Changes in Clinical and Microbiological Periodontal Profiles Relate to Progression of Carotid Intima‐Media Thickness: The Oral Infections and Vascular Disease Epidemiology Study
- Moïse Desvarieux, MD, PhD⇑;
- Ryan T. Demmer, PhD, MPH;
- David R. Jacobs, PhD;
- Panos N. Papapanou, DDS, PhD;
- Ralph L. Sacco, MD, MS;
- Tatjana Rundek, MD, PhD
- 1Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY (M.D., R.T.D.)
- 2INSERM U738 Paris,
- 3École des Hautes Études en Santé Publique, Rennes, France (M.D.)
- 4Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN (D.R.J.)
- 5Department of Nutrition, University of Oslo, Oslo, Norway (D.R.J.)
- 6Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, Columbia University, New York, NY (P.N.P.)
- 7Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL (R.L.S., T.R.)
- Correspondence to:
Moïse Desvarieux, MD, PhD, Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 W 168th Street, Room 525, New York, NY 10032. E‐mail:
Background No prospective studies exist on the relationship between change in periodontal clinical and microbiological status and progression of carotid atherosclerosis.
Methods and Results The Oral Infections and Vascular Disease Epidemiology Study examined 420 participants at baseline (68±8 years old) and follow‐up. Over a 3‐year median follow‐up time, clinical probing depth (PD) measurements were made at 75 766 periodontal sites, and 5008 subgingival samples were collected from dentate participants (average of 7 samples/subject per visit over 2 visits) and quantitatively assessed for 11 known periodontal bacterial species by DNA‐DNA checkerboard hybridization. Common carotid artery intima‐medial thickness (CCA‐IMT) was measured using high‐resolution ultrasound. In 2 separate analyses, change in periodontal status (follow‐up to baseline), defined as (1) longitudinal change in the extent of sites with a ≥3‐mm probing depth (Δ%PD≥3) and (2) longitudinal change in the relative predominance of bacteria causative of periodontal disease over other bacteria in the subgingival plaque (Δetiologic dominance), was regressed on longitudinal CCA‐IMT progression adjusting for age, sex, race/ethnicity, diabetes, smoking status, education, body mass index, systolic blood pressure, and low‐density lipoprotein cholesterol and high‐density lipoprotein cholesterol. Mean (SE) CCA‐IMT increased during follow‐up by 0.139±0.008 mm. Longitudinal IMT progression attenuated with improvement in clinical or microbial periodontal status. Mean CCA‐IMT progression varied inversely across quartiles of longitudinal improvement in clinical periodontal status (Δ%PD≥3) by 0.18 (0.02), 0.16 (0.01), 0.14 (0.01), and 0.07 (0.01) mm (P for trend<0.0001). Likewise, mean CCA‐IMT increased by 0.20 (0.02), 0.18 (0.02), 0.15 (0.02), and 0.12 (0.02) mm (P<0.0001) across quartiles of longitudinal improvement in periodontal microbial status (Δetiologic dominance).
Conclusion Longitudinal improvement in clinical and microbial periodontal status is related to a decreased rate of carotid artery IMT progression at 3‐year average follow‐up.
- Received April 28, 2013.
- Accepted August 16, 2013.
- © 2013 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
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