The present study aimed to investigate the link between the severity of periodontal disease (PD), coronary calcifications and unstable plaque features in patients who underwent coronary computed tomography for unstable angina (UA). Fifty-two patients with UA, included in the ATHERODENT trial (NCT03395041), underwent computed tomographic coronary angiography (CCTA) and dental examination. Based on the median value of the periodontal index (PI), patients were assigned to the low periodontal index (LPI) group (PI < 22) and a high periodontal index (HPI) group (PI > 22). Patients with HPI had higher plaque volume (p = 0.013) and noncalcified plaque volume (p = 0.0003) at CCTA. In addition, the presence of vulnerability features in the atheromatous plaques was significantly correlated with PI (p = 0.001). Among periodontal indices, loss of gingival attachment (p = 0.009) and papillary bleeding index (p = 0.002) were strongly associated with high-risk plaques. PI significantly correlated with coronary calcium score (r = 0.45, p = 0.0008), but not with traditional markers of subclinical atherosclerosis. Overall, this subgroup analysis of the ATHERODENT study indicates that patients with advanced PD and UA present a higher amount of calcium in the coronary tree and have a more vulnerable phenotype of their culprit plaques.

Both periodontal disease and atherosclerosis are chronic disorders with an inflammatory substrate that leads to alteration of the host’s immune response. In PD, inflammation is responsible for bone tissue destruction, while in atherosclerosis, it leads to atheromatous plaque formation. These modifications result from the action of pro-inflammatory cytokines that are secreted both locally at gingival or coronary sites, and systemically. Recently, it was observed that in patients with PD or with cardiovascular disease, COVID-19 infection is prone to be more severe. While the association between PD, inflammation and cardiovascular disease is well-known, the impact of COVID-19-related inflammation on the systemic complications of these conditions has not been established yet. The purpose of this review is to bring light upon the latest advances in understanding the link between periodontal–cardiovascular diseases and COVID-19 infection.

The present study aimed to investigate the association between apolipoprotein B (Apo B) and classical features associated with clinical or subclinical atherosclerosis. A total of 811 adult patients from the general Romanian population, included in the national SEPHAR registry on hypertension, were divided into two groups based on Apo B value (low versus high Apo B with a cut-off established at 130 mg/dL) and subsequently into four subgroups according to the cut-offs recommended by the 2021 ESC Guidelines on Cardiovascular Disease Prevention. In all patients, lipid profile, uric acid, full blood count and presence of significant carotid plaques were assessed. Apo B levels were positively correlated with proatherogenic lipids (total cholesterol, triglycerides and LDL-cholesterol, p < 0.0001) and negatively correlated with HDL cholesterol (all p < 0.05). In comparison with patients with low Apo B levels, those with elevated Apo B levels more frequently presented significant carotid plaques (17% vs. 19% vs. 28% vs. 46%, p < 0.0001). Univariate regression analysis identified a strong association between the level of uric acid and increased value of Apo B in the four subgroups (uric acid 4.8 +/− 1.3 vs. 5 +/− 1.6 vs. 5.1 +/− 1.5 vs. 5.8 +/− 1.6, r = 0.2, p < 0.0001). The results of this nationwide registry on hypertension in Romania indicate that high Apo B may be considered as a risk factor for CVD, promoting atherosclerosis and associated with increased expression of classical markers of clinical or subclinical CVD.