American Journal of Epidemiology Vol. 169, No.

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ª The Author 2009. Published by the Johns Hopkins Bloomberg School of Public Health. DOI: 10.1093/aje/kwn399
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Original Contribution

Is Maternal Periodontal Disease a Risk Factor for Preterm Delivery?

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Vitool Lohsoonthorn, Kajorn Kungsadalpipob, Prohpring Chanchareonsook,
Sompop Limpongsanurak, Ornanong Vanichjakvong, Sanutm Sutdhibhisal,
Nopmanee Wongkittikraiwan, Chulamanee Sookprome, Wiboon Kamolpornwijit,
Surasak Jantarasaengaram, Saknan Manotaya, Vatcharapong Siwawej, William E. Barlow,
Annette L. Fitzpatrick, and Michelle A. Williams

Initially submitted September 1, 2008; accepted for publication December 1, 2008.

Several studies have suggested an association between maternal periodontal disease and preterm delivery, but
this has not been a consistent finding. In 2006–2007, the authors examined the relation between maternal peri-
odontal disease and preterm delivery among 467 pregnant Thai women who delivered a preterm singleton infant
(<37 weeks’ gestation) and 467 controls who delivered a singleton infant at term (
37 weeks’ gestation). Peri-
odontal examinations were performed within 48 hours after delivery. Participants’ periodontal health status was
classified into 4 categories according to the extent and severity of periodontal disease. Logistic regression was
used to estimate odds ratios and 95% confidence intervals. Preterm delivery cases and controls were similar with
regard to mean probing depth, mean clinical attachment loss, and mean percentage of sites exhibiting bleeding on
probing. After controlling for known confounders, the authors found that severe clinical periodontal disease was not
associated with an increased risk of preterm delivery (odds ratio ¼ 1.20, 95% confidence interval: 0.67, 2.16). In
addition, there was no evidence of a linear increase in risk of preterm delivery or its subtypes associated with
increasing severity of periodontal disease (Ptrend > 0.05). The results of this case-control study do not provide
convincing evidence that periodontal disease is associated with preterm delivery or its subtypes among Thai
women.

periodontal diseases; premature birth

Abbreviations: CI, confidence interval; OR, odds ratio.

Preterm delivery continues to be one of the most signif-
icant unsolved problems of public health and perinatology
(1–3). Preterm infants are at elevated risk for mortality and
infant morbidity, including neurodevelopmental disabilities,
cognitive impairment, and behavioral disorders (4–6). Al-
though the pathophysiology of preterm delivery remains
unknown, accumulating evidence suggests that subclinical
infections and chronic inflammation may account for a ma-
jority of preterm deliveries. Some investigators have indi-
cated that infections are major causes of preterm deliveries,
responsible for 30%–50% of all cases (7, 8). Moreover,
there is increasing evidence that suggests that other infec-
tious processes occurring elsewhere in the body may con-
tribute to preterm delivery (9). Periodontal disease may be
one such infection (9).
Offenbacher et al. (10) were the first group of investiga-
tors to report a link between poor maternal periodontal
health and adverse pregnancy outcomes including preterm
delivery. This early finding has subsequently been corrobo-
rated by some (11–19), although not all (20–24), investiga-
tors. Two relatively large studies in the United Kingdom
failed to find an association between maternal periodontal
disease and risk of preterm delivery (21, 22). The reasons
for the differences in findings are unclear. In the United
States, associations between periodontal disease and pre-
term delivery appear to be stronger and more consistent in

Correspondence to Dr. Vitool Lohsoonthorn, Department of Preventive and Social Medicine, Faculty of Medicine, Chulalongkorn University, 1873
Rama 4 Road, Patumwan, Bangkok 10330, Thailand (e-mail: vitool@gmail.com).

