Periodontitis is a common multifactorial disease characterized by clinical attachment loss and bone loss and may result in tooth loss, if not treated effectively.1 Periodontitis occurs in most age groups, but it is most prevalent among adults over the age of 30, affecting 42% of the US adult population, of which 7% have severe periodontitis.2 Over the last 40-years, numerous studies have demonstrated an association between periodontal disease and several chronic diseases.3-5 These studies have reported an association among periodontal disease and diabetes mellitus, osteoporosis, rheumatoid arthritis, chronic obstructive pulmonary disease, and cardiovascular diseases (CVDs).6,-8 Several case-control and cross-sectional studies have discussed the relationship between periodontal diseases and coronary heart disease (CHD).9,-11 These studies indicated that patients with periodontitis have a 1.14 times higher relative risk of developing coronary heart disease and a 25% increased risk compared with control subjects.11, 12 In addition, several studies have suggested that atherosclerosis may be exacerbated by periodontitis. 13-15
Chronic periodontal infections may stimulate endothelial dysfunction through systemic inflammation that is exacerbated by elevated levels of interleukin-6 and fibrinogen. Moreover, bacterial products from Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, including gingipains and soluble bacterial components, can induce endothelial dysfunction.16 Inflammation plays a role in the entire pathogenesis with atherosclerosis, starting from the expression of the endothelial adhesion molecules, including intercellular adhesion molecule I and vascular cell adhesion molecule I. These molecules are expressed in response to soluble inflammatory mediators, such as interleukin 1 and 6, in the bloodstream, leading to endothelial permeability, leukocyte migration, and adhesion. Fatty streaks and calcifications become phagocytosed within macrophages, resulting in the increasing release of pro-inflammatory cytokines (e.g., interleukin-1, interleukin-6 and tumor necrosis factor alpha). The disintegrated endothelial layer leads to the production of thrombin from prothrombin and the formation of fibrin to fibrinogen that can result in thrombosis and, consequently, to cerebrovascular accidents or myocardial infarction.7, 17 According to a polymerase chain reaction study on samples taken from carotid endarterectomies, 44% of atheromas were found positive for at least one periodontal bacteria and P. gingivalis and Tannerella forsythia were observed in 26% and 30%, respectively, of the surgical specimens. These periodontal pathogens are strongly related to bleeding on probing and deep pocket depths.10, 18 Extracranial carotid artery calcifications (ECACs) may be visualized in panoramic radiographs beneath the mandibular angle proximal to the cervical vertebrae at the C3 and C4 levels. These calcifications were detected among 10% to 12% of male patients and 10% to 16% of female patients, either unilaterally or bilaterally.19 Regarding the accuracy of panoramic radiographs for detection of ECACs, one study compared ultrasonography with conventional panoramic radiographs. The authors found that the panoramic radiographs had a sensitivity of 66.6%, and a positive predictive value of 45% was found for the detection of carotid artery calcifications in patients whose angiograms confirmed the presence of coronary artery disease and a sensitivity of 50% in patients with a normal angiogram.20 However, the sensitivity and specificity reached 76% and 98% in digital panoramic X-rays, respectively, in the portrayal of carotid artery calcifications.21 In addition, a statistically significant association was found between the presence of ECACs in panoramic radiographs and the percentage of alveolar bone loss in patients with periodontitis.19
Intracranial carotid artery calcifications (ICACs) are one type of calcification that may be detected as incidental findings in cone-beam computed tomography (CBCT). A cross-sectional study by Khosropanah and co-workers compared the prevalence of intracranial and extracranial artery calcifications in 705 CBCT scans. They reported that more than 60% of the scans were positive for ICACs and 39.9% were positive for ECACs. The findings also showed that there was a correlation between ICACs and ECACs 22 and another study by de Weert reported that ICACs were independently associated with smoking, hypercholesterolemia, and history of cardiac and/or ischemic cerebrovascular diseases.23 A dental practitioner who prescribes CBCT imaging is responsible for the interpretation of the entire scanned volume. This interpretation is based on a thorough knowledge of the anatomical structures, variations, and abnormalities on radiographic images. It is crucial to examine the entire volume systematically, which may include paranasal sinuses, airway spaces, the base of the skull, the cervical spine, and temporomandibular joints. To the best of the current authors’ knowledge, no research has examined the association between internal carotid artery calcifications and periodontitis. Therefore, this retrospective study aimed to examine the prevalence of ICACs on CBCT images and their associations among age, gender, chronic periodontitis, and patient-reported CVDs.
From an article published in the Journal of Periodontology.