Conclusion: Oral hygiene and tooth loss are associated with increased levels of carotid stenosis and predict future progression of carotid artery atherosclerosis. Summary: There may be a link between periodontal and dental disease and atherosclerosis. It is suggested that chronic inflammation triggered by periodontitis plays a role in the etiology of atherosclerosis. In this study, the authors studied a subset of patients from the Inflammation and Carotid Artery Risk for Atherosclerosis study. This is a prospective study involving serial ultrasound assessments of patients likely to have clinically relevant atherosclerosis of the carotid artery. For the current study, 411 patients were randomly selected from the 1268 participants in the Inflammation and Carotid Artery Risk for Atherosclerosis study. Patients were evaluated for dental and periodontal status and oral hygiene at study entrance using three World Health Organization validated indices: DMFT (decayed, missing, filled teeth), SLI (Silness-Lowe index), and CPITN (community periodontal index for treatment needs), respectively. Carotid duplex ultrasound was used to measure carotid stenosis at baseline and after a median of 7.5 months (range, 6 to 9 months). DMFT (P < .01), SLI (P = .048), CPITN (P = .007), and edentulousness (P = .007) all were associated with baseline levels of carotid stenosis. During this study period, progression of carotid stenosis was noted in 48 of 411 patients (11.7%). Adjusted odds ratios were 1.11 (95% confidence interval [CI], 1.01 to 1.22, P = .032) for DMFT, 1.77 (95% CI, 1.09 to 2.79) for SLI, and 1.51 (95% CI, 0.89 to 2.45, P = 0.16) for CPITN. DMFT and SLI predicted disease progression independent of cardiovascular risk factors and baseline degree of stenosis. Edentulous patients also had a higher risk for disease progression compared with patients with teeth (adjusted odds ratio, 2.10; 95% CI, 106 to 4.16; P = .033). Comment: The role of dental and periodontal disease in atherosclerosis is controversial. There are many possible explanations for an observed association between dental disease and atherosclerosis, and unmeasured cofounders like socioeconomics status may modify observed associations. It may be that dental disease merely serves as an added inflammatory component to an already inflammatory vascular disease or that transient bacteriemia associated with poor dental hygiene affects the development of atherosclerotic plaques. Speculation with regard to the role of dental disease and the etiology of atherosclerosis will continue. There are so many potential known and unknown confounding variables that it is very unlikely this question will ever be settled to anyone’s satisfaction.