731 Am J Epidemiol 2009;169:731–739

732 Lohsoonthorn et al.
studies that include higher proportions of subjects from
African-American racial/ethnic groups and subjects who
smoke during pregnancy (25, 26). Several investigators have
noted that positive associations were more commonly observed
in US studies where the proportion of African-American sub-
jects exceeded 60% (10–12).
Results from randomized clinical controlled trials have
also been inconsistent. Two relatively small studies have
suggested that treatment of periodontal disease during preg-
nancy may reduce the risk of preterm delivery (27, 28).
However, these findings were not subsequently confirmed
when reevaluated in a larger multicenter randomized trial
(29). Given the inconsistent findings across studies, and
given the emerging evidence suggesting that associations
may be influenced by population characteristics, we as-
sessed the relation between maternal periodontal disease
and the risk of preterm delivery among Thai women.
MATERIALS AND METHODS
Study population and selection of cases and controls
A case-control study was conducted among women who
delivered livebirths at King Chulalongkorn Memorial Hos-
pital, Rajavithi Hospital, and Police General Hospital,
Bangkok, Thailand, between July 2006 and November
2007. Cases were women with singleton pregnancies who
delivered before 37 completed weeks’ gestation (22–36
weeks’ gestation). Preterm delivery cases were identified
by daily monitoring of all new deliveries at postpartum
wards of participating hospitals. Of the 478 eligible cases
approached, 467 (97.7%) agreed to participate in the study.
Controls were women who delivered a singleton infant at
term (
37 weeks’ gestation) and were selected from the
same hospital of delivery. An eligible control, delivering
immediately after a case, was approached and recruited
for the study. Of the 482 eligible controls approached, 467
(96.9%) agreed to participate in the study.
All participants provided informed consent, and the
research protocol was reviewed and approved by ethics
committees at the Faculty of Medicine, Chulalongkorn
University, Rajavithi Hospital, and Police General Hospital,
as well as by the Institutional Review Board, Division of
Human Subjects Research, University of Washington.
Data collection
After obtaining informed consent, we asked the women to
participate in a 45-minute in-person interview in which
trained research personnel used a structured questionnaire
to elicit information regarding maternal sociodemography,
lifestyle habits, oral health history, and medical and repro-
ductive histories. Participants’ labor and delivery and pre-
natal medical records were reviewed by trained research
nurses who used a standardized abstraction form. Informa-
tion abstracted from medical records included participants’
prepregnancy weight, height, and blood pressure; pregnancy
complications; and condition of the newborn.
Study participants underwent a full-mouth periodontal
examination by 1 of the 6 trained and calibrated periodon-
tists who were blinded to case-control status. The weighted
kappa coefficients for measurements within 61 mm be-
tween each pair of examiners and within each examiner
ranged from 0.80 to 0.97 and from 0.79 to 1.00, respectively.
Periodontal examinations were performed at the bedside on
the postpartum wards by using mouth mirrors and manual
periodontal probes (North Carolina periodontal probe UNC-
15; Hu Friedy Manufacturing, Inc., Chicago, Illinois) with
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an external light source within 48 hours after delivery. Prob-
ing depth and recession were measured on all teeth except
for the third molar in 6 locations (mesiobuccal, midbuccal,
distobuccal, mesiolingual, midlingual, and distolingual).
These measurements were made in millimeters and were
rounded down to the whole millimeter. The level of clinical
attachment loss was calculated from probing depth and
recession, and it represented the distance from the cemento-
enamel junction to the base of the periodontal pocket. Plaque
and bleeding on probing were recorded dichotomously as
either present or absent. Bleeding on probing was determined
to be positive if hemorrhage occurred within 15 seconds after
probing. At the end of the periodontal examination, each
participant was given instructions regarding dental treatment
needs.
Analytical variable specification
Preterm delivery. The diagnosis of preterm delivery was
made by use of American College of Obstetricians and
Gynecologists (ACOG) guidelines (30). Gestational age
was based on the last menstrual period or ultrasound exam-
ination. If information on the last menstrual period and ul-
trasound dating (before 20 weeks’ gestation) were available
and the 2 agreed within 14 days, we used the former to
assign gestational age. If the 2 dates differed by more than
14 days, we used the ultrasound date. The ultrasonography
was available in 52.5% of preterm cases and 56.3% of term
controls. In order to account for possible heterogeneity in
the etiology of preterm delivery, we categorized preterm
delivery cases according to the 3 pathophysiologic groups
previously described (i.e., spontaneous preterm labor and
delivery, preterm premature rupture of membranes, and
medically indicated preterm delivery) (31, 32). We also cat-
egorized preterm delivery cases according to gestational age
at delivery (i.e., very preterm delivery (22–31 weeks), mod-
erate preterm delivery (32–33 weeks), and mild preterm
delivery (34–36 weeks)).
Maternal periodontal disease. Participants’ periodontal
health status was classified, a priori, into 4 categories ac-
cording to the extent and severity of periodontal disease by
using the following criteria advocated by Albandar (33):
severe periodontitis (2 or more nonadjacent teeth with in-
terproximal sites showing
6 mm of clinical attachment
loss and
4 mm of probing depth); moderate periodontitis
(2 or more nonadjacent teeth with interproximal sites show-
ing
5 mm of clinical attachment loss and
4 mm of prob-
ing depth); and mild periodontitis (1 or more teeth with
interproximal sites showing
4 mm of clinical attachment
loss and
4 mm of probing depth). Individuals who did not
fulfill any of the above criteria were classified as not having
detectable levels of periodontitis. We empirically evaluated
Am J Epidemiol 2009;169:731–739
 Maternal Periodontal Disease and Preterm Delivery 733

