risk of incident CHD events (hazard ratio 1.42, 95% CI 1.03-1.97), which was partially mediated by coronary atherosclerosis.

Severe periodontitis is positively associated with subclinical coronary atherosclerosis, EAT alterations reflecting inflammatory activity, and CHD event incidence. These results position periodontitis as a marker of increased coronary risk, warranting targeted cardiovascular risk assessment.