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Localized Oral Infections and Systemic
Inflammation: The Oral Infections and
Vascular Disease Epidemiology Study
Ryan Demmer, MPH
Pre-doctoral Fellow
Division of Epidemiology, School of Public Health
University of Minnesota
No disclosures to make
Coauthors:
Moïse Desvarieux, MD, PhD
Panos Papapanou, DDS, PhD
Bernadette Boden-Albala, DrPH, MPH
David Jacobs, PhD
Ralph Sacco, MD, MS
Scientific Question:
How might infection influence
atherosclerosis?
Are current local oral infections
associated with elevated markers of
systemic inflammation?
METHODS
INVEST Design
• Prospective cohort study
investigating the relationship
between oral infection and
atherosclerotic progression
• Cross-sectional results presented
here
– Addressing potential mechanism by
which infections and atherosclerosis
might be related
Methods:
INVEST Eligibility
• Hispanic, Black or White
• Age 55 or older
• No baseline history of stroke, MI, or other
chronic inflammatory conditions
• Living in a defined geographic area of
Northern Manhattan
• Ability to come to clinic for in-person
assessment
Methods:
Clinical Oral Examination
• Pocket (probing) depth (PD) measures
were made at six locations per tooth using
a UNC-15 manual probe
– Measured in mm
– Measured in up to 192 sites per mouth
• PD is a strong correlate of current
infection
probe
Methods:
Summary Exposure Definition
• Periodontal disease is defined by
severity and extent of infection
• Severity (depth of pocket)
– 4 mm selected as cutpoint
• Extent (# or % of infected sites per
mouth)
Methods:
Summary Exposure Definition
• Number of sites per mouth with PD ≥
4 mm
– Burden of infection
• Percent of sites per mouth with PD ≥
4 mm
– Intensity of infection
Methods:
White Blood Cell Count (WBC)
• Fasting blood samples
• Whole blood collected in 5-cm3 EDTA-
anticoagulated tubes
• White Blood Cell Count (WBC) (# cells x
109/L) assessed with automated cell
counter using standardized laboratory
techniques
– Coulter STK-R and Coulter STK-S, Coulter Electronics, and Sysmex SE-9500,
TOA Medical Electronics
Methods: Risk Factor Assessment
(The following conventional CVD risk factors were
included in adjusted analyses)
• In person interviews
– Age on last birthday
– Race/ethnicity
– Smoking (current, former or never)
• pack-years added no additional information
– Gender
– Education (completed high school)
• Diabetes (yes/no via interview)
– Or fasting glucose > 126
• Blood pressure (continuous mm Hg)
– Assessed in person by trained research
assistants
Results
General Characteristics
n = 911
Variable % Variable Mean +/- SD
Female 60% Age 66 ± 8
Race/Ethnicity # missing teeth 14 ± 8
Hispanic 63% SBP 142 ± 20
Black 21% DBP 81 +/- 12
White 16%
Smoking
Ever 53%
Current 15%
Edentulous 19%
White Blood Cells Distribution
140
120
100
Number of Subjects
80
60
40
20
0
1.
2.
3.
4.
5.
6.
7.
8.
9.
10
11
12
13
14
50
50
50
50
50
50
50
50
50
.5
.5
.5
.5
.5
0
0
0
0
0
White Blood Count (Cells x 10^9/L)
Mean = 6.20 ± 1.90; Median = 5.90
Mean WBC values across quartiles of
% PD≥4 mm: Intensity of infection
n = 911; p for trend across quartiles = 0.27;
p for trend including edentulous = 0.52
6.60
6.40
WB C (cells x 10^9)
6.20
6.00
5.80
5.60
5.40
0% - 2% 3% - 10% 11% - 25% gt 25% edentulous (n =
(n=176) (n=180) (n=195) (n=185) 175)
Unadjusted Percent of sites with PD >= 4mm
Adjusted
Adjusted model includes: age, gender, smoking, diabetes, race/ethn., education and SBP
Mean WBC values across quartiles
of # PD≥4 mm: Burden of infection
n = 911; p for trend across quartiles = 0.25;
p for trend including edentulous = 0.06
6.60
6.40
WBC (cells x 10^9)
6.20
6.00
5.80
5.60
5.40
0 - 2 (n=175) 2 - 8 (n=185) 9 - 26 (n=184) gt 26 (n=188) edentulous
(n=175)
Unadjusted Number of sites with PD >= 4 mm
Adjusted
Adjusted model includes: age, gender, smoking, diabetes, race/ethn., education and SBP
Red line = Mean tooth loss across quartiles
of quartiles of # PD ≥ 4 mm
Unadjusted WBC
Adjusted WBC
# Missing Teeth
6.60 20
18
6.40
16
14
6.20
# M issing Teeth
12
WBC
6.00 10
8
5.80
6
4
5.60
2
5.40 0
0 - 2 (n=175) 2 - 8 (n=185) 9 - 26 (n=184) gt 26 (n=188) edentulous
Number of sites with PD >= 4 mm (n=175)
Adjusted model includes: age, gender, smoking, diabetes, race/ethn., education and SBP
Conclusions
• WBC appears to be positively related to
extent of periodontal infection – although
not in a monotonic fashion
• Relationship between periodontal status
and WBC may be random in these data
– Weak relationship relative to literature
– Relationship may vary with age
• Burden (# of sites) of infection may be
more important than intensity of infection
Limitations
• Cross-sectional
• Use of pocket depth alone as exposure
– misclassification
• No neutrophil data
– Other studies have shown neutrophils to be
explanatory
• CRP, IL-6 and Fibrinogen results
unavailable at this time
Discussion
• Tooth loss may distort overall periodontal
health
• WBC in edentulous difficult to interpret
– Potential for infection is reduced
– History of severe infection likely
• Edentulous have elevated levels of carotid
artery plaque
– After careful adjustment for health behaviors
and other life style factors
– Implication: removal of infection may alleviate
periodontal disease but not eliminate CVD
risk?
Moïse Desvarieux, M.D., Ph.D.
Principal Investigator
• Project Coordinator
– George T. Loo, MPA, MPH
Co-Investigators and Consultants
• Research Assistants
• Columbia University
– Mariana Cukier, DDS
– Panos Papapanou, DDS, PhD
– Palma Gervasi, BA
– Ralph L. Sacco MD, MS
– Giselle Santivanez, BS
– Ira Lamster, DDS, MS
• Core Laboratory (CALM)
• University of Minnesota
– Daniel J. Fink, MD, MPH
– Aaron Folsom, MD
– Kihn M. Kiu, BS
– Mark Herzberg, DDS, PhD
• Ultrasound Specialists
– David Jacobs, PhD
– Tanja Rundek, MD, PhD
– Russell Luepker, MD, MS
• NOMASS Research Director
• University of Paris
– Bernadette Boden-Albala,
– Pierre-Jean Touboul, MD
DrPH, MPH
• Wake Forest University
• NOMASS Project Coordinator
– Ward Riley, PhD
– Janet de Rosa, MPH
• Periodontal Laboratory
Technicians
– Miriam S. Herrera-Abreu, BS
– Romanita S. Celenti, MS
• Predoctoral Fellow
– Ryan Demmer, MPH