the extent to which associations between maternal periodon- Table 1. Characteristics of Study Members According to Preterm
tal disease and preterm delivery are dependent upon the Case and Control Status, Bangkok, Thailand, 2006–2007
various case definitions used to classify women’s periodon- Preterm
tal health status. Using a single data set (467 preterm Controls
Cases
Maternal Characteristics (n 5 467)
delivery cases and 467 term controls), we classified partic- (n 5 467)
ipants’ periodontal disease status using case definitions No. % No. %
advocated by the Centers for Disease Control and Prevention- Maternal age, years
American Academy of Periodontology Working Group (34),
63 13.5 81 17.3

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<20
Offenbacher et al. (13), Contreras et al. (35), Lopez et al. (36),
Radnai et al. (18), and Canakci et al. (37). 20–24 130 27.8 129 27.6
25–29 145 31.0 110 23.6
30–34 83 17.8 86 18.4
Statistical analysis

35 46 9.9 61 13.1
The distribution of maternal sociodemographic character- Maternal education, years
istics and medical and reproductive histories according to 6 153 32.8 155 33.2
preterm and term delivery status was examined. To estimate
7–12 282 60.4 278 59.5
the relative association between maternal periodontal dis-
ease and preterm delivery, we performed conditional logis- >12 32 6.9 34 7.3
tic regression procedures, taking into account the matching Marital status
of cases and controls for hospital of delivery, to calculate Married 231 49.5 229 49.0
maximum likelihood estimates of odds ratios and 95% con- Living with partner 219 46.9 208 44.5
fidence intervals, adjusted for potential confounding factors
Separated 17 3.6 30 6.4
(38, 39). We considered the following covariates as possible
confounders: maternal age, parity, marital status, maternal Parity
educational attainment, prepregnancy body mass index, on- Nulliparous 249 53.3 275 58.9
set of prenatal care, alcohol consumption, and smoking sta- Multiparous 218 46.7 192 41.1
tus during pregnancy. All postulated potential confounders Smoked during pregnancy
were adjusted and then deleted one-by-one in a stepwise Yes 8 1.7 12 2.6
approach until the odds ratio had changed from the fully
No 459 98.3 455 97.4
adjusted odds ratio by at least 10% (39). Variables of a priori
interest (e.g., maternal educational attainment, parity, alco- Alcohol use during
pregnancy
hol consumption, and smoking status during pregnancy)
were forced into final models. These analytical procedures Yes 22 4.7 16 3.4
were also used in stratified analyses designed to assess the No 445 95.3 451 96.6
risk of subtypes of preterm delivery (i.e., spontaneous pre- Prepregnancy body
term labor and delivery, preterm premature rupture of mem- mass index, kg/m2
branes, medically indicated preterm delivery, very preterm Underweight (<18.5) 80 17.6 119 26.9
delivery, moderate preterm delivery, and mild preterm de- Normal (18.5–24.9) 315 69.4 268 60.5
livery). All statistical analyses were performed with STATA, Overweight (25.0–29.9) 45 9.9 38 8.6
version 10.0, software (StataCorp LP, College Station,
Obesity (
30.0) 14 3.1 18 4.1
Texas). All reported P values are 2 tailed, and confidence
intervals were calculated at the 95% level. Onset of prenatal care
None 12 2.6 41 8.8
<14 weeks’ gestation 199 42.6 159 34.0
RESULTS
14 weeks’ gestation 256 54.8 267 57.2
Prior history of preterm
The maternal sociodemographic, medical, and reproduc- delivery
tive characteristics of preterm cases and term controls are
Yes 14 6.4 43 22.4
presented in Table 1. Overall, preterm cases and term con-
trols were similar with regard to maternal age, educational No 204 93.6 149 77.6
attainment, marital status, parity, smoking, and alcohol con- Not applicable (nulliparous) 249 275
sumption status. Preterm cases, however, were more likely
to report a history of previous preterm delivery, were more
likely to be underweight, and were less likely to have uti-
lized prenatal care services than were controls. with plaque (75.6% vs. 76.1%), and mean percentage of
As seen in Table 2, no clinically meaningful differences sites exhibiting bleeding on probing (35.6% vs. 36.1%).
were observed between preterm cases and controls with There were no clinically meaningful differences in the mean
regard to mean probing depth (2.41 vs. 2.46 mm), mean percentage of sites with periodontal probing depth
4 mm
clinical attachment loss (2.39 vs. 2.42 mm), mean number (10.4% vs. 10.7%) or clinical attachment loss
4 mm (9.8%
of missing teeth (1.19 vs. 1.24), mean percentage of sites vs. 9.7%).

Am J Epidemiol 2009;169:731–739
734 Lohsoonthorn et al.

Table 2. Periodontal Parameters Between Controls and Preterm Delivery Cases, Bangkok,
Thailand, 2006–2007

Controls (n 5 467) Preterm Cases (n 5 467)

Periodontal Parameters 95% 95%

Mean Confidence Mean Confidence
Interval Interval

Probing depth, mm 2.46 2.42, 2.49 2.41 2.37, 2.45

Clinical attachment loss, mm 2.42 2.38, 2.46 2.39 2.35, 2.44

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No. of missing teeth 1.24 1.08, 1.41 1.19 0.99, 1.39
Percent of sites with
Probing depth
4 mm 10.7 9.6, 11.8 10.4 9.3, 11.6
Clinical attachment loss
4 mm 9.7 8.5, 10.8 9.8 8.6, 11.0
Plaque 76.1 74.5, 77.8 75.6 73.9, 77.3
Exhibiting bleeding on probing 36.1 34.0, 38.2 35.6 33.4, 37.7

Participants’ periodontal health status was classified,
a priori, into 4 categories (i.e., periodontal healthy and mild,
moderate, and severe periodontitis) according to the extent
and severity of periodontal disease (33). We calculated odds
ratios for preterm delivery for each level of clinical peri-
odontal disease. Overall, we found very little evidence of an
association between maternal periodontal health status and
preterm delivery risk. Women with severe periodontitis, as
compared with periodontally healthy women, had only a 7%
increased risk of preterm delivery (odds ratio (OR) ¼ 1.07,
95% confidence interval (CI): 0.62, 1.85), and this was not
statistically significant. Adjustment for possible confound-
ing by maternal age, educational attainment, parity, prepreg-
nancy body mass index, alcohol consumption, and smoking
status did not substantially alter the magnitude of the ob-
served association (adjusted OR ¼ 1.20, 95% CI: 0.67,
2.16). In addition, there was no evidence of a linear increase
in risk of preterm delivery associated with increasing sever-
ity of periodontal disease (Ptrend ¼ 0.36) (Table 3).
Because results from prior studies suggest that there may
be some heterogeneity in the epidemiology of preterm de-
livery according to the pathophysiology and gestational age
of delivery (31, 32), we repeated the analyses allowing for
this possibility. As seen in Table 4, there was no clear evi-
dence of a positive association between maternal periodon-
tal disease and risk of spontaneous preterm delivery or risk
of preterm premature rupture of membrane. However, we
noted a weak, though statistically nonsignificant, associa-
tion between moderate (adjusted OR ¼ 1.37, 95% CI:
0.70, 2.69) and severe (adjusted OR ¼ 1.39, 95% CI:
0.60, 3.22) periodontitis and the risk of medically indicated
preterm delivery. The association between periodontal dis-
ease and severity of preterm delivery was also studied. After
controlling for known confounders, we found no clear evi-
dence of a positive association between maternal periodon-
tal disease and severity of preterm delivery (Table 5).
We next evaluated the extent to which the various case
definitions and criteria for diagnosis of periodontal disease
used in previous studies impacted the association between
maternal periodontal disease and risk of preterm delivery
(Figure 1). The magnitude and direction of associations
between maternal periodontal disease and preterm delivery
risk were largely similar when different periodontal disease
diagnostic criteria were utilized. When we used the criteria
advocated by Albandar (33), there was no statistically sig-
nificant association between severe periodontitis and pre-
term delivery risk (adjusted OR ¼ 1.20, 95% CI: 0.67,
2.16). The adjusted odds ratios of association between

Table 3. Odds Ratio and 95% Confidence Interval of Preterm Delivery According to Levels of Periodontal Disease, Bangkok, Thailand,
2006–2007

Preterm
Controls Unadjusted 95% Adjusted 95%
Levels of Periodontal Cases
(n 5 467) Odds Confidence Odds Confidence
Disease (n 5 467)
Ratio Interval Ratioa Interval
No. % No. %

Periodontal healthy 120 25.7 119 25.5 1.00 Referent 1.00 Referent
Mild periodontitis 241 51.6 230 49.3 0.96 0.70, 1.32 1.01 0.73, 1.41
Moderate periodontitis 74 15.8 84 18.0 1.14 0.76, 1.71 1.20 0.79, 1.84
Severe periodontitis 32 6.9 34 7.3 1.07 0.62, 1.85 1.20 0.67, 2.16
Ptrend ¼ 0.56 Ptrend ¼ 0.36
a
Adjusted for hospital of delivery, maternal age, educational attainment, parity, prepregnancy body mass index, alcohol consumption, and
smoking status during pregnancy.

Am J Epidemiol 2009;169:731–739
 Maternal Periodontal Disease and Preterm Delivery 735

Table 4. Odds Ratio and 95% Confidence Interval of Preterm Delivery Subtypes According to Levels of Periodontal Disease, Bangkok, Thailand,
2006–2007

Spontaneous Preterm Preterm Premature Rupture Medically Indicated Preterm

Controls Delivery (n 5 230) of Membrane (n 5 120) Delivery (n 5 117)
Levels of Periodontal
(N 5 467), 95% 95% 95%
Disease Odds Odds Odds
No. No. Confidence No. Confidence No. Confidence
Ratioa Ratioa Ratioa
Interval Interval Interval

Periodontal healthy 120 58 1.00 Referent 35 1.00 Referent 26 1.00 Referent

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Mild periodontitis 241 122 1.16 0.77, 1.75 57 0.86 0.51, 1.45 51 0.99 0.56, 1.76
Moderate periodontitis 74 38 1.25 0.72, 2.15 20 1.14 0.59, 2.21 26 1.37 0.70, 2.69
Severe periodontitis 32 12 1.21 0.54, 2.74 8 1.07 0.42, 2.70 14 1.39 0.60, 3.22
Ptrend ¼ 0.44 Ptrend ¼ 0.73 Ptrend ¼ 0.27
a
Adjusted for hospital of delivery, maternal age, educational attainment, parity, prepregnancy body mass index, alcohol consumption, and
smoking status during pregnancy.

severe periodontitis and preterm delivery were 1.21 (95%
CI: 0.61, 2.37) using the criteria of Offenbacher et al. (13),
1.07 (95% CI: 0.61, 1.85) using the criteria of Contreras
et al. (35), and 0.98 (95% CI: 0.57, 1.69) using the criteria
proposed by the Centers for Disease Control and Prevention-
American Academy of Periodontology Working Group (34).
DISCUSSION
We found no association between maternal periodontal
disease and preterm delivery among Thai women (OR ¼
1.20, 95% CI: 0.67, 2.16). In addition, we found no evidence
of a linear increase in risk of preterm delivery with increas-
ing severity of periodontal disease (Ptrend ¼ 0.36). Thus,
these results do not support the hypothesis that periodontal
disease is an independent risk factor of preterm delivery
among Thai women. Few studies have investigated associ-
ations between periodontal disease and adverse pregnancy
outcomes (e.g., preterm delivery, low birth weight, preterm
low birth weight) among Asians, and findings from these
studies are inconsistent. For instance, Dasanayake (14), in
a matched case-control study (n ¼ 55 pairs), reported that
Thai women with more healthy areas of gingiva, defined by
the Community Periodontal Index Treatment Need, had
a lower risk of giving birth to a low birth weight infant
(OR ¼ 0.30, 95% CI: 0.12, 0.72). In contrast, Buduneli
et al. (20), in their study of 53 preterm low birth weight
cases and 128 term controls in Turkey, found no statistically
significant differences between preterm low birth weight
cases and controls with regard to maternal dental and peri-
odontal parameters.
Results from previous observational studies and random-
ized clinical controlled trials conducted in other populations
have also been inconsistent. The reasons for these inconsis-
tencies are unclear. Xiong et al. (26), in their systematic
review of periodontal disease and adverse pregnancy out-
comes, suggested that the effects of periodontal disease on
adverse pregnancy outcomes may be different according to
maternal socioeconomic status and access to dental care.
North and South American studies that include high propor-
tions of subjects from African-American ethnic groups and
subjects from economically disadvantaged families (10–13)
tend to more consistently document statistically significant
associations between maternal periodontal disease and the
risk of preterm delivery. In contrast, most studies conducted
in European countries, where their citizens are offered

Table 5. Odds Ratio and 95% Confidence Interval of Mild, Moderate, and Very Preterm Delivery According to Levels of Periodontal Disease,
Bangkok, Thailand, 2006–2007

Mild Preterm Delivery Moderate Preterm Delivery Very Preterm Delivery

Controls (34–36 Weeks) (n 5 305) (32–33 Weeks) (n 5 84) (22–31 Weeks) (n 5 78)
Levels of Periodontal
(N 5 467), 95% 95% 95%
Disease Odds Odds Odds
No. No. Confidence No. Confidence No. Confidence
Ratioa Ratioa Ratioa
Interval Interval Interval

Periodontal healthy 120 70 1.00 Referent 22 1.00 Referent 27 1.00 Referent

Mild periodontitis 241 165 1.30 0.90, 1.89 39 0.72 0.39, 1.35 26 0.50 0.26, 0.96
Moderate periodontitis 74 50 1.32 0.81, 2.15 17 0.99 0.46, 2.13 17 1.16 0.55, 2.44
Severe periodontitis 32 20 1.28 0.65, 2.50 6 0.87 0.30, 2.53 8 1.19 0.43, 3.28
Ptrend ¼ 0.30 Ptrend ¼ 0.95 Ptrend ¼ 0.57
a
Adjusted for hospital of delivery, maternal age, educational attainment, parity, prepregnancy body mass index, alcohol consumption, and
smoking status during pregnancy.

Am J Epidemiol 2009;169:731–739
736 Lohsoonthorn et al.
Figure 1. Odds ratios and 95% confidence intervals of preterm delivery in relation to periodontal disease defined by various case definitions,
Bangkok, Thailand, 2006–2007. Odds ratios were adjusted for hospital of delivery, maternal age, educational attainment, parity, prepregnancy
body mass index, alcohol consumption, and smoking status during pregnancy. AAP, American Academy of Periodontology; CDC, Centers for
Disease Control and Prevention.
universal health care, fail to document positive associations
between maternal periodontal disease and preterm delivery
(21–23). For instance, Davenport et al. (21), in their case-
control study of 236 preterm low birth weight cases and 507
term controls in the United Kingdom, found no positive
association between maternal periodontal disease and the
risk of preterm low birth weight after controlling for con-
founding. Moore et al. (22), in their large prospective study
of 3,738 women in the United Kingdom, found no signifi-
cant association between the severity of periodontal disease
and the risk of either preterm delivery or low birth weight.
The lack of consistency raises the possibility that previ-
ously observed associations are noncausal. Vergnes and
Sixou (40), in their meta-analysis of the association between
maternal periodontal disease and preterm low birth weight,
suggested that periodontal disease may not cause preterm
delivery, but there may be some underlying mechanism such
as a genetic predisposition for a hyperinflammatory re-
sponse causing both periodontal disease and preterm deliv-
ery. Alternatively, associations between clinical periodontal
disease and preterm delivery may be evident only in some
susceptible populations, made so by the presence of other
environmental or genetic risk factors. For example, differ-
ences in the distribution and virulence of specific periodon-
tal pathogens may contribute to heterogeneity across
studies. This thesis is supported by studies documenting
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differences in the periodontal pathogens detected across
populations sampled from diverse geographic locations
(41–43). Future studies that investigate specific character-
istics of the types and virulence of periodontal pathogens
may help to move this literature forward.
Periodontal pathogens are thought to gain access to feto-
placental tissues via blood-borne pathways and then are
thought to elicit inflammatory and prostaglandin cascades
(44–47) that precipitate preterm labor. However, few inves-
tigators have isolated periodontal pathogens in the fetopla-
cental tissues collected after preterm labor and delivery.
Goepfert et al. (11), in their study of 59 preterm delivery
cases and 44 controls, isolated periodontal pathogens in
only 2 of 59 preterm placentas and in only 3 of 44 term
placentas. Similarly, despite isolating periodontal pathogens
in dental plaques collected from women who delivered pre-
term and who had periodontitis, Dortbudak et al. (15) failed
to isolate microorganisms in amniotic fluid. Yet other inves-
tigators have postulated that periodontal disease may pro-
mote preterm delivery via mechanisms that involve chronic
diffuse endothelial dysfunction and inflammation secondary
to oral infections (48–50). Further studies are needed to
more thoroughly explore these mechanistic hypotheses, par-
ticularly in those populations where associations between
periodontal disease and preterm delivery have been consis-
tently observed (i.e., African Americans).
Am J Epidemiol 2009;169:731–739

This study has several strengths, including the relatively
large sample of preterm delivery cases and controls and the
fact that we used only well-trained, calibrated, and blinded
periodontists to examine all participants. The high partici-
pation rates for cases and controls (97.7% and 96.9%) also
served to attenuate concerns about selection bias. Several
limitations, however, should be considered when interpret-
ing results from our study. First, an unavoidable short-
coming of the case-control design is that controls were
evaluated for periodontal parameters at a time when they
were not at risk for preterm delivery. Comparing periodon-
tal parameters in women delivering preterm with the same
parameters assessed at term may produce potential bias if
the periodontal parameters change rapidly during the third
trimester of pregnancy. However, accumulating evidence
suggests that progression of attachment loss occurs slowly
with progression rates varying between 0.02 and 0.24 mm/
year (51–53). Additionally, Gürsoy et al. (54), in their study
of clinical changes in the periodontium during pregnancy,
reported that there was no change in clinical attachment loss
during pregnancy. Collectively, these data suggest that the
magnitude of bias is likely to be small. Second, our study
did not specifically characterize the pathobiology of oral
infection (i.e., bacterial counts or antibody levels to peri-
odontal pathogens). Although the full-mouth recording of
periodontal parameters used in our study has been shown to
be more effective in determining periodontal disease, sev-
eral authors suggested that clinical measures of periodonti-
tis may not adequately represent the systemic burden of
periodontal disease (55, 56). Because the clinical signs of
periodontal disease are a result of periodontal pathogens
interacting with the host’s immune and inflammatory re-
sponse, it is likely that including measurements of this in-
teraction between microorganisms and maternal host
response may provide a means to more fully characterize
the exposure that we think of as periodontal disease (57).
Third, 52.5% of preterm cases and 56.3% of term controls
had a sonographically confirmed gestational length. Given
concerns about errors in gestational age based on the last
menstrual period, we completed subanalyses restricted to
pregnancies with sonographically confirmed gestational
age. The results from these restricted analyses were not
materially different from those analyses reported for the
entire study populations in Table 3. The adjusted odds ratios
for preterm delivery among women with sonographically
confirmed gestational age were 1.04 (95% CI: 0.67, 1.62),
1.26 (95% CI: 0.70, 2.26), and 1.22 (95% CI: 0.54, 2.75) for
mild, moderate, and severe periodontitis, respectively.
Fourth, although we adjusted for many potential confound-
ers, we cannot exclude the possibility that some residual
confounding by factors not measured in our study (e.g.,
urinary tract infection, bacterial vaginosis, chorioamnioni-
tis) may have influenced the reported risk estimates. Fifth,
some authors have argued that failure to assess effect mod-
ification by smoking may contribute to variation in the re-
sults across studies (58, 59). However, the prevalence of
cigarette smoking during pregnancy among Thai women
was very low (<3%). We did not have sufficient statistical
power to evaluate the association between periodontal dis-
ease and the risk of preterm delivery among women who
Am J Epidemiol 2009;169:731–739
Maternal Periodontal Disease and Preterm Delivery 737
smoked during pregnancy. Finally, our study was designed
to have 95% statistical power to detect a 1.80-fold increase
in preterm delivery risk associated with maternal periodon-
tal disease. Although we consider it unlikely that limited
power could be responsible for our null findings, we cannot
rule out the likelihood of missing weaker associations or
associations that may be present only among specific pre-
term delivery subtypes.
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In conclusion, the results of this case-control study do not
provide convincing evidence that periodontal disease is as-
sociated with preterm delivery or preterm delivery subtypes
among Thai women. Future studies that investigate specific
characteristics of periodontal pathogens, as well as maternal
immune and inflammatory responses, may help to move this
literature forward.
ACKNOWLEDGMENTS
Author affiliations: Department of Preventive and Social
Medicine, Faculty of Medicine, Chulalongkorn University,
Bangkok, Thailand (Vitool Lohsoonthorn); Department of
Periodontology, Faculty of Dentistry, Chulalongkorn Uni-
versity, Bangkok, Thailand (Kajorn Kungsadalpipob,
Ornanong Vanichjakvong, Sanutm Sutdhibhisal); Depart-
ment of Dentistry, Rajavithi Hospital, Bangkok, Thailand
(Prohpring Chanchareonsook, Nopmanee Wongkittikraiwan,
Chulamanee Sookprome); Department of Obstetrics and
Gynecology, Faculty of Medicine, Chulalongkorn University,
Bangkok, Thailand (Sompop Limpongsanurak, Saknan
Manotaya); Department of Obstetrics and Gynecology,
Rajavithi Hospital, Bangkok, Thailand (Wiboon
Kamolpornwijit, Surasak Jantarasaengaram); Department
of Obstetrics and Gynecology, Police General Hospital,
Bangkok, Thailand (Vatcharapong Siwawej); Department
of Biostatistics, School of Public Health and Community
Medicine, University of Washington, Seattle, Washington
(William E. Barlow); and Department of Epidemiology,
School of Public Health and Community Medicine,
University of Washington, Seattle, Washington (Vitool
Lohsoonthorn, Annette L. Fitzpatrick, Michelle A. Williams).
This research was supported by the Rachadapiseksompoj
Faculty of Medicine Research Fund (RA 20/49), Chulalong-
korn University, and the Multidisciplinary International
Research Training (MIRT) Program of the School of Public
Health and Community Medicine, University of Washing-
ton. The MIRT Program is supported by an award from the
National Center on Minority Health and Health Disparities,
National Institutes of Health (T37-MD001449).
The authors wish to thank all the staff nurses at King
Chulalongkorn Memorial Hospital, Rajavithi Hospital, and
the Police General Hospital in Bangkok, Thailand, for their
assistance in data collection.
This research was done as partial fulfillment for the re-
quirements of a Ph.D. degree by one of the authors (V. L.) in
the Department of Epidemiology, School of Public Health
and Community Medicine, University of Washington, Seat-
tle, Washington.
Conflict of interest: none declared.
738 Lohsoonthorn et al.
